Role of AVP in pressor responses during activation of central TxA2/PGH2 receptors.
Administration of thromboxane A2/prostaglandin H2 (TxA2/PGH2)-receptor agonist U-46619 (2.86 nmol/kg i.v.) to conscious rats increased mean arterial pressure (MAP) by 17 +/- 2 mmHg (n = 6; P < 0.001) and plasma arginine vasopressin (AVP) by 3.5 +/- 1.1 IU/ml (n = 6; P < 0.001). Ifetroban (TxA2/PGH2 antagonist; intracerebroventricularly) prevented both responses. Intracerebroventricular U-46619 increased MAP in Long-Evans rats (n = 6) more than in AVP-deficient Brattleboro rats. AVP V1-receptor antagonist d(CH2)5Tyr(Me)AVP (3 microg/kg i.v.) blocked 67 +/- 5% and 69 +/- 7% of pressor response to intravenous AVP and intracerebroventricular U-46619, respectively. AVP (10 ng/kg i.v.) increased 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 pressor response.