Alpha 2-adrenoceptor antagonism attenuates the diuretic response to acute cold exposure

Abstract

Renal alpha 2-adrenoreceptors modulate the hydrosmotic action of arginine vasopressin (AVP) through suppression of AVP-stimulated adenosine 3',5'-cyclic monophosphate (cAMP) accumulation. Circulating catecholamines, likely candidates for the endogenous ligand, are elevated during cold exposure (CE). These studies therefore tested the hypothesis that the diuresis observed with acute CE in rats is due in part to modulation of AVP's tubular action via alpha 2-adrenoceptor activation. Subjects were five male Brattleboro homozygous diabetes insipidus (DI) rats (358 +/- 8 g) receiving chronic AVP replacement (1 microgram.kg-1 x day-1) and seven Long-Evans (LE) normal rats (395 +/- 5 g). In a CE protocol, baseline measurements at room temperature (RT, 24 +/- 0.3 degrees C) were followed by 60-min exposure to 5 +/- 0.5 degrees C. Results were compared with those from a RT time control protocol. The selective alpha 2-antagonist yohimbine (YOH; 10 micrograms.kg-1 x min-1) or vehicle (VEH) was infused throughout the CE and RT protocols. In VEH-infused rats, CE increased urine flow by 63 +/- 12 (DI rats) and 31 +/- 4 microliters.min-1 x 100 g body wt-1 (LE rats), and mean arterial pressure by 36 +/- 1 (DI rats) and 32 +/- 2 mmHg (LE rats). The increased flow was largely a water diuresis, with changes in free water clearance averaging 45 +/- 11 (DI rats) and 28 +/- 3 microliters.min-1 x 100 g body wt-1 (LE rats). YOH treatment completely blunted the cold-induced diuresis in both strains but did not alter the CE-induced hypertension. Glomerular filtration rate was not affected by either CE or YOH infusion.(ABSTRACT TRUNCATED AT 250 WORDS)