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The role of angiotensin II in the renal responses to somatic nerve stimulation in the rat.

机译:血管紧张素II在大鼠对体神经刺激的肾脏反应中的作用。

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摘要

1. Electrical stimulation of the brachial nerves at 3 Hz (15 V, 0.2 ms), in sodium pentobarbitone-anaesthetized rats whose renal arterial pressure was held constant, elicited a 26% increase in systemic blood pressure, a 15% rise in heart rate, an 11% reduction in renal blood flow, did not alter glomerular filtration rate and significantly reduced absolute and fractional sodium excretions and urine flow by 44, 49 and 31%, respectively. 2. In a separate group of rats, brachial nerve stimulation at 3 Hz increased plasma renin activity approximately 2-fold, while in animals in which the brachial nerves were not stimulated plasma renin activity did not change. 3. Following inhibition of the renin-angiotensin system with captopril or sar-1-ile-8-angiotensin II, brachial nerve stimulation resulted in similar increases in systemic blood pressure and heart rate as in the animals with an intact renin-angiotensin system but, in captopril-infused rats, did not change renal haemodynamics or urine flow while absolute and fractional sodium excretions were reduced by 20 and 25%, respectively. In sar-1-ile-8-angiotensin II-infused animals, similar nerve stimulation decreased renal blood flow by 12%, glomerular filtration rate by 7% and absolute and fractional sodium excretions and urine flow by 25, 18 and 18%, respectively. These decreases in sodium and water output were significantly smaller than those observed in animals with an intact renin-angiotensin system. 4. Stimulation of the brachial nerves increased post-ganglionic efferent renal nerve activity by 20% and the magnitude of this response was unaffected following inhibition of the renin-angiotensin system. 5. The results show that low rates of brachial nerve stimulation in the rat can increase efferent renal nerve activity and result in an antinatriuresis and antidiuresis which is dependent on the presence of angiotensin II, and appears to be due to an action of angiotensin II at the level of the kidney.
机译:1.在戊巴比妥钠麻醉的大鼠中,以3 Hz(15 V,0.2 ms)以3 Hz(15 V,0.2 ms)电刺激肱神经,其肾动脉压保持恒定,导致全身血压升高26%,心率升高15%肾血流量减少11%并没有改变肾小球滤过率,并且绝对和部分钠排泄和尿流量分别减少了44%,49%和31%。 2.在另一组大鼠中,以3 Hz刺激臂神经使血浆肾素活性增加约2倍,而在未刺激臂神经的动物中,血浆肾素活性没有改变。 3.用卡托普利或sar-1-ile-8-血管紧张素II抑制肾素-血管紧张素系统后,臂神经刺激导致的全身血压和心率升高与具有完整的肾素-血管紧张素系统的动物相似,但在注入卡托普利的大鼠中,钠的绝对排泄量和分数钠排泄分别减少了20%和25%,但并未改变肾脏的血液动力学或尿流。在注入sar-1-ile-8-血管紧张素II的动物中,类似的神经刺激使肾血流量减少了12%,肾小球滤过率减少了7%,绝对排泄钠和部分钠排泄以及尿液分别减少了25%,18%和18%。 。钠和水输出量的这些减少明显小于具有完整的肾素-血管紧张素系统的动物中观察到的减少。 4.刺激肱神经使神经节后传出的肾神经活动增加20%,并且在抑制肾素-血管紧张素系统后该反应的程度不受影响。 5.结果表明,大鼠肱臂神经刺激率低会增加传出的肾神经活动,并导致排尿利尿和抗利尿,这取决于血管紧张素II的存在,并且似乎是由于血管紧张素II的作用肾脏的水平。

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