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Am J Physiol Heart Circ Physiol 273: H1927-H1932, 1997;
0363-6135/97 $5.00
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Vol. 273, Issue 4, H1927-H1932, October 1997

Role of AVP in pressor responses during activation of central TxA2/PGH2 receptors

Christopher S. Wilcox, Hubin Gao, Joseph G. Verbalis, and William J. Welch

Division of Nephrology and Hypertension and Division of Endocrinology and Metabolism, Georgetown University Medical Center, Washington, District of Columbia 20007

Administration of thromboxane A2/prostaglandin H2 (TxA2/PGH2)-receptor agonist U-46619 (2.86 nmol/kg iv) 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 µg/kg iv) blocked 67 ± 5% and 69 ± 7% of pressor response to intravenous AVP and intracerebroventricular U-46619, respectively. AVP (10 ng/kg iv) 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.

vasopressin; thromboxane A2/prostaglandin H2 receptors; ifetroban; brain; U-46619


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