Paraventricular nucleus injections of noradrenaline: cardiovascular effects in conscious Long-Evans and Brattleboro rats.

The cardiovascular effects of noradrenaline injected into the hypothalamic paraventricular nucleus (PVN) were investigated in conscious Long-Evans (control) rats and homozygous vasopressin (AVP)-deficient Brattleboro rats. Unilateral microinjection of noradrenaline (3-30 nmol) into the PVN produced dose-dependent increases in systolic and diastolic blood pressure of Long-Evans rats, and a concomitant decrease in heart rate. Only the highest dose of noradrenaline tested (30 nmol) caused a significant pressor response in Brattleboro rats (9 +/- 4/9 +/- 4 mm Hg, systolic/diastolic, n = 7) which was significantly smaller than the response produced by the same dose of noradrenaline in Long-Evans rats (32 +/- 8/27 +/- 6 mm Hg, n = 7). Intravenous pretreatment of Long-Evans rats with the V1-receptor antagonist, d(CH2)5Tyr[Et]DAVP, almost completely abolished the pressor effect of noradrenaline (10 nmol) without significantly attenuating the bradycardia. The alpha 2-adrenoceptor antagonist, idazoxan (4 nmol), injected into the PVN abolished the pressor response produced by noradrenaline (10 nmol) in Long-Evans rats but had no significant effect on the bradycardia. Pretreatment with the alpha 1-adrenoceptor antagonist, prazosin (0.7 nmol), significantly attenuated both the pressor and bradycardic effects of noradrenaline in Long-Evans rats. These results suggest that the pressor response produced by microinjection of noradrenaline into the hypothalamic PVN of conscious Long-Evans rats is mediated largely through stimulation of alpha 2-adrenoceptors and is dependent, in part, on release of AVP into the circulation. A component of the bradycardia seen with this intervention may be mediated through stimulation of alpha 1-adrenoceptors in the PVN.