Role of calcium ions in the pressure control of renin secretion from the kidneys

Abstract

Abstract. 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 retool/1 ("normal") or zero calcium concentrations (calcium-free perfusate with 0.5 mmol/1 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 t~mol/1) stimulated RSR in a pressure-dependent fashion at a calcium concentration of 1.5 mmol/1. 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/1) in the range between 40 mmHg and 140mmHg (5-19kPa) 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.

Role of cGMP-kinase II in the control of renin secretion and renin expression.

“…Because cGK activation also inhibited renin secretion induced by low extracellular calcium, a condition for example under which the inhibitory effect of angiotensin II on renin secretion is completely abolished (52), it may be inferred that the inhibitory effect of cGKII is not mediated by the inhibitory calcium pathway controlling renin secretion and renin synthesis. Further studies will therefore be necessary to define the inhibitory effect of cGKII at the level of the JG cell.…”

Connexins: Key Mediators of Endocrine Function

“…As in many other secretory cells, renin secretion is controlled by an interplay of several intracellular second messengers (472). However, and at variance with many other secretory mechanisms which are stimulated when the free cytosolic concentration of free Ca 2ϩ increases (401,402,572), it is a lowering in the cytosolic levels of the cation that trigger renin secretion (281,465,466). Conversely, the renin-producing cells are locally inhibited by an increase in either blood pressure or blood volume and flow, as well as by elevated circulating levels of angiotensin II and Na ϩ (32, 472).…”

Effect of amlodipine on renin secretion and renin gene expression in rats

“…In renal JG cells an elevation of cytosolic calcium appears to inhibit the secretion of renin, a phenomenon that has been called the 'calcium paradox' of renin secretion (Hackenthal et al, 1990). There is good evidence that calcium is required for the inhibitory action of angiotensin II on renin secretion (Vandongen & Peart, 1974;Antonipillai & Horton, 1985;Scholz et al, 1994) and also for the baroreceptor control of renin secretion, in particular for the inhibition of renin secretion at higher perfusion pressure (Fray 1976;Fray & Park, 1979;Jones & Churchill, 1993). Recent findings, moreover, suggest that calcium is not only inhibitory for renin secretion but also for renin gene expression on the level of renal JG cells (Della Bruna et al, 1995).…”