The Experts below are selected from a list of 105 Experts worldwide ranked by ideXlab platform
W. Keith Mcelroy - One of the best experts on this subject based on the ideXlab platform.
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Influence of chlordimeform on Alpha-Adrenergic Receptor-associated mechanisms of hormonal regulation in the rat: pituitary and adrenocortical secretion.
Toxicology, 1991Co-Authors: Tammy E. Stoker, Jerome M. Goldman, Ralph L. Cooper, W. Keith McelroyAbstract:The acaricide chlordimeform (CDF) has been reported to have effects on the central nervous system that appear to involve an interaction with Alpha-Adrenergic Receptor-mediated mechanisms of neurotransmission. The present study examined the effects of CDF on adrenocortical and pituitary prolactin secretion, which are known to involve central Adrenergic Receptors. Male Long-Evans rats were injected i.p. with 20 or 50 mg/kg CDF and killed after 1, 4, 8 or 24 h. Both noninjected and saline-injected controls were included. Dosing was structured so that trunk blood could be collected during the morning nadir of circulating corticosterone (CORT). Assays for plasma adrenocorticotropic hormone (ACTH), CORT and prolactin (PRL) showed that with 50 mg/kg, all three hormones rose sharply by 1 h. CORT increased in a dose-dependent fashion and declined over the ensuing 8 h. Other rats were treated with the Alpha-Adrenergic antagonist phenoxybenzamine (PBZ, 20 mg/kg) or the Alpha-agonist clonidine (CLON, 0.6 mg/kg) 40 min before and killed 1 h after CDF (25 mg/kg) injection. CLON was found to completely suppress the CDF-induced rise in CORT, while PBZ enhanced the CORT/ACTH response to CDF. CLON also significantly elevated PRL, an alteration not seen in the CLON-pretreated CDF rats. Dexamethasone was able to block the CDF-induced rise in CORT and significantly suppressed PRL levels in both saline- and CDF-treated groups. These effects indicate that CDF is interfering with a regulatory signal mediated by Alpha-Adrenergic Receptor-associated activity.
Martin C. Michel - One of the best experts on this subject based on the ideXlab platform.
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the Alpha 1a Adrenergic Receptor subtype mediates biochemical molecular and morphologic features of cultured myocardial cell hypertrophy
Journal of Biological Chemistry, 1993Co-Authors: Kirk U Knowlton, Martin C. Michel, M Itani, H E Shubeita, K Ishihara, Joan Heller Brown, Kenneth R ChienAbstract:Alpha 1-Adrenergic agonists induce a hypertrophic phenotype in cultured neonatal rat ventricular myocytes. Quantifiable markers of this phenotype include stimulation of phosphoinositide hydrolysis, transcriptional induction of atrial natriuretic factor (ANF) gene expression, and an increase in myocardial cell size. The aim of the present work was to determine which Alpha 1-Adrenergic Receptor subtype mediates the acquisition of these parameters of myocardial cell hypertrophy. Phosphoinositide hydrolysis is inhibited by low concentrations of 5-methylurapidil (log Ki = -8.7) and (+)-niguldipine (log Ki = -10.6). The Alpha-Adrenergic Receptor-induced increase in transcriptional activation of an ANF luciferase reporter gene is inhibited over the same range of concentrations of 5-methylurapidil (log Ki = -8.2) and (+)-niguldipine (log Ki = -11.2) that inhibit phosphoinositide hydrolysis. In addition, the increase in cell size that accompanies Alpha-Adrenergic Receptor stimulation of cultured ventricular myocytes is blocked by similar concentrations of 5-methylurapidil (log Ki = -8.0) and (+)-niguldipine (log Ki = -10.6). In contrast, treatment with the Alpha 1B selective antagonist chlorethylclonidine at a concentration of 10 microM had no effect on the Adrenergically mediated induction of ANF luciferase reporter gene expression or the Adrenergically induced increase in myocardial cell size. These findings demonstrate that pharmacologically identifiable Alpha 1A-Adrenergic Receptors mediate not only the early effects of Alpha 1-Adrenergic stimulation such as phosphoinositide hydrolysis, but that they activate the signaling pathways that control transcriptional induction of the ANF luciferase reporter gene and an increase in myocardial cell size. Studies using Alpha 1-Adrenergic Receptor cDNAs to delineate and alter the direct interaction of this Receptor subtype with proximal signaling molecules, e.g. GTP binding proteins, should provide a powerful means of assessing their role in the induction of the molecular and morphologic parameters of myocardial cell hypertrophy.
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On the role of renal Alpha-Adrenergic Receptors in spontaneously hypertensive rats.
Hypertension (Dallas Tex. : 1979), 1992Co-Authors: Martin C. Michel, Paul A. Insel, S Jäger, R. Casto, Rainer Rettig, C Graf, Morton P. Printz, T Philipp, Otto-erich BroddeAbstract:We tested the hypothesis that a genetically determined increase in renal Alpha-Adrenergic Receptor density might be a pathophysiologically important factor in the spontaneously hypertensive rat model of genetic hypertension. In a first study, we compared renal Alpha 1 and Alpha 2-Adrenergic Receptor density with systolic blood pressure in 45 rats of an F2 generation of Wistar-Kyoto x spontaneously hypertensive rat hybrids but were unable to detect significant cosegregation between either Receptor density or blood pressure. In a second study, we determined renal Alpha 1- and Alpha 2-Adrenergic Receptor density in Wistar-Kyoto and spontaneously hypertensive rat kidneys that were transplanted into an F1 generation of Wistar-Kyoto x spontaneously hypertensive rat hybrids. Although Wistar-Kyoto kidneys lowered blood pressure in these animals and spontaneously hypertensive rat kidneys increased blood pressure, renal Alpha-Adrenergic Receptor densities were similar in membranes from both types of kidneys. Since rat kidney coexpresses Alpha 1A- and Alpha 1B-Adrenergic Receptors, we also investigated whether differential regulation of these two subtypes might conceal ongoing alterations. The Alpha 1A/Alpha 1B-Adrenergic Receptor ratio, however, was similar in Wistar-Kyoto rats, spontaneously hypertensive rats, and F1 rats transplanted with a kidney from either strain. Taken together these data do not support the hypothesis that genetically determined alterations of renal Alpha-Adrenergic Receptor numbers play an important role in the development of elevated blood pressure in the spontaneously hypertensive rat.
Claus G. Roehrborn - One of the best experts on this subject based on the ideXlab platform.
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Efficacy of Alpha-Adrenergic Receptor Blockers in the Treatment of Male Lower Urinary Tract Symptoms.
Reviews in urology, 2009Co-Authors: Claus G. RoehrbornAbstract:Male lower urinary tract symptoms (LUTS) are one of the most common causes for a consultation with a health care provider, and one of the most common causes of male LUTS is benign prostatic hyperplasia (BPH). In recent decades, medical therapy has established itself as viable and cost effective for the majority of men. For the treatment of male LUTS in the United States, the 5 currently available Alpha-Adrenergic Receptor blockers are alfuzosin, doxazosin, silodosin, terazosin, and tamsulosin. Alpha-Blockers remain one of the mainstays in the treatment of male LUTS and clinical BPH. They exhibit an early onset of efficacy (within less than 1 week) with regard to both symptoms and flow rate improvement, maintain such improvements in open-label and controlled trials for up to 5 years, and have been shown to prevent symptomatic progression.
Maria T E Hopman - One of the best experts on this subject based on the ideXlab platform.
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the role of the Alpha Adrenergic Receptor in the leg vasoconstrictor response to orthostatic stress
Acta Physiologica, 2009Co-Authors: Miriam Kooijman, Gerard A Rongen, Paul Smits, H J M Van Kuppevelt, Maria T E HopmanAbstract:AIM: The prompt increase in peripheral vascular resistance, mediated by sympathetic Alpha-Adrenergic stimulation, is believed to be the key event in blood pressure control during postural stress. However, despite the absence of central sympathetic control of the leg vasculature, postural leg vasoconstriction is preserved in spinal cord-injured individuals (SCI). This study aimed at assessing the contribution of both central and local sympathetically induced Alpha-Adrenergic leg vasoconstriction to head-up tilt (HUT) by including healthy individuals and SCI, who lack central sympathetic baroreflex control over the leg vascular bed. METHODS: In 10 controls and nine SCI the femoral artery was cannulated for drug infusion. Upper leg blood flow (LBF) was measured bilaterally using venous occlusion strain gauge plethysmography before and during 30 degrees HUT throughout intra-arterial infusion of saline or the non-selective Alpha-Adrenergic Receptor antagonist phentolamine respectively. Additionally, in six controls the leg vascular response to the cold pressor test was assessed during continued infusion of phentolamine, in order to confirm complete Alpha-Adrenergic blockade by phentolamine. RESULTS: During infusion of phentolamine HUT still caused vasoconstriction in both groups: leg vascular resistance (mean arterial pressure/LBF) increased by 10 +/- 2 AU (compared with 12 +/- 2 AU during saline infusion), and 13 +/- 3 AU (compared with 7 +/- 3 AU during saline infusion) in controls and SCI respectively. CONCLUSION: Effective Alpha-Adrenergic blockade did not reduce HUT-induced vasoconstriction, regardless of intact baroreflex control of the leg vasculature. Apparently, redundant mechanisms compensate for the absence of sympathetic Alpha-adrenoceptor leg vasoconstriction in response to postural stress.
Tammy E. Stoker - One of the best experts on this subject based on the ideXlab platform.
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Influence of chlordimeform on Alpha-Adrenergic Receptor-associated mechanisms of hormonal regulation in the rat: pituitary and adrenocortical secretion.
Toxicology, 1991Co-Authors: Tammy E. Stoker, Jerome M. Goldman, Ralph L. Cooper, W. Keith McelroyAbstract:The acaricide chlordimeform (CDF) has been reported to have effects on the central nervous system that appear to involve an interaction with Alpha-Adrenergic Receptor-mediated mechanisms of neurotransmission. The present study examined the effects of CDF on adrenocortical and pituitary prolactin secretion, which are known to involve central Adrenergic Receptors. Male Long-Evans rats were injected i.p. with 20 or 50 mg/kg CDF and killed after 1, 4, 8 or 24 h. Both noninjected and saline-injected controls were included. Dosing was structured so that trunk blood could be collected during the morning nadir of circulating corticosterone (CORT). Assays for plasma adrenocorticotropic hormone (ACTH), CORT and prolactin (PRL) showed that with 50 mg/kg, all three hormones rose sharply by 1 h. CORT increased in a dose-dependent fashion and declined over the ensuing 8 h. Other rats were treated with the Alpha-Adrenergic antagonist phenoxybenzamine (PBZ, 20 mg/kg) or the Alpha-agonist clonidine (CLON, 0.6 mg/kg) 40 min before and killed 1 h after CDF (25 mg/kg) injection. CLON was found to completely suppress the CDF-induced rise in CORT, while PBZ enhanced the CORT/ACTH response to CDF. CLON also significantly elevated PRL, an alteration not seen in the CLON-pretreated CDF rats. Dexamethasone was able to block the CDF-induced rise in CORT and significantly suppressed PRL levels in both saline- and CDF-treated groups. These effects indicate that CDF is interfering with a regulatory signal mediated by Alpha-Adrenergic Receptor-associated activity.