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Artery Tone

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John J Morrison – 1st expert on this subject based on the ideXlab platform

  • umbilical Artery Tone in maternal obesity
    Reproductive Biology and Endocrinology, 2009
    Co-Authors: Mark P Hehir, Audrey T Moynihan, Siobhan V Glavey, John J Morrison

    Abstract:

    The increasing prevalence of obesity constitutes a major health problem in obstetrics with implications for feto-maternal growth and wellbeing. This study investigated and compared the contractile properties of umbilical arteries excised from obese women, with those excised from women with a normal body mass index (BMI). Sections of umbilical Artery were obtained from umbilical cord samples immediately after delivery and mounted for isometric recording in organ tissue baths under physiological conditions. Cumulative additions of 5-Hydroxytryptamine (5-HT) and Prostaglandin F-2alpha (PgF2alpha) were added in the concentration range of 1 nmol/L to 10 micromol/L. Control vessels were exposed to Krebs physiological salt solution (PSS) only. The resultant effects of each drug addition were measured using the Powerlab hardware unit. 5-HT exerted a significant effect on human umbilical Artery Tone at concentrations of 100 nmol/L, 1 micromol/L, and 10 micromol/L in normal (n = 5; P 0.05). These findings support the hypothesis that endogenous regulation of umbilical Artery Tone is altered in association with maternal obesity. This may be linked to the cardiovascular effects of secretory products of adipose tissue, with implications for the feto-maternal circulation.

  • Umbilical Artery Tone in maternal obesity
    Reproductive Biology and Endocrinology, 2009
    Co-Authors: Mark P Hehir, Audrey T Moynihan, Siobhan V Glavey, John J Morrison

    Abstract:

    Background The increasing prevalence of obesity constitutes a major health problem in obstetrics with implications for feto-maternal growth and wellbeing. This study investigated and compared the contractile properties of umbilical arteries excised from obese women, with those excised from women with a normal body mass index (BMI). Methods Sections of umbilical Artery were obtained from umbilical cord samples immediately after delivery and mounted for isometric recording in organ tissue baths under physiological conditions. Cumulative additions of 5-Hydroxytryptamine (5-HT) and Prostaglandin F-2alpha (PgF2alpha) were added in the concentration range of 1 nmol/L to 10 micromol/L. Control vessels were exposed to Krebs physiological salt solution (PSS) only. The resultant effects of each drug addition were measured using the Powerlab hardware unit. Results 5-HT exerted a significant effect on human umbilical Artery Tone at concentrations of 100 nmol/L, 1 micromol/L, and 10 micromol/L in normal (n = 5; P < 0.05) and obese (n = 5; P < 0.05) women. The contractile effect was significantly greater in vessels from obese women {Mean Maximum Tension (MMT) = 4.2532 g} than in those from women of normal BMI (MMT = 2.97 g; P < 0.05). PgF2alpha exerted a significant contractile effect on vessels at 1 micromol/L and 10 micromol/L concentrations when compared with controls (n = 5; P < 0.05). There was a non-significant trend towards an enhanced Tone response in vessels from obese women (MMT = 3.02 g; n = 5), in comparison to vessels from women of a normal BMI (MMT = 2.358 g; n = 5; P > 0.05). Conclusion These findings support the hypothesis that endogenous regulation of umbilical Artery Tone is altered in association with maternal obesity. This may be linked to the cardiovascular effects of secretory products of adipose tissue, with implications for the feto-maternal circulation.

  • Umbilcal Artery Tone in maternal obesity
    American Journal of Obstetrics and Gynecology, 2006
    Co-Authors: Mark P Hehir, Audrey T Moynihan, John J Morrison

    Abstract:

    Background
    The increasing prevalence of obesity constitutes a major health problem in obstetrics with implications for feto-maternal growth and wellbeing. This study investigated and compared the contractile properties of umbilical arteries excised from obese women, with those excised from women with a normal body mass index (BMI).

Claude A. Piantadosi – 2nd expert on this subject based on the ideXlab platform

  • bicarbonate dependent superoxide release and pulmonary Artery Tone
    American Journal of Physiology-heart and Circulatory Physiology, 2003
    Co-Authors: Eva Nozikgrayck, Martha Sue Carraway, Yuh-chin T. Huang, Claude A. Piantadosi

    Abstract:

    Pulmonary vasoconstriction is influenced by inactivation of nitric oxide (NO) with extracellular superoxide (\batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepacka…

  • Vascular Signaling by Free Radicals Bicarbonate-dependent superoxide release and pulmonary Artery Tone
    , 2003
    Co-Authors: Eva Nozik-grayck, Yuh-chin T. Huang, Martha Sue Carraway, Claude A. Piantadosi

    Abstract:

    Nozik-Grayck, Eva, Yuh-Chin T. Huang, Martha Sue Carraway, and Claude A. Piantadosi. Bicarbonate-dependent superoxide release and pulmonary Artery Tone. Am J Physiol Heart Circ Physiol 285: H2327–H2335, 2003. First published July 3, 2003; 10.1152/ajpheart.00507.2003.—Pulmonary vasoconstriction is influenced by inactivation of nitric oxide (NO) with extracellular superoxide (O2 ). Because the short-lived O2 anion cannot diffuse across plasma membranes, its release from vascular cells requires specialized mechanisms that have not been well delineated in the pulmonary circulation. We have shown that the bicarbonate (HCO3 )-chloride anion exchange protein (AE2) expressed in the lung also exchanges O2 for HCO3 . Thus we determined whether O2 release involved in pulmonary vascular Tone depends on extracellular HCO3 . We assessed endotheliumdependent vascular reactivity and O2 release in the presence or absence of HCO3 in pulmonary Artery (PA) rings isolated from normal rats and those exposed to hypoxia for 3 days. Lack of extracellular HCO3 in normal PA rings significantly attenuated endothelial O2 release, opposed hypoxic vasoconstriction, and enhanced acetylcholine-mediated vasodilation. Release of O2 was also inhibited by an AE2 inhibitor (SITS) and abolished in normoxia by an NO synthase inhibitor (NG-nitro-L-arginine methyl ester). In contrast, hypoxia increased PA AE2 protein expression and O2 release; the latter was not affected by NG-nitro-L-arginine methyl ester or other inhibitors of enzymatic O2 generation. Enhanced O2 release by uncoupling NO synthase with geldanamycin was attenuated by hypoxia or by HCO3 elimination. These results indicate that O2 produced by endothelial NOS in normoxia and unidentified sources in hypoxia regulate pulmonary vascular Tone via AE2.

  • bicarbonate dependent superoxide release and pulmonary Artery Tone vascular signaling by free radicals
    American Journal of Physiology-heart and Circulatory Physiology, 2003
    Co-Authors: Eva Nozikgrayck, Martha Sue Carraway, Yuh-chin T. Huang, Claude A. Piantadosi

    Abstract:

    Pulmonary vasoconstriction is influenced by inactivation of nitric oxide (NO) with extracellular superoxide (O – 2 ○). Because the short-lived O – 2 ○ anion cannot diffuse across plasma membranes, its release from vascular cells requires specialized mechanisms that have not been well delineated in the pulmonary circulation. We have shown that the bicarbonate (HCO – 3)-chloride anion exchange protein (AE2) expressed in the lung also exchanges O – 2 ○ for HCO – 3 . Thus we determined whether O – 2 ○ release involved in pulmonary vascular Tone depends on extracellular HCO – 3. We assessed endothelium-dependent vascular reactivity and O – 2 ○ release in the presence or absence of HCO – 3 in pulmonary Artery (PA) rings isolated from normal rats and those exposed to hypoxia for 3 days. Lack of extracellular HCO – 3in normal PA rings significantly attenuated endothelial O – 2 ○ release, opposed hypoxic vasoconstriction, and enhanced acetylcholine-mediated vasodilation. Release of O – 2 ○ was also inhibited by an AE2 inhibitor (SITS) and abolished in normoxia by an NO synthase inhibitor (N G -nitro-L-arginine methyl ester). In contrast, hypoxia increased PA AE2 protein expression and O – 2 ○ release; the latter was not affected by N G -nitro-L-arginine methyl ester or other inhibitors of enzymatic O – 2 ○ generation. Enhanced O – 2 ○ release by uncoupling NO synthase with geldanamycin was attenuated by hypoxia or by HCO3 elimination. These results indicate that O – 2 ○ produced by endothelial NOS in normoxia and unidentified sources in hypoxia regulate pulmonary vascular Tone via AE2.

Steffensebastian Bolz – 3rd expert on this subject based on the ideXlab platform

  • Sphingosine-1-Phosphate acutely modulates the CFTR (Cystic Fibrosis Transmembrane Regulator) transporter in an AMPK-dependent manner
    The FASEB Journal, 2010
    Co-Authors: Firhan Atir Malik, Anja Meissner, Christine E. Bear, Steffensebastian Bolz

    Abstract:

    IntroductionSphingosine-1-Phosphate (S1P) is a primary modulator of resistance Artery Tone. Its bioavailability is controlled by a rheostat between sphingosine kinase 1 and intracellular S1P phosph…

  • role of sphingosine 1 phosphate phosphohydrolase 1 in the regulation of resistance Artery Tone
    Circulation Research, 2008
    Co-Authors: Bernhard Friedrich Peter, Darcy Lidington, Aki Harada, Hanno J Bolz, Lukas Vogel, Scott P Heximer, Sarah Spiegel, Ulrich Pohl, Steffensebastian Bolz

    Abstract:

    Sphingosine-1-phosphate (S1P), which mediates pleiotropic actions within the vascular system, is a prominent regulator of microvascular Tone. By virtue of its S1P-degrading function, we hypothesized that S1P-phosphohydrolase 1 (SPP1) is an important regulator of Tone in resistance arteries. Hamster gracilis muscle resistance arteries express mRNA encoding SPP1. Overexpression of SPP1 (via transfection of a SPP1wt) reduced resting Tone, Ca2+ sensitivity, and myogenic vasoconstriction, whereas reduced SPP1 expression (antisense oligonucleotides) yielded the opposite effects. Expression of a phosphatase-dead mutant of SPP1 (SPP1H208A) had no effect on any parameter tested, suggesting that catalytic activity of SPP1 is critical. The enhanced myogenic Tone that follows overexpression of S1P-generating enzyme sphingosine kinase 1 (Sk1wt) was functionally antagonized by coexpression with SPP1wt but not SPP1H208A. SPP1 modulated vasoconstriction in response to 1 to 100 nmol/L exogenous S1P, a concentration range that was characterized as S1P2-dependent, based on the effect of S1P2 inhibition by antisense oligonucleotides and 1 μmol/L JTE013. Inhibition of the cystic fibrosis transmembrane regulator (CFTR) (1) restored S1P responses that were attenuated by SPP1wt overexpression; (2) enhanced myogenic vasoconstriction; but (3) had no effect on noradrenaline responses. We conclude that SPP1 is an endogenous regulator of resistance Artery Tone that functionally antagonizes the vascular effects of both Sk1wt and S1P2 receptor activation. SPP1 accesses extracellular S1P pools in a manner dependent on a functional CFTR transport protein. Our study assigns important roles to both SPP1 and CFTR in the physiological regulation of vascular Tone, which influences both tissue perfusion and systemic blood pressure.

  • sphingosine 1 phosphate modulates spiral modiolar Artery Tone a potential role in vascular based inner ear pathologies
    Cardiovascular Research, 2006
    Co-Authors: Darcy Lidington, Ulrich Pohl, Elias Q Scherer, Elmar Oestreicher, W Arnold, Steffensebastian Bolz

    Abstract:

    Objective The mechanisms regulating spiral modiolar Artery (SMA) Tone are not known, yet their characterization is pivotal for understanding inner ear blood flow regulation. Sphingosine-1-phosphate (S1P), known to stimulate vasoconstriction in several vascular beds, is a candidate regulator of SMA Tone with potential pathophysiological relevance.

    Methods Gerbil SMAs were isolated, cannulated and pressurized (30 mm Hg transmural) for experimentation under near-in vivo conditions. For functional experiments, vascular diameter and intracellular Ca2+ were simultaneously measured. Standard RT-PCR and immunohistochemical techniques were also employed.

    Results mRNA transcripts encoding sphingosine kinase, S1P phosphohydrolase and three S1P receptors (S1P1–3) were detected in the SMA. S1P induced dose-dependent vasoconstriction of the SMA (EC50=115nmol/L), and enhanced the apparent Ca2+-sensitivity of the contractile apparatus. Noradrenaline did not elicit vasoconstriction. The Rho kinase inhibitor Y27632 (1μmol/L) reversed S1P-induced vasoconstriction and the S1P-mediated enhancement of Ca2+-sensitivity. RhoA was observed to translocate to the plasma membrane in response to stimulation with 30μmol/L S1P.

    Conclusion We conclude that all key signalling pathway constituents are present at the mRNA level for S1P to act as an endogenous regulator of SMA Tone. S1P stimulates potent, RhoA/Rho kinase-dependent SMA vasoconstriction and Ca2+ sensitization. The high sensitivity to S1P suggests that SMA vasoconstriction is likely to occur under pathological conditions that increase intramural S1P concentrations (i.e., inflammation). From a clinical perspective, the present study identifies new potential therapeutic targets for the treatment of vascular-based, “stroke-like” inner ear pathologies: the enzymes responsible for S1P bioavailability and the S1P receptors.