Johnson R A, Freeman R H
Department of Physiology, University of Missouri School of Medicine, Columbia 65212.
Am J Physiol. 1994 Jun;266(6 Pt 2):R1723-9. doi: 10.1152/ajpregu.1994.266.6.R1723.
The influence of renal perfusion pressure on renin release was examined in rats administered the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME). Compared with the control plasma renin of 6.0 +/- 0.7 ng angiotensin I (ANG I).ml-1.h-1, plasma renin activity was suppressed (1.8 +/- 0.2 ng ANG I.ml-1.h-1, P < 0.05) in L-NAME-treated animals in which the renal perfusion pressure was permitted to increase and reached 141 +/- 8 mmHg. Plasma renin activity also was suppressed (2.5 +/- 0.4 ng ANG I.ml-1.h-1, P < 0.05) in a second L-NAME-treated group in which the renal perfusion pressure was controlled to a level of 105 +/- 5 mmHg via tightening of a suprarenal aortic snare. Plasma renin activity was increased (12.0 +/- 1.4 ng ANG I.ml-1.h-1, P < 0.05) in a third L-NAME-treated group in which renal perfusion pressure was reduced to 59 +/- 1 mmHg. Overall, these findings suggest that the intrarenal pressure-sensing mechanism for renin release does not stringently require nitric oxide synthesis. In a second experimental series, bilaterally renal-denervated rats were administered L-NAME, and again plasma renin activity was suppressed significantly whether renal perfusion pressure was permitted to increase or was controlled. Thus L-NAME also suppressed plasma renin activity independently of reflex reductions in renal neuroadrenergic activity even when renal perfusion pressure was controlled. Infusions of sodium nitroprusside completely inhibited L-NAME-induced suppression of plasma renin activity in these renal-denervated rats. Nitric oxide may function as a paracrine stimulatory mechanism for the local regulation of renin release.
在给予一氧化氮合酶抑制剂NG-硝基-L-精氨酸甲酯（L-NAME）的大鼠中，研究了肾灌注压对肾素释放的影响。与对照组血浆肾素水平6.0±0.7 ng血管紧张素I（ANG I）·ml⁻¹·h⁻¹相比，在肾灌注压允许升高并达到141±8 mmHg的L-NAME处理动物中，血浆肾素活性受到抑制（1.8±0.2 ng ANG I·ml⁻¹·h⁻¹，P<0.05）。在第二个L-NAME处理组中，通过收紧肾上腺主动脉圈套器将肾灌注压控制在105±5 mmHg水平，血浆肾素活性也受到抑制（2.5±0.4 ng ANG I·ml⁻¹·h⁻¹，P<0.05）。在第三个L-NAME处理组中，肾灌注压降至59±1 mmHg，血浆肾素活性升高（12.0±1.4 ng ANG I·ml⁻¹·h⁻¹，P<0.05）。总体而言，这些发现表明，肾素释放的肾内压力传感机制并非严格需要一氧化氮合成。在第二个实验系列中，对双侧肾去神经大鼠给予L-NAME，无论肾灌注压是允许升高还是受到控制，血浆肾素活性再次受到显著抑制。因此，即使肾灌注压受到控制，L-NAME也能独立于肾神经肾上腺素能活性的反射性降低而抑制血浆肾素活性。硝普钠输注完全抑制了这些肾去神经大鼠中L-NAME诱导的血浆肾素活性抑制。一氧化氮可能作为旁分泌刺激机制参与肾素释放的局部调节。
