ROLE OF AVP IN PRESSOR-RESPONSES DURING ACTIVATION OF CENTRAL TXA(2) PGH(2) RECEPTORS/

Administration of thromboxane A(2)/prostaglandin Hz (TxA(2)/PGH(2))-re ceptor agonist U-46619 (2.86 nmol/kg iv) to conscious rats increased m ean arterial pressure (P6AP) by 17 +/- 2 mmHg (n = 6; P < 0.001) and p lasma arginine vasopressin (AVP) by 3.5 +/- 1.1 IU/ml (n = 6; P < 0.00 1). Ifetroban (TxA(2)/PGH(2) antagonist; intracerebroventricularly) pr evented both responses. Intracerebroventricular U-46619 increased MAP in Long-Evans rats (n = 6) more than in AVP-deficient Brattleboro rats . AVP VL-receptor antagonist d(CH2)(5)Tyr(Me)AVP (3 mu g/kg iv) blocke d 67 +/- 5% and 69 +/- 7% of presser response to intravenous AVP and i ntracerebroventricular U-46619, respectively. AVP (10 ng/kg iv) increa sed AVP by 4.7 +/- 0.5 pg/ml, comparable to the increase of 3.5 +/- 1. 2 pg/ml with intracerebroventricular U-46619 (2.86 nmol/ kg), but the rise in MAP was only one-half as great (+8 +/- 3 mmHg for AVP vs. +17 +/- 2 mmHg for U-46619; P < 0.05). In conclusion, U-46619 raises blood pressure and releases AVP by activating brain receptors. AVP explains approximately one-half of the presser response.