The role of α‐adrenoceptors in the regulation of renal tubular sodium reabsorption and renin secretion in the rabbit
The role of α‐adrenoceptors in the regulation of renal tubular sodium reabsorption and renin secretion in the rabbit
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α-肾上腺素受体在兔肾小管钠重吸收和肾素分泌调节中的作用
DOI：
--
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发表时间：
1985
影响因子：
7.3
通讯作者：
E. Johns
中科院分区：
文献类型：
--
作者：
I. Hesse;E. Johns
1在麻醉兔子中进行了一项研究，对负责增加肾小管钠重吸收和肾素分泌的α肾上腺素受体亚型进行分类。在不改变肾血流量或肾小球滤过率的剂量下，肾内给予去甲肾上腺素可显著降低尿流量、绝对钠排泄量和钠排泄分数，降幅在26%至29%之间。选择性α1-肾上腺素受体拮抗剂哌唑嗪可消除这些肾脏对去甲肾上腺素的反应，而选择性α2-肾上腺素受体拮抗剂咪唑克生则不能消除这些反应。[2]去甲肾上腺素，肾内给药，使肾素分泌增加2 ~ 3倍，这种反应不受哌唑嗪或咪唑克生的影响。3肾内给予选择性α肾上腺素受体激动剂苯肾上腺素和甲氧胺，剂量率不改变肾血流动力学，显著减少尿流量，绝对和部分钠排泄量15%至33%，但剂量减少血流量和滤过率11%至26%，尿流量，钠排泄的绝对值和分数下降了42%-49%。4.在无肾脏血流动力学作用的剂量下，输注胍那苄（选择性α2-肾上腺素受体激动剂）可使尿流量、绝对钠排泄和钠排泄分数增加11%至15%，而在血流量减少7%的剂量下，这些其他变量没有变化。5给予UK 14304（选择性α2-肾上腺素受体激动剂）分别使血流量和滤过率降低3%和9%，但没有其他可测量的作用。在较高剂量下，血流量降低14%，滤过率降低24%，尿流量、绝对和部分钠排泄量下降27%至50%。6.高剂量的苯肾上腺素和UK 14304可显著增加肾素分泌，而低剂量的这些药物则无此作用。7这些研究表明，肾小管钠重吸收的肾上腺素能刺激涉及α1-而不是α2-肾上腺素受体的激活。此外，肾上腺素能激活肾小球细胞释放肾素似乎不涉及α1或α2肾上腺素受体。
1 A study was undertaken in the anaesthetized rabbit to classify the α‐adrenoceptor subtypes responsible for increasing renal tubular sodium reabsorption and renin secretion. Intrarenal administration of noradrenaline, at doses which did not change renal blood flow or glomerular filtration rate, significantly decreased urine flow, absolute and fractional sodium excretion by between 26% and 29%. These renal responses to noradrenaline were abolished by the selective α1‐adrenoceptor antagonist, prazosin, but not by the selective α2‐adrenoceptor antagonist, idazoxan. 2 Noradrenaline, given intrarenally, increased renin secretion between two and three fold and this response was not modified by either prazosin or idazoxan. 3 Intrarenal administration of the selective α‐adrenoceptor agonists, phenylephrine and methoxamine, at dose rates which did not change renal haemodynamics, significantly reduced urine flow, absolute and fractional sodium excretion by 15% to 33%, but at doses which reduced blood flow and filtration rate, by between 11% and 26%, urine flow, absolute and fractional sodium excretion decreased between 42% and 49%. 4 Infusion of guanabenz (selective α2‐adrenoceptor agonist), at doses with no renal haemodynamic action, increased urine flow, absolute and fractional sodium excretion by 11% to 15%, while at doses which decreased blood flow by 7%, these other variables did not change. 5 Administration of UK 14304 (selective α2‐adrenoceptor agonist) reduced blood flow and filtration rate by 3% and 9% respectively but had no other measurable action. At higher doses, which decreased blood flow by 14% and filtration rate by 24%, urine flow, absolute and fractional sodium excretion fell by between 27% and 50%. 6 Renin secretion was significantly increased by the high doses of phenylephrine and UK 14304 but not by the low doses of these drugs. 7 These studies show that adrenergic stimulation of renal tubular sodium reabsorption involves the activation of α1‐ but not α2‐adrenoceptors. Further, adrenergic activation of the juxtaglomerular cells to release renin does not appear to involve either α1‐ or α2‐adrenoceptors.
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DOI：
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发表时间：
1985
期刊：
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影响因子：
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作者：
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DOI：
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DOI：
10.1152/ajprenal.1982.243.6.f576
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期刊：
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影响因子：
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DOI：
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期刊：
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影响因子：
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DOI：
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发表时间：
1983
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
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作者：
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