Dopaminergic control of angiotensin II-induced vasopressin secretion in vitro
Rossi, N.F.
American Journal of Physiology 275(4): E687-E693
1998
ISSN/ISBN: 0002-9513 PMID: 9755089 Document Number: 491476
Because dopamine influences arginine vasopressin (AVP) release, the present studies were designed to ascertain the dopamine receptor subtype that potentiates angiotensin II-induced AVP secretidon in cultured hypothalamo-neurohypophysial explants. Dopamine (a nonselective D1/D2 agonist), apomorphine (a D2 mchgt D1 agonist), and SKF-38393 (a selective D1 agonist) dose dependently increased AVP secretion. Maximal AVP release was observed with 5 muM dopamine, 307 +- 66% explant-1cntdoth-1, 1 muM SYF-38393, 369 +- 41%cntdotexplant-1cntdoth-1, and 0.1 muM apomorphine, 374 +- 67%cntdotexplant-1 cntdotH-1. Selective D1 antagonism with 1 muM SCH-23390 blocked AVP secretion to values no different from basal. Domperidone (D2 antagonist), phenoxybenzamine (nonselective adrenergic antagonist), and prazosin (alpha1-antagonist) failed to prevent release. D1 antagonism also prevented AVP secretion to 1 muM angiotensin II (angiotensin II, 422 +- 87%cntdotexplant-1cntdoth-1 vs. angiotensin II plus SCH-23390, 169 +- 28%cntdotexplant-1cntdoth-1 (P < 0.05)), but D2 and alpha1-adrenergic blockade did not. In contrast, AT1 receptor inhibition with 0.5 muM losartan blocked angiotensin II- but not dopamine-induced AVP release. AT2 antagonism had no effect. Although subthreshold doses of the agonists did not increase AVP secretion (0.05 muM dopamine, 133 +- 44%cntdotexplant-1cntdoth-1; 0.01 muM SKF-38393, 116 +- 26%cntdotexplant-1cntdoth-1), and 0.001 muM angiotensin II, 104 +- 29%cntdotexplant-1 cntdoth-1), the combination of dopamine and angiotensin II provoked a significant rise in AVP (420 +- 83%cntdotexplant-1cntdoth-1 (P < 0.01)). Similar results were observed with SKF-38393 and angiotensin II, and the AVP response was blocked to basal levels by either D1 or AT1 antagonism. These findings support a role for D1 receptor activation to increase AVP release and mediate angiotensin II-induced AVP release within the hypothalamo-neurohyPophysial system. The data also suggest that the combined subthreshold stimulation of receptors that use distinct intracellular pathways can prompt substantial AVP release.