title: [3H]nitrendipine binding to adrenal capsular membranes.
abstract: The physiologic regulation of aldosterone secretion is dependent on extracellular calcium and appears to be mediated by increases in cytosolic free calcium concentration in the zona glomerulosa cell. A specific role for voltage-dependent calcium channels was suggested by previous studies with the calcium channel antagonist verapamil. We therefore studied the [3H]nitrendipine calcium channel binding site in adrenal capsules. These studies revealed a single class of saturable, high affinity sites with KD = .26 +/- .04 nM and Bmax = 105 +/- 5.7 fmol/mg protein. Specific binding of [3H]nitrendipine was inhibited by calcium channel antagonists with potencies nitrendipine = nifedipine much greater than verapamil, while diltiazem had no inhibitory effect. In the rat, binding sites for [3H]nitrendipine were located in the adrenal capsule and medulla and were undetectable in the zona fasciculata. Physiologic studies with collagenase-dispersed adrenal glomerulosa cells demonstrated that nifedipine selectively inhibited angiotensin-II and potassium-stimulated steroidogenesis. These observations suggest both a pharmacologic and physiologic role for the nitrendipine binding site in aldosterone production.
mesh_terms: D000313:Adrenal Medulla / Q000378:metabolism*; D000450:Aldosterone / Q000096:biosynthesis; D000818:Animals; D001665:Binding Sites; D001667:Binding, Competitive; D004110:Diltiazem / Q000378:metabolism; D007700:Kinetics; D008566:Membranes / Q000378:metabolism; D009543:Nifedipine / Q000031:analogs & derivatives* / Q000378:metabolism; D009568:Nitrendipine; D051381:Rats; D014700:Verapamil / Q000378:metabolism
chemical_list: D000450:Aldosterone; D009568:Nitrendipine; D014700:Verapamil; D004110:Diltiazem; D009543:Nifedipine