Cinotti G A
J Hypertens Suppl. 1983 Oct;1(1):43-51.
Resetting of the 'pressure-natriuresis' balance may result from subtle changes in renal vascular resistance or an independent defect in sodium excretion. The renin-angiotensin system, renal kinins and prostaglandins are all implicated in the regulation of glomerular filtration rate (GRF), renal blood flow (RBF) and urinary sodium excretion. Experimental and clinical evidence is reported demonstrating intimate, but poorly understood, interactions between these systems. Locally synthetized vasodilatory hormones (kinins, prostaglandins) modulate the effects of angiotensin II (AII), norepinephrine and alpha-adrenergic stimuli on renal vasculature and sodium excretion. It is suggested that an alteration of this interplay may be responsible for some forms of experimental and human hypertension.
“压力-利钠”平衡的重置可能源于肾血管阻力的细微变化或钠排泄的独立缺陷。肾素-血管紧张素系统、肾激肽和前列腺素均参与肾小球滤过率（GRF）、肾血流量（RBF）和尿钠排泄的调节。有实验和临床证据表明这些系统之间存在密切但尚不清楚的相互作用。局部合成的血管舒张激素（激肽、前列腺素）可调节血管紧张素II（AII）、去甲肾上腺素和α-肾上腺素能刺激对肾血管系统和钠排泄的影响。有人提出，这种相互作用的改变可能是某些形式的实验性高血压和人类高血压的原因。
