Stretch receptor model for renin release with evidence from perfused rat kidney

Abstract

Control of renin release was studied in isolated rat kidneys perfused with Krebs-Henseleit solution containing albumin. Cumulative perfusate renin activity (PRA) as measured by radioimmunoassay was increased by low perfusion pressure and suppressed by high pressure. Renal vasoconstriction induced by infusion of phenylephrine or methoxamine increased PRA, whereas vasodilatation by papaverine suppressed renin activity. The increased renin activity induced by phenylephrine was blocked by high pressure or papaverine. Changing sodium concentration in the perfusion medium had no effect on basal renin release. A mathematical analysis for an intrarenal stretch receptor indicates that renin release is related to the elastic modulus, the internal and external hydrostatic pressures, and the internal and external radii. Calculations based on this model also indicate that renin release is most sensitive to changes in the ratio of the radii. It is proposed that basodilatation or high perfusion pressure may increase the stretch of the afferent arteriole and depolarize the granular cell membrane, whereas vasoconstriction or low pressure may decrease stretch and thus hyperpolarize the cell.