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首页> 外文期刊>Hypertension: An Official Journal of the American Heart Association >Renal mechanisms for suppression of renin secretion by atrial natriuretic factor.
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Renal mechanisms for suppression of renin secretion by atrial natriuretic factor.

机译:房性利钠因子抑制肾素分泌的肾脏机制。

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摘要

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)
机译:在具有单个滤过肾或单个去神经非滤过肾的麻醉犬中检查了合成心钠素对肾素分泌的影响。在具有单个滤肾功能的犬(系列1,n = 6)中,初始剂量的心钠素(2微克/千克,静脉注射),然后以200和400 ng / kg / min的剂量持续静脉输注20分钟每一种都会使肾素分泌显着下降(p小于0.05),从每分钟1083 +/- 322降到205 +/- 120和286 +/- 168 ng血管紧张素I。肾素分泌的下降与肌酐清除率,尿液流量,钠排泄和钠的过滤负荷显着增加(p小于0.05)有关。肾血流量仅短暂增加。在具有单个神经非滤过非过滤性肾脏的犬(系列2,n = 6)中,以这些剂量输注心房利钠因子也会对肾素分泌产生明显的抑制作用(p小于0.05),从311 +/- 98到72 +/-。每分钟22和91 +/- 37 ng的血管紧张素I。与系列I中的肾脏血流相反,整个输注过程中的肾脏血流仍然显着升高(p小于0.05)。在持续的持续过程中,第三条狗(n = 6)中有单个失神经的非滤过肾脏获得了相似的结果肾内输注心钠素。这些结果表明,通过心房利钠因子递送至黄斑抑制肾素分泌的钠负荷的增加是通过其与两种肾内受体机制,即肾血管受体和黄斑牙本质的相互作用而介导的。(摘要摘录于250字)

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