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Hiromu Kawasaki - One of the best experts on this subject based on the ideXlab platform.
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acute hyperglycemia and hyperinsulinemia enhance Adrenergic vasoconstriction and decrease calcitonin gene related peptide containing Nerve mediated vasodilation in pithed rats
Hypertension Research, 2008Co-Authors: Yoshito Zamami, Shingo Takatori, Kousuke Yamawaki, Satoko Miyashita, Mitsunobu Mio, Yoshihisa Kitamura, Hiromu KawasakiAbstract:Recent clinical studies have demonstrated that transient postprandial hyperglycemia and hyperinsulinemia may contribute to the development of hypertension. Therefore, we investigated the influence of acute hyperglycemia and/or hyperinsulinemia induced by glucose or insulin infusion on neuronal and humoral control of vascular tone in rats. Euglycemic male Wistar rats were pithed under anesthesia and arterial blood pressure was measured. Changes in vascular responses to spinal cord stimulation (SCS) and intravenous bolus injections of noradrenaline, angiotensin II, calcitonin gene-related peptide (CGRP), acetylcholine and sodium nitroprusside (SNP) were studied by infusing various concentrations of glucose or insulin. Continuous glucose infusion, which increased both blood glucose and serum insulin levels, significantly augmented Adrenergic Nerve-mediated pressor responses to SCS without affecting pressor responses to injection of noradrenaline or angiotensin II. In pithed rats with artificially increased blood pressure and blockade of autonomic outflow, glucose infusion attenuated CGRPergic Nerve-depressor responses to SCS without affecting depressor responses to injection of CGRP, acetylcholine or SNP. In pithed rats treated with octreotide, which increased blood glucose without increasing serum insulin levels, glucose infusion caused only significant augmentation of Adrenergic Nerve-mediated pressor responses. Combined infusion of insulin and glucose, which resulted in increased serum insulin levels with euglycemia, significantly augmented Adrenergic Nerve-mediated pressor responses and attenuated CGRPergic Nerve-mediated depressor responses. The present results suggest that acute hyperglycemia and hyperinsulinemia increase Adrenergic Nerve-mediated vasoconstriction, which in turn blunts CGRPergic Nerve function, and that the increase in plasma insulin concentration associated with hyperglycemia may be responsible for the alteration of neuronal vascular regulation.
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effect of postprandial hyperglycemia and hyperinsulinemia on vascular responsiveness
Yakugaku Zasshi-journal of The Pharmaceutical Society of Japan, 2008Co-Authors: Yoshito Zamami, Shingo Takatori, Yukiko Iwatani, Kousuke Yamawaki, Satoko Miyashita, Nana Yabumae, Fusako Takayama, Mitsunobu Mio, Hiromu KawasakiAbstract:Recent clinical studies demonstrated that transient postprandial hyperglycemia and hyperinsulinemia may contribute to the development of hypertension. Therefore, we investigated influence of acute hyperglycemia and/or hyperinsulinemia induced by glucose or insulin infusion on neuronal and humoral control of vascular tone in rats. Euglycemic male Wistar rats were pithed under anesthesia and arterial blood pressure was measured. Changes in vascular responses to spinal cord stimulation (SCS) and intravenous bolus injections of noradrenaline, angiotensin II, calcitonin gene-related peptide (CGRP), acetylcholine and sodium nitroprusside (SNP) were studied by infusing various concentration of glucose or insulin. Continuous glucose infusion, which increased both blood glucose and serum insulin levels, significantly augmented Adrenergic Nerve-mediated pressor responses to SCS without affecting injection of pressor responses to noradrenaline or angiotensin II. In pithed rats with artificially increased blood pressure and blockade of autonomic outflow, glucose infusion attenuated CGRPergic Nerve-depressor responses to SCS without affecting depressor responses to injection of CGRP, acetylcholine or SNP. In pithed rats treated with octreotide, which increased blood glucose without increasing serum insulin levels, glucose infusion caused only significant augmentation of Adrenergic Nerve-mediated pressor responses. Combined infusion of insulin and glucose, which resulted in increased serum insulin levels with euglycemic, significantly augmented Adrenergic Nerve-mediated pressor responses and attenuated CGRPergic Nerve-mediated depressor responses. The present results suggest that acute hyperglycemia and hyperinsulinemia increases Adrenergic Nerve-mediated vasoconstriction, which is partly associated with the blunted CGRPergic Nerve function, and that plasma insulin concentration associated with hyperglycemia may be responsible for alteration of neuronal vascular regulation.
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α3β4 nicotinic receptors mediate Adrenergic Nerve and peptidergic cgrp Nerve dependent vasodilation induced by nicotine in rat mesenteric arteries
British Journal of Pharmacology, 2007Co-Authors: Shinji Eguchi, Satoko Miyashita, Yoshihisa Kitamura, Hiromu KawasakiAbstract:Background and purpose: Previous studies demonstrated that nicotine-induced endothelium-independent vasodilation is mediated by perivascular Adrenergic Nerves and Nerves releasing calcitonin gene-related peptide (CGRPergic Nerves). We characterized the nicotinic acetylcholine (ACh) receptor subtype underlying the vasodilation in response to nicotine in rat mesenteric arteries. Experimental approach: Rat mesenteric vascular beds without endothelium were contracted by perfusion with Krebs solution containing methoxamine and the perfusion pressure was measured with a pressure transducer. Key results: Perfusion of nicotine (1–100 μM) for 1 min caused a concentration-dependent decrease in perfusion pressure due to vasodilation. Perfusion of (±)-epibatidine (1–100 nM) (non-selective agonist) or (−)-cytisine (1–100 μM) (partial agonist for nicotinic β2 subtype and full agonist for nicotinic β4 subtype) induced vasodilation in a concentration-dependent manner. Vasodilation induced by nicotine, (−)-cytisine- and (±)-epibatidine was markedly attenuated by guanethidine (5 μM) and pretreatment with capsaicin (1 μM). Mecamylamine (relatively selective antagonist for α3β4 subtype), but not dihydro-β-erythroidine (selective antagonist for α4β2 subtype) or α-bungarotoxin (selective antagonist for α7 subtype), markedly inhibited nicotine-induced vasodilation. Nicotine-induced vasodilation was inhibited by methyllycaconitine at high concentrations (>1 μM), which non-selectively antagonize nicotinic receptors, while a low concentration of 10 nM, which selectively antagonizes α7 subtype, had no effect. (−)-Cytisine and (±)-epibatidine-induced vasodilation were abolished by mecamylamine Conclusion and implications: These results suggest that the nicotinic α3β4 receptor subtype, but not the α7 and α4β2 subtypes, is responsible for the vasodilation in rat mesenteric arteries induced by nicotine- and nicotinic ACh receptor agonists through stimulation of Adrenergic and CGRPergic perivascular Nerves. British Journal of Pharmacology (2007) 151, 1216–1223. doi:10.1038/sj.bjp.0707331
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chronic hyperinsulinemia enhances Adrenergic vasoconstriction and decreases calcitonin gene related peptide containing Nerve mediated vasodilation in pithed rats
Hypertension Research, 2006Co-Authors: Yuji Kurosaki, Yoshito Zamami, Shingo Takatori, Mitsunobu Mio, Hiromu KawasakiAbstract:The present study investigated the influence of chronic hyperinsulinemia on vascular responsiveness induced by Adrenergic Nerves and calcitonin gene-related peptide-containing (CGRPergic) Nerves in pithed rats with insulin resistance. Male Wistar rats (6 weeks old) received 15% fructose solution in drinking fluid for 10 weeks (fructose-drinking rats: FDR), which resulted in significant increases in plasma levels of insulin, total cholesterol and triglyceride, and systolic blood pressure, as compared with control rats. Pithed FDR showed greater Adrenergic Nerve-mediated pressor response to spinal cord stimulation (SCS) at the lower thoracic vertebra (Th 9-12) and pressor response to exogenous noradrenaline than control rats. In pithed FDR with blood pressure artificially increased by continuous infusion of methoxamine and blockade of autonomic ganglia by hexamethonium, CGRPergic Nerve-mediated depressor responses to SCS were significantly smaller than those in control rats, but depressor responses to other vasodilators such as acetylcholine, CGRP and sodium nitroprusside were similar to those in control rats. These results suggest that chronic hyperinsulinemia in FDR facilitates Adrenergic Nerve-mediated vasoconstriction, which is associated with attenuated CGRPergic Nerve-mediated vasodilation.
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vanilloid receptors mediate Adrenergic Nerve and cgrp containing Nerve dependent vasodilation induced by nicotine in rat mesenteric resistance arteries
British Journal of Pharmacology, 2004Co-Authors: Shinji Eguchi, Satoko Tezuka, Narumi Hobara, Shinji Akiyama, Yuji Kurosaki, Hiromu KawasakiAbstract:Previous studies showed that nicotine induces Adrenergic Nerve-dependent vasodilation that is mediated by endogenous calcitonin gene-related peptide (CGRP) released from CGRP-containing (CGRPergic) Nerves. The mechanisms underlying the nicotine-induced vasodilation were further studied. Rat mesenteric vascular beds without endothelium were contracted by perfusion with Krebs solution containing methoxamine, and the perfusion pressure was measured with a pressure transducer. Perfusion of nicotine (1–100 μM) for 1 min caused concentration-dependent vasodilation. Capsazepine (vanilloid receptor-1 antagonist; 1–10 μM) and ruthenium red (inhibitor of vanilloid response; 1–30 μM) concentration-dependently inhibited the nicotine-induced vasodilation without affecting the vasodilator response to exogenous CGRP. Nicotine-induced vasodilation was not inhibited by treatment with 3,4-dihydroxyphenylalanine (DOPA) receptor antagonist (L-DOPA cyclohexyl ester; 0.001–10 μM), dopamine D1 receptor-selective antagonist (SCH23390; 1–10 μM), dopamine D2 receptor antagonist (haloperidol; 0.1–0.5 μM), ATP P2x receptor-desensitizing agonist (α,β-methylene ATP; 1–10 μM), adenosine A2 receptor antagonist (8(p-sulfophenyl)theophylline; 10–50 μM) or neuropeptide Y (NPY)-Y1 receptor antagonist (BIBP3226; 0.1–0.5 μM). Immunohistochemical staining of the mesenteric artery showed dense innervation of CGRP- and vanilloid receptor-1-positive Nerves, with both immunostainings appearing in the same neuron. The mesenteric artery was also densely innervated by NPY-positive Nerves. Double immunostainings showed that both NPY and CGRP immunoreactivities appeared in the same neuron of the artery. These results suggest that nicotine acts on presynaptic nicotinic receptors to release Adrenergic neurotransmitter(s) or related substance(s), which then stimulate vanilloid receptor-1 on CGRPergic Nerves, resulting in CGRP release and vasodilation. British Journal of Pharmacology (2004) 142, 1137–1146. doi:10.1038/sj.bjp.0705773
Sue P. Duckles - One of the best experts on this subject based on the ideXlab platform.
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Adrenergic Nerve Smooth Endoplasmic Reticulum Calcium Buffering Declines with Age
Neurobiology of Aging, 1998Co-Authors: Henry Tsai, W. J. Pottorf, John N. Buchholz, Sue P. DucklesAbstract:Calcium buffering capacity declines with age in sympathetic Nerves of rat tail artery. To test whether smooth endoplasmic reticulum (SER) calcium buffering declines with age, effects of two SER calcium-ATPase inhibitors on norepinephrine release and intracellular calcium were determined. Thapsigargin or cyclopiazonic acid caused a significant increase in stimulation-evoked norepinephrine release from 6 month tail arteries with much less effect in 20 months. In isolated superior cervical ganglion cells, the rate of rise of calcium with K+-depolarization increased only in young cells with either cyclopiazonic acid or thapsigargin, with no effect in the old. In young cells, cyclopiazonic acid significantly influenced time to peak, rate of decline, and time to basal of K+-evoked calcium transients, but had no effect in old cells. Thapsigargin caused a significant increase in rate of decline in young, but not old, cells. These differential effects suggest an age-related decline in function of SER calcium buffering mechanisms in the sympathetic nervous system causing older Nerves to become more reliant on mitochondria to buffer calcium.
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ovariectomy eliminates sex differences in rat tail artery response to Adrenergic Nerve stimulation
American Journal of Physiology-heart and Circulatory Physiology, 1997Co-Authors: Diana N. Krause, Suzanne Doolen, Sue P. DucklesAbstract:The influence of gonadal hormones on vasoconstrictor responses to Adrenergic Nerve stimulation was investigated by comparing tail arteries from intact and gonadectomized male and female Fisher 344 rats. Arterial ring segments from females were significantly less responsive to transmural Nerve stimulation (1-8 Hz) than arteries from age-matched males. Significant male-female differences persisted after correcting the contractile responses for sex-related differences in arterial mass, optimal resting tension, and maximal contractile force. Arteries were taken from cycling, intact females in either proestrus, estrus, metestrus, or diestrus, but no significant differences were found among the four stages for vasoconstrictor responses to either Adrenergic Nerve stimulation or exogenous norepinephrine. These data suggest Adrenergic function in the artery is not affected by hormonal variations during the estrous cycle. After bilateral ovariectomy, however, contractile responses of female arteries to Adrenergic Nerve stimulation were increased to levels similar to those observed in male arteries. Orchidectomy of males, in contrast, had no effect on neural-evoked contraction. Low concentrations of norepinephrine also produced greater contractile responses in male compared with female arteries; however, this sex-related difference was eliminated by orchidectomy but not ovariectomy. Taken together, the results indicate that circulating gonadal hormones contribute to gender differences observed in rat tail artery. Vasoconstrictor responses to exogenous norepinephrine appear to be enhanced by testicular hormones. In contrast, vasoconstriction induced by Adrenergic Nerve stimulation appears to be influenced by chronic exposure to circulating ovarian hormones, resulting in a smaller vascular response in female arteries.
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Melatonin receptors mediate potentiation of contractile responses to Adrenergic Nerve stimulation in rat caudal artery
European journal of pharmacology, 1995Co-Authors: Diana N. Krause, Victor E. Barrios, Sue P. DucklesAbstract:Abstract The hormone melatonin potentiated contractile responses to Adrenergic Nerve stimulation in isolated ring segments of rat caudal artery. This effect was inhibited by the melatonin receptor antagonist luzindole but not by the serotonin 5-HT 2 receptor antagonist ketanserin. Melatonin had no direct effects on vascular tone. Melatonin agonists potentiated contractile responses with a relative order of potency (2-iodomelatonin, EC 50 = 0.6 nM; melatonin, EC 50 = 4.7 nM; N -acetylserotonin, EC 50 = 1.5 μM) that is consistent with the melatonin ML 1 receptor subtype. Melatonin also potentiated contractions elicited by exogenous norepinephrine and produced its effects in the absence of an intact endothelium. These data suggest that melatonin acts on receptors in the smooth muscle. The caudal artery provides a useful functional assay for pharmacological analysis of melatonin receptors. Physiologically, melatonin may activate its receptors at night to influence thermoregulation in the rat by enhancing the effects of sympathetic input to the caudal artery.
Daniela Cavallotti - One of the best experts on this subject based on the ideXlab platform.
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Adrenergic Nerve fibres and mast cells correlation in rat thymus
Immunology Letters, 2002Co-Authors: M Artico, Carlo Cavallotti, Daniela CavallottiAbstract:The interactions between Adrenergic Nerve fibres and mast cells (MCs) were studied in the thymus of adult and old rats by morphological methods and by quantitative analysis of images (QAIs). The whole thymus was drawn in adult (12 months old) rats: normal, sympathectomized or electrostimulated. Thymuses from the above-mentioned animals were weighed, measured and dissected. Thymic slices were stained with eosin orange for detection of microanatomical details and with Bodian's method for identification of the whole Nerve fibres. Thymic MCs were stained with Astrablau. Histofluorescence microscopy was used for staining of Adrenergic Nerve fibres. Finally, all morphological results were submitted to the QAIs and statistical analysis of data. Our results suggest that after surgical sympathectomy, the greater part of Adrenergic Nerve fibres disappear while related MCs appear to show less evident fluorescence and few granules. On the contrary, electrostimulation of the cervical superior ganglion induced an increase in the fluorescence of Adrenergic Nerve fibres and of related MCs.
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occurrence of Adrenergic Nerve fibers in human thymus during immune response
Neurochemistry International, 2002Co-Authors: Daniela Cavallotti, M Artico, Gian Domenico Iannetti, Carlo CavallottiAbstract:The Adrenergic Nerve fibers (ANF), the neuropeptide Y-like immunoreactive Nerve fibers (NPY-NF) and the noradrenaline (NA) amount were studied in the human thymus in subjects previously treated or not treated with interferon therapy with the aim to identify the changes due to the interferon therapy. This therapy has been used in patients affected by multiple sclerosis (MS). Biochemical and morphological methods were used associated with quantitative analysis of images. The whole thymuses were removed during autopsies in young and adult patients not treated with interferon. Moreover, samples of thymus were removed from patients, either young or adult who had previously been treated with interferon therapy, and subjected, for diagnostic reasons, to thymic biopsy. All samples of thymus were weighed, measured and dissected. Thymic slices were stained with Eosin-orange for detection of the microanatomical details, or with Bodian's reaction for recognition of nervous structures. Histofluorescence microscopy was used for detection of ANF, and immunofluorescence microscopy for recognition of NPY-like immunoreactive structures. All morphological results were subjected to quantitative analysis of images. Noradrenaline contained in thymic structures was measured by biochemical methods. Our results only concerned the effects of the therapy and suggested that treatment with interferon therapy induces many changes in the thymic structures: (1) The protein content of thymus is significantly increased; (2) the NA content in the thymus is also significantly increased; (3) NPY-like immunoreactive structures in the thymus are significantly increased; (4) occurrence of NPY-like immunoreactivity is particularly and significantly increased both in thymic microenvironment and in structures resembling Nerve fibers; (5) ANF are significantly increased in the same thymic structures in which NPY-like immunoreactivity is also increased (i.e. thymic microenvironment and structures resembling Nerve fibers). The morphological and biochemical changes observed can also explain the immunological changes induced in the thymus after immunostimulating therapy.
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occurrence of Adrenergic Nerve fibers and of noradrenaline in thymus gland of juvenile and aged rats
Immunology Letters, 1999Co-Authors: Carlo Cavallotti, M Artico, Daniela CavallottiAbstract:Adrenergic Nerve fibers (ANF) were studied in juvenile, adult and old rats by biochemical and morphological methods and by quantitative analysis of images (QAI). After chemical sympathectomy with neurotoxin 6-OH dopamine, the greater part of ANF disappeared. The whole thymus was drawn in juvenile normal or sympathectomized rats, in adult normal or sympathectomized rats and in old normal or sympathectomized rats. Thymuses from the above-mentioned animals were weighed, measured and dissected. Thymic slices were stained with eosin orange for the detection of the microanatomical details and with Bodian's method for the recognition of the whole Nerve fibers. Histofluorescence microscopy was used for staining of ANF while immunofluorescence microscopy was employed for staining of neuropeptide Y (NPY)-like immunoreactivity. Biochemical dosage of proteins and of noradrenaline amount was performed. Finally, all morphological results were subjected to QAI. Our results suggest that: (1) total innervation of the thymus increases with age; (2) ANF do not change with age; (3) the content of noradrenaline in the thymus increases with age; and (4) NPY-like immunoreactive structures in the thymus decrease with age. Biochemical results are in accordance with the morphological ones and both are confirmed by means of QAI. The probable function of sympathetic innervation of rat thymus is also discussed.
Shingo Takatori - One of the best experts on this subject based on the ideXlab platform.
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acute hyperglycemia and hyperinsulinemia enhance Adrenergic vasoconstriction and decrease calcitonin gene related peptide containing Nerve mediated vasodilation in pithed rats
Hypertension Research, 2008Co-Authors: Yoshito Zamami, Shingo Takatori, Kousuke Yamawaki, Satoko Miyashita, Mitsunobu Mio, Yoshihisa Kitamura, Hiromu KawasakiAbstract:Recent clinical studies have demonstrated that transient postprandial hyperglycemia and hyperinsulinemia may contribute to the development of hypertension. Therefore, we investigated the influence of acute hyperglycemia and/or hyperinsulinemia induced by glucose or insulin infusion on neuronal and humoral control of vascular tone in rats. Euglycemic male Wistar rats were pithed under anesthesia and arterial blood pressure was measured. Changes in vascular responses to spinal cord stimulation (SCS) and intravenous bolus injections of noradrenaline, angiotensin II, calcitonin gene-related peptide (CGRP), acetylcholine and sodium nitroprusside (SNP) were studied by infusing various concentrations of glucose or insulin. Continuous glucose infusion, which increased both blood glucose and serum insulin levels, significantly augmented Adrenergic Nerve-mediated pressor responses to SCS without affecting pressor responses to injection of noradrenaline or angiotensin II. In pithed rats with artificially increased blood pressure and blockade of autonomic outflow, glucose infusion attenuated CGRPergic Nerve-depressor responses to SCS without affecting depressor responses to injection of CGRP, acetylcholine or SNP. In pithed rats treated with octreotide, which increased blood glucose without increasing serum insulin levels, glucose infusion caused only significant augmentation of Adrenergic Nerve-mediated pressor responses. Combined infusion of insulin and glucose, which resulted in increased serum insulin levels with euglycemia, significantly augmented Adrenergic Nerve-mediated pressor responses and attenuated CGRPergic Nerve-mediated depressor responses. The present results suggest that acute hyperglycemia and hyperinsulinemia increase Adrenergic Nerve-mediated vasoconstriction, which in turn blunts CGRPergic Nerve function, and that the increase in plasma insulin concentration associated with hyperglycemia may be responsible for the alteration of neuronal vascular regulation.
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effect of postprandial hyperglycemia and hyperinsulinemia on vascular responsiveness
Yakugaku Zasshi-journal of The Pharmaceutical Society of Japan, 2008Co-Authors: Yoshito Zamami, Shingo Takatori, Yukiko Iwatani, Kousuke Yamawaki, Satoko Miyashita, Nana Yabumae, Fusako Takayama, Mitsunobu Mio, Hiromu KawasakiAbstract:Recent clinical studies demonstrated that transient postprandial hyperglycemia and hyperinsulinemia may contribute to the development of hypertension. Therefore, we investigated influence of acute hyperglycemia and/or hyperinsulinemia induced by glucose or insulin infusion on neuronal and humoral control of vascular tone in rats. Euglycemic male Wistar rats were pithed under anesthesia and arterial blood pressure was measured. Changes in vascular responses to spinal cord stimulation (SCS) and intravenous bolus injections of noradrenaline, angiotensin II, calcitonin gene-related peptide (CGRP), acetylcholine and sodium nitroprusside (SNP) were studied by infusing various concentration of glucose or insulin. Continuous glucose infusion, which increased both blood glucose and serum insulin levels, significantly augmented Adrenergic Nerve-mediated pressor responses to SCS without affecting injection of pressor responses to noradrenaline or angiotensin II. In pithed rats with artificially increased blood pressure and blockade of autonomic outflow, glucose infusion attenuated CGRPergic Nerve-depressor responses to SCS without affecting depressor responses to injection of CGRP, acetylcholine or SNP. In pithed rats treated with octreotide, which increased blood glucose without increasing serum insulin levels, glucose infusion caused only significant augmentation of Adrenergic Nerve-mediated pressor responses. Combined infusion of insulin and glucose, which resulted in increased serum insulin levels with euglycemic, significantly augmented Adrenergic Nerve-mediated pressor responses and attenuated CGRPergic Nerve-mediated depressor responses. The present results suggest that acute hyperglycemia and hyperinsulinemia increases Adrenergic Nerve-mediated vasoconstriction, which is partly associated with the blunted CGRPergic Nerve function, and that plasma insulin concentration associated with hyperglycemia may be responsible for alteration of neuronal vascular regulation.
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chronic hyperinsulinemia enhances Adrenergic vasoconstriction and decreases calcitonin gene related peptide containing Nerve mediated vasodilation in pithed rats
Hypertension Research, 2006Co-Authors: Yuji Kurosaki, Yoshito Zamami, Shingo Takatori, Mitsunobu Mio, Hiromu KawasakiAbstract:The present study investigated the influence of chronic hyperinsulinemia on vascular responsiveness induced by Adrenergic Nerves and calcitonin gene-related peptide-containing (CGRPergic) Nerves in pithed rats with insulin resistance. Male Wistar rats (6 weeks old) received 15% fructose solution in drinking fluid for 10 weeks (fructose-drinking rats: FDR), which resulted in significant increases in plasma levels of insulin, total cholesterol and triglyceride, and systolic blood pressure, as compared with control rats. Pithed FDR showed greater Adrenergic Nerve-mediated pressor response to spinal cord stimulation (SCS) at the lower thoracic vertebra (Th 9-12) and pressor response to exogenous noradrenaline than control rats. In pithed FDR with blood pressure artificially increased by continuous infusion of methoxamine and blockade of autonomic ganglia by hexamethonium, CGRPergic Nerve-mediated depressor responses to SCS were significantly smaller than those in control rats, but depressor responses to other vasodilators such as acetylcholine, CGRP and sodium nitroprusside were similar to those in control rats. These results suggest that chronic hyperinsulinemia in FDR facilitates Adrenergic Nerve-mediated vasoconstriction, which is associated with attenuated CGRPergic Nerve-mediated vasodilation.
Alessandro Giordano - One of the best experts on this subject based on the ideXlab platform.
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cardiac Adrenergic Nerve function and microvascular dysfunction in patients with cardiac syndrome x
Heart, 2008Co-Authors: Antonio Di Monaco, Isabella Bruno, Roberto Nerla, Priscilla Lamendola, Lucy Barone, Antonio Bagnato, Alfonso Sestito, Alessandro Giordano, Chiara Pisanello, Gaetano Antonio LanzaAbstract:Objective: To assess whether abnormalities in cardiac uptake of 123 I-metaiodobenzylguanidine (MIBG) correlate with coronary microvascular dysfunction in patients with cardiac syndrome X (CSX). Setting: University hospital. Patients: 29 patients (aged 59 (SD 7) years, 11 men) with typical CSX and a matched group of 20 healthy subjects (aged 56 (7) years, 8 men) were studied. Interventions: Planar and single photon emission computed tomography (SPECT) MIBG myocardial scintigraphy was performed in all subjects. Coronary flow response (CFR) to adenosine and to cold pressor test (CPT) in the left anterior descending (LAD) coronary artery was assessed in all CSX patients and in 12 controls by transthoracic Doppler echocardiography. Main outcome measures: Abnormalities in cardiac MIBG scintigraphy were observed in 25 CSX patients (86.2%), but in no healthy control (p Conclusion: Our data show striking abnormalities in cardiac Adrenergic Nerve function and in coronary microvascular function in CSX patients. However, no significant relation between the two abnormalities was found. Further studies are needed to clarify the mechanisms and the role of MIBG defects in CSX patients.
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effect of spinal cord stimulation on cardiac Adrenergic Nerve function in patients with cardiac syndrome x
Journal of Nuclear Cardiology, 2008Co-Authors: Antonella Spinelli, Antonio Di Monaco, Isabella Bruno, Maria Lucia Calcagni, Priscilla Lamendola, Lucy Barone, Gaetano Antonio Lanza, Alfonso Sestito, Gregory A Sgueglia, Alessandro GiordanoAbstract:Background. In patients with cardiac syndrome X (CSX) who present with refractory angina episodes, spinal cord stimulation (SCS) has beneficial effects. The mechanisms of SCS, however, remain speculative. We assessed the effects of SCS on cardiac sympathetic function in these patients. Methods and Results. We studied 11 CSX patients treated by SCS for refractory angina (mean age, 60±9 years; 5 men and 6 women), both during SCS therapy (SCS-ON) and after withdrawal of SCS therapy (SCS-OFF), using a randomized crossover design. Planar and single photon emission computed tomography iodine 123 metaiodobenzylguanidine (MIBG) myocardial scintigraphy and technetium 99m sestamibi (MIBI) bicycle exercise stress testing were performed at the end of each period. Compared with 10 healthy control subjects, CSX patients showed a lower heart-mediastinum ratio for MIBG uptake (2.19±0.3 vs 1.69±0.3,P=.001) and a higher cardiac MIBG uptake score (4.0±2.5 vs 19.7±27,P=.08). There were no differences in CSX patients during the SCS-ON and SCS-OFF phases of the study in heart-mediastinum ratio (1.74±0.3 vs 1.69±0.3,P=.13), cardiac washout rate of MIBG (42.9%±14% vs 43.3%±14%,P=.08), or MIBG defect score (18.7±25 vs 19.7±27,P=.22). Reversible perfusion defects during the SCS-OFF phase were detected in 8 patients; an improvement in perfusion defects was observed in 2 patients (25%) during the SCS-ON phase. Conclusions. Our data confirm the presence of abnormal cardiac Adrenergic Nerve function in CSX patients. SCS was unable to result in significant improvement of cardiac MIBG uptake abnormalities, suggesting that its therapeutic effects are unlikely to be mediated by modulation of cardiac Adrenergic Nerve activity.
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abnormal cardiac Adrenergic Nerve function in patients with syndrome x detected by 123i metaiodobenzylguanidine myocardial scintigraphy
Circulation, 1997Co-Authors: Gaetano Antonio Lanza, Maria Lucia Calcagni, Alessandro Giordano, Christian Pristipino, G Meduri, Carlo Trani, Rodolfo Franceschini, Filippo Crea, L Troncone, Attilio MaseriAbstract:Background Previous studies have suggested that an abnormal cardiac Adrenergic tone may have a pathophysiological role in syndrome X (effort angina, positive exercise testing, angiographically normal coronary arteries). Methods and Results To evaluate cardiac Adrenergic Nerve function, we performed [123I]metaiodobenzylguanidine (MIBG) myocardial scintigraphy in 12 patients with syndrome X and 10 control subjects. Cardiac MIBG uptake was assessed by the heart/mediastinum (H/M) ratio and by an MIBG uptake defect score (higher values=lower uptake). In syndrome X patients, we also correlated MIBG scintigraphic findings with stress myocardial perfusion as assessed by 201Tl scintigraphy. An inferior MIBG defect was observed in only 1 control subject, whereas 9 patients (P<.01) showed MIBG defects. The heart was totally or almost totally invisible on MIBG images in 5 patients, and predominantly regional defects were observed in 4. The H/M ratio was lower (1.70±0.6 versus 2.2±0.3, P=.03) and MIBG uptake defect sc...