ROLE OF CALCIUM-IONS IN THE PRESSURE CONTROL OF RENIN SECRETION FROM THE KIDNEYS

In this study we examined the role of calcium ions in the control of renin release by the renal artery pressure. For this purpose renin secretion rates (RSR) were measured in isolated rat kidneys perfused at pressures of 140, 100, 80 and 40 mmHg [19, 13, 11, 5 kPa) with media containing either 1.5 mmol/l (''normal'') or zero calcium concentrations (calcium-free perfusate with 0.5 mmol/l EGTA). At normal calcium the RSR was inversely related to the renal artery pressure, whereas calcium withdrawal resulted in an almost linear and proportional relationship between RSR and perfusion pressure. As a consequence, RSR at 140 mmHg (19 kPa) with a calcium-free medium was similar to renin release at 40 mmHg (5 kPa) with normal calcium. The nitric oxide (NO) donor sodium nitroprusside (1 mu mol/l) stimulated RSR in a pressure-dependent fashion at a calcium concentration of 1.5 mmol/l. With a calcium-free perfusate, sodium nitroprusside did not restore the inverse pressure dependence of RSR seen with normal calcium but almost doubled the RSR across the whole pressure range. Whilst RSR was significantly reduced by angiotensin II (1 nmol/l) in the range between 40 mmHg and 140 mmHg (5-19 kPa) with normal calcium, withdrawal of extracellular calcium ions practically abolished the inhibitory action of angiotensin II. Since angiotensin II attenuated RSR especially at low renal perfusion pressure, our results indicate that renin release in this pressure range is still inhibitable by calcium mobilization in renal juxtaglomerular cells. Thus, the enhancement of renin secretion at lower pressures cannot be explained by a decreased sensitivity of renin release towards calcium ions. Instead, our data support the hypothesis that the ''baroreceptor'' control of renin secretion is maintained through a pressure-related calcium influx mechanism into juxtaglomerular cells which counteracts the stimulatory effect of locally released NO.