Adrenergic Stimulation of Renin Secretion in the Isolated Perfused Rat Kidney
Adrenergic Stimulation of Renin Secretion in the Isolated Perfused Rat Kidney
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离体灌注大鼠肾中肾素分泌的肾上腺素刺激
DOI：
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发表时间：
1973
期刊：
影响因子：
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通讯作者：
GRAHAME W. Boyd
中科院分区：
文献类型：
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作者：
R. Vandongen;W. S. Peart;GRAHAME W. Boyd
为了避免复杂的全身效应，肾上腺素能激素对肾素分泌的影响进行了检查，在离体大鼠肾脏灌注Krebs-葡聚糖溶液在恒定的平均压力和流速。异丙肾上腺素和胰高血糖素产生了一致的增加，在不改变灌注压和流量的肾素分泌。同样地，在用酚苄明消除血管收缩作用后，仍然观察到去甲肾上腺素引起的肾素分泌增加，这与强烈的血管收缩和灌注压升高有关。异丙肾上腺素刺激的肾素分泌，不受酚苄明，明显抑制dl-普萘洛尔，但不是由d-普萘洛尔。dl-普萘洛尔未能抑制肾素对胰高血糖素的反应，这证实了在其他组织中的观察结果，并表明涉及其他受体或替代机制。这些发现支持肾上腺素能激素对肾素分泌的直接肾内作用，并且这种作用可能在儿茶酚胺的情况下由β受体特异性介导。
To avoid complicating systemic effects, the influence of adrenergic hormones on renin secretion was examined in the isolated rat kidney perfused with Krebs-dextran solution at a constant mean pressure and flow rate. Isoproterenol and glucagon produced a consistent increase in renin secretion without a change in perfusion pressure and flow. Similarly the increase in renin secretion with norepinephrine, which was associated with intense vasoconstriction and raised perfusion pressure, was still observed after the vasoconstrictive effect was abolished with phenoxybenzamine. Isoproterenol- stimulated renin secretion, unaffected by phenoxybenzamine, was markedly suppressed by dl-propranolol but not by d-propranolol. The failure of dl-propranolol to suppress the renin response to glucagon confirms observations in other tissues and suggests involvement of other receptors or alternative mechanisms. These findings support a direct intrarenal effect of adrenergic hormones on renin secretion, and this effect may be mediated specifically by beta receptors in the case of catecholamines.