INFLUENCE OF DOPAMINE-RECEPTOR AND ADRENOCEPTOR BLOCKADE ON THE HEMOCONCENTRATING AND HYPOTENSIVE ACTIONS OF ATRIAL-NATRIURETIC-PEPTIDE

Atrial natriuretic peptide (ANP) lowers mean arterial pressure (MAP) a nd increases hematocrit through reduction in plasma volume caused by a transcapillary shift of plasma fluid and protein toward the interstit ium. We examined the consequences of blockade of the dopaminergic and adrenergic systems on the hypotensive and hemoconcentrating responses to ANP. Changes in MAP, hematocrit, and plasma protein concentration ( PPC) were measured in anesthetized acutely binephrectomized rats, duri ng infusion of ANP alone (1 mu g.kg(-1).min(-1) for 45 min) or in the presence of haloperidol (20 mu g.kg(-1).min(-1)), phentolamine (15 mu g.kg(-1).min(-1)), or propranolol (10 mu g.kg(-1).min(-1)). Infusion o f ANP reduced MAP by 8.6 +/- 1.3% and increased hematocrit by 9.0 +/- 0.6% (both p < 0.005 vs. vehicle). PPC increased (4.4 +/- 0.6%; p < 0. 005 vs. vehicle) significantly less than hematocrit, indicating extrav asation of proteins. The ANP-evoked reduction in MAP was not affected in haloperidol- or phentolamine-treated rats (-8.8 +/- 2.3 and -10.5 /- 2.4%, respectively; both p < 0.005 vs. vehicle) but was abolished i n propranolol-treated rats (+3.2 +/- 1.3%; p = ns vs. vehicle). The AN P-induced increase in hematocrit was slightly attenuated in haloperido l-, phentolamine-, and propranolol-treated rats (7.5 +/- 0.7, 7.3 +/- 0.8, and 6.0 +/- 1%, respectively). In addition, the coefficient of re flection, an index of the permeability to proteins, was higher in thes e three groups (0.41 +/- 0.06, 0.49 +/- 0.08, and 0.57 +/- 0.14, respe ctively) than in control rats infused with ANP (0.27 +/- 0.03), indica ting an attenuation of the ANP-induced extravasation of proteins. Thus , in binephrectomized rats, the hypotensive activity of ANP requires a beta-adrenergic component, whereas its hemoconcentrating action is, a t least in part, dependent upon dopaminergic and adrenergic activation .