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Renal control of renin secretion and some actions of the angiotensins in the kidney of the teleost Salmo gairdneri Bailey, John Richard

Abstract

The renin-angiotensin system is a hormonal system found throughout the vertebrate phylogenetic scale with the exception of elasmobranchs and cyclostomes. This sytem has only been extensively studied in mammalian species to date. Renin secretion, in the mammals studied, is influenced by a number of factors such as renal perfusion pressure, renal tubular sodium levels, circulating catecholamines and the sympathetic nervous sytem. In fishes factors which influence renin secretion had not been investigated but it was known that dehydration of fishes caused a depletion of renal renin stores. This action may be due to two possible causes either a decline in blood volume with a consequent decrease in blood pressure or an increased blood osmotic pressure due to water loss. Therefore the effects of changing either blood pressure or blood osmolarity (using sodium as the osmotically active paricle) on renin release were investigated. Further some actions of the angiotensins on the trout kidney were investigated to determine the action of the renin-angiotensin system in combatting dehydration. Since it is very difficult to assay renin per se, it is necessary to assay renin activity, i.e., to determine the amount of product formed from the renin-renin substrate reaction. This has been done by means of a bioassay but since the bioassay technique tends to be time consuming, a radioimmunoassay technique was developed. A significant correlation between blood loss and plasma renin activity was established. Further work using an isolated non-filtering perfused kidney preparation showed that a decline in renal perfusion pressure caused an increase in renin release as evidenced by an increase in renin activity. This appeared to be a direct effect on the renin-secreting cells as sympathetic blocking agents had no effect on the response. Increasing renal perfusion pressure has little or no effect on renin secretion but the end product of the system, angiotensin II, will apparently inhibit further renin secretion by a short-loop negative feedback type system. Plasma sodium levels do not appear to affect renin secretion in the trout as hypertonic sodium perfusion of the isolated non-filtering kidney had no effect on renin release. Similarily, hypertonic sodium perfusion of the isolated filtering kidney had'no apparent effect on renin release, which indicates that renal tubular sodium loads have no effect on renin secretion in this species. Angiotensin II is known to have several diverse actions in mammalian kidneys but its action in the fish kidney was obscure. It was found that angiotensin I has little or no effect on urine flow rates but has an apparent antinatriuretic effect on the renal tubules. Angiotensin II on the other hand has both a diuretic and an antidiuretic effect, depending on which part of the renal vasculature is stimulated. In addition, the angiotensin II has an antinatriuretic effect which is of similar magnitude to that exerted by angiotensin I arid this may also be a direct effect on the renal tubule. These data indicate that the angiotensins may have a role in the maintenance of blood volume and blood osmolarity in the trout. They also indicate that the angiotensin I may have been the primitive messenger of the system as this compound is not highly active in mammalian species.

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