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心房利钠因子抑制肾素分泌的肾脏机制。

Renal mechanisms for suppression of renin secretion by atrial natriuretic factor.

作者信息

Villarreal D, Freeman R H, Davis J O, Verburg K M, Vari R C

出版信息

Hypertension. 1986 Jun;8(6 Pt 2):II28-35. doi: 10.1161/01.hyp.8.6_pt_2.ii28.

Abstract

The effects of synthetic atrial natriuretic factor on renin secretion were examined in anesthetized dogs with either a single filtering kidney or a single denervated nonfiltering kidney. In dogs with a single filtering kidney (Series 1, n = 6), a priming dose of atrial natriuretic factor (2 micrograms/kg, i.v.) followed by sustained intravenous infusions at doses of 200 and 400 ng/kg/min for 20 minutes each produced striking decrements (p less than 0.05) in renin secretion, from 1083 +/- 322 to 205 +/- 120 and 286 +/- 168 ng of angiotensin I per minute. This fall in renin secretion was associated with significant increases (p less than 0.05) in creatinine clearance, urine flow, sodium excretion, and the filtered load of sodium. Renal blood flow increased only transiently. In dogs with a single denervated nonfiltering kidney (Series 2, n = 6), infusion of atrial natriuretic factor at these doses also produced marked inhibition (p less than 0.05) of renin secretion, from 311 +/- 98 to 72 +/- 22 and 91 +/- 37 ng of angiotensin I per minute. Renal blood flow remained significantly elevated (p less than 0.05) throughout the infusion, in contrast to renal blood flow in Series I. Similar results were obtained in a third series of dogs (n = 6) with a single denervated nonfiltering kidney, during sustained intrarenal arterial infusions of atrial natriuretic factor. These results suggest that an increase in the sodium load delivered to the macula suppression of renin secretion by atrial natriuretic factor is mediated through its interactions with the two intrarenal receptor mechanisms, the renal vascular receptor and the macula densa.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在麻醉的犬身上,研究了合成心房利钠因子对肾素分泌的影响,这些犬有的只有一个滤过肾,有的只有一个去神经支配的非滤过肾。在有一个滤过肾的犬(第1组,n = 6)中,先给予一次负荷剂量的心房利钠因子(2微克/千克,静脉注射),随后以200和400纳克/千克/分钟的剂量持续静脉输注,各持续20分钟,肾素分泌显著减少(p < 0.05),从每分钟1083±322纳克血管紧张素I降至205±120和286±168纳克。肾素分泌的这种下降与肌酐清除率、尿流量、钠排泄以及钠滤过负荷的显著增加(p < 0.05)相关。肾血流量仅短暂增加。在有一个去神经支配的非滤过肾的犬(第2组,n = 6)中,以这些剂量输注心房利钠因子也显著抑制(p < 0.05)肾素分泌,从每分钟311±98纳克血管紧张素I降至72±22和91±37纳克。与第1组的肾血流量不同,在整个输注过程中,第2组的肾血流量一直显著升高(p < 0.05)。在第三组有一个去神经支配的非滤过肾的犬(n = 6)中,在持续肾内动脉输注心房利钠因子期间也得到了类似结果。这些结果表明,心房利钠因子通过与两种肾内受体机制(肾血管受体和致密斑)相互作用,介导了输送到致密斑的钠负荷增加对肾素分泌的抑制作用。(摘要截短于250字)

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