Interactions of renin, kinins and prostaglandins.
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.
D000818:Animals; D001095:Arachidonic Acids / Q000378:metabolism; D001477:Bartter Syndrome / Q000378:metabolism; D004232:Diuretics / Q000494:pharmacology; D011464:Epoprostenol / Q000494:pharmacology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000378:metabolism; D007610:Kallikreins / Q000378:metabolism; D007705:Kinins / Q000378:metabolism*; D011247:Pregnancy; D011453:Prostaglandins / Q000378:metabolism*; D012083:Renin / Q000378:metabolism*; D012084:Renin-Angiotensin System / Q000187:drug effects
D001095:Arachidonic Acids; D004232:Diuretics; D007705:Kinins; D011453:Prostaglandins; D011464:Epoprostenol; D007610:Kallikreins; D012083:Renin