Noradrenaline receptor mechanisms modulate the angiotensin II-induced water intake in the subfornical organ in rats.

The present study was carried out to clarify the role of noradrenergic systems in the mediation of drinking response to angiotensin II (ANG II) in the rat subfornical organ (SFO). Microinjection of ANG II (10 pmol, 50 nl) into the SFO caused a robust drinking response (water volume, 1.8-8.7 ml for 20 min). Injections of either noradrenaline (NA; 0.1, 1 and 10 nmols, 50 nl) into the SFO did not produce a significant water intake. Phenylephrine (Phen; 0.1, 1, 10 nmols, 50 nl), an α-adrenoceptor agonist, injected into the SFO elicited little drinking in the rats tested (water volume, 0.4-1.5 ml for 20 min). Previous injections of NA (0.1 and 1 nmols) or Phen (0.1, 1 and 10 nmols) significantly enhanced the water intake elicited by the injection of ANG II into the SFO. Neither the α-adrenoceptor agonist clonidine (Clon; 10 nmol, 50 nl) nor the β-adrenoceptor agonist isoprenaline (Isop; 10 nmol, 50 nl) into the SFO caused a significant water intake. Previous injections of Clon (0.1, 1 and 10 nmol, 50 nl) into the SFO were without effect on the water intake produced by the ANG II injection into the SFO. Pretreatment with Isop (1 and 10 nmols), on the other hand, significantly attenuated the drinking response to ANG II. Vehicle (artificial cerebrospinal fluid, 50 nl) had no effect on the ANG II-induced water intake. These results suggest that both α1-(facilitatory) and β-(inhibitory) adrenoceptor mechanisms may be implicated in the control of drinking response induced by angiotensinergic activation of SFO neurons.