Physiological Evolution of the Renin-Angiotensin System

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Abstract
The renin-angiotensin system (RAS) in mammals may participate in the controls of blood pressure and aldosterone secretion, and possibly in the regulation of renal function. It was shown that renin release is controlled by: 2 intrarenal receptors, the renal arteriolar receptor and the macula densa; the sympathetic nervous system; several humoral agents. Recent studies indicate interrelations between the RAS and renal prostaglandins and the kallikrein-kinin system. Comparative studies revealed that renal renin and the juxtaglomerular (JG) cells emerged during the early evolution of bony fishes, whereas the macula densa evolved later in the vertebrate phylogeny. Exogenously administered angiotensins and renin produce vasopressor actions in representative species of all vertebrate classes from elasmobranchs to mammals, and increase secretions of mineralocorticoids from the adrenal cortex (interrenal) in amphibians, reptiles and possibly in teleosts. Angiotensin causes glomerular diuresis in teleosts and lungfishes, which may be ascribed to increased dorsal aortic pressure, while angiotensin may have both glomerular and tubular actions in some amphibians. Intracranial injection of angiotensin stimulates drinking in teleosts, reptiles, and birds, but not in amphibians. Hemorrhage and acute hypotension are potent stimuli for causing renin release in an aglomerular teleost and a bird. Since anatomical evidence shows that the evolution of the JG cells preceded that of the macula densa, it appears that the RAS evolved with a close relationship to blood pressure homeostasis. There is no clear evidence that the RAS is activated in depleted teleosts and amphibians.