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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Modulation of noradrenaline-induced vasoconstriction in isolated perfused mesenteric arterial beds from obese Zucker rats in the presence and absence of insulin.
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Modulation of noradrenaline-induced vasoconstriction in isolated perfused mesenteric arterial beds from obese Zucker rats in the presence and absence of insulin.

机译：在存在和不存在胰岛素的情况下，肥胖Zucker大鼠离体灌注的肠系膜动脉床中去甲肾上腺素诱导的血管收缩的调节。

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The genetically obese Zucker rat (fa/fa) is an insulin-resistant animal model with early-onset severe hyperinsulinemia that eventually develops mild hypertension. Thus, it represents a model in which the effect of hyperinsulinemia - insulin resistance associated with hypertension on vascular reactivity can be examined. The purpose of this study was to investigate the contribution of endogenous nitric oxide (NO) and prostaglandins to reactivity to noradrenaline (NA) in the presence and absence of insulin in mesenteric arterial beds (MAB) from 25-week-old obese Zucker rats and their lean, gender-matched littermates. In the absence of insulin, bolus injection of NA (0.9-90 nmol) produced a dose-dependent increase in perfusion pressure in MAB from both lean and obese rats. Although there was no significant difference in NA pD2 (-log ED50) values, the maximum response of MAB from obese rats to NA was slightly but significantly reduced compared with that of MAB from lean rats. The nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA, 300 microM) enhanced and indomethacin (20 microM) inhibited pressor responses to NA in MAB from both obese and lean rats. Perfusion with insulin (200 mU/L, a level similar to that in obese rats in vivo) potentiated only the responses of the obese MAB to the two lowest doses of NA tested (0.9 and 3 nmol). In the presence of L-NMMA, insulin further potentiated the NA response in MAB from obese rats. Indomethacin, the prostaglandin H2/thromboxane A2 receptor antagonist SQ 29548 (0.3 microM), and the nonselective endothelin-1 (ET-1) receptor antagonist bosentan (3 microM) all abolished insulin potentiation of the NA response in obese MAB. These data suggest that concurrent release of NO and vasoconstrictor cyclooxygenase product(s) in MAB from both obese and lean Zucker rats normally regulates NA-induced vasoconstrictor responses. Furthermore, insulin increases the release of contracting cyclooxygenase product(s) and enhances reactivity to low doses of NA in MAB from obese rats. The effects of insulin may be partially mediated by ET-1 via ET receptors and are buffered to some extent by concomitant NO release. This altered action of insulin may play a role in hypertension in this hyperinsulinemic - insulin-resistant model.
机译：遗传性肥胖的Zucker大鼠（fa / fa）是一种胰岛素抵抗性动物模型，具有早期发作的严重高胰岛素血症，最终发展为轻度高血压。因此，它代表了一种模型，其中可以检查高胰岛素血症-与高血压相关的胰岛素抵抗对血管反应性的影响。这项研究的目的是调查存在和不存在25周龄肥胖Zucker大鼠的肠系膜动脉床（MAB）中存在胰岛素和不存在胰岛素时内源性一氧化氮（NO）和前列腺素对去甲肾上腺素（NA）反应性的贡献。他们的精瘦，性别匹配的同窝仔。在不存在胰岛素的情况下，推注NA（0.9-90 nmol）可以使瘦鼠和肥胖鼠的MAB灌注压力产生剂量依赖性的增加。尽管NA pD2（-log ED50）值无显着差异，但肥胖大鼠对MA的最大反应与瘦大鼠MAB的最大反应相比有轻微但显着降低。一氧化氮合酶抑制剂NG-单甲基-L-精氨酸（L-NMMA，300 microM）增强，消炎痛（20 microM）抑制肥胖和瘦大鼠MAB对NA的升压反应。胰岛素灌注（200 mU / L，与体内肥胖大鼠体内的水平相似）仅增强了肥胖MAB对两种最低NA剂量（0.9和3 nmol）的反应。在存在L-NMMA的情况下，胰岛素进一步增强了肥胖大鼠MAB中的NA反应。消炎痛，前列腺素H2 /血栓烷A2受体拮抗剂SQ 29548（0.3 microM）和非选择性内皮素-1（ET-1）受体拮抗剂波生坦（3 microM）都消除了肥胖MAB中胰岛素抵抗的胰岛素增强作用。这些数据表明，肥胖和瘦Zucker大鼠同时释放MAB中的NO和血管收缩剂环氧合酶产物通常可调节NA诱导的血管收缩剂反应。此外，胰岛素增加了收缩性环氧合酶产物的释放，并增强了肥胖大鼠对MAB中低剂量NA的反应性。胰岛素的作用可能由ET-1经由ET受体部分介导，并在一定程度上被伴随的NO释放所缓冲。胰岛素的这种改变的作用可能在这种高胰岛素-胰岛素抵抗模型中在高血压中起作用。

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