Role of Ca2+ in response of aldosterone to stimulation by angiotensin II in vivo.

The role of Ca2+ in stimulation of aldosterone secretion (ASR) has been evaluated in vivo using conscious sheep with an adrenal cervical autotransplant. The calcium antagonists verapamil, nisoldipine, and lanthanum and the calcium ionophore BAY K 8644 were infused into the adrenal arterial supply before or concomitantly with angiotensin II. Nisoldipine reversed stimulation of ASR (n = 4) from 13.6 +/- 3.2 to 4.8 +/- 1.2 nmol/h (P less than 0.01; control 2.3 +/- 0.6 nmol/h), as did verapamil. Lanthanum had an intermediate effect. In contrast, pretreatment with nisoldipine (n = 5) did not affect the response to angiotensin II, with ASR being 3.8 +/- 0.9 nmol/h after nisoldipine alone and 12.8 +/- 1.3 nmol/h after nisoldipine plus angiotensin II. In response to graded infusion of angiotensin II, nisoldipine blunted (P less than 0.01) to a small degree the response at all doses of the peptide. Close adrenal arterial infusion of the ionophore BAY K 8644 similarly reversed stimulation of ASR by angiotensin II. It also blocked the initiation of response to the peptide. These data are consistent with the involvement of two pools of calcium in the zona glomerulosa response to angiotensin II, an intracellular pool that is primarily responsible for the initiation of response and a transmembrane extracellular pool that is primarily involved in the "sustained" response to angiotensin II.