Abstract
Arginine vasopressin may contribute to cardiovascular regulation by causing vasoconstriction and stimulating renal water absorption through V1 and V2 receptors, respectively. Arginine vasopressin may play an important role in congestive heart failure. Recently, oral vasopressin V1 and V2 receptor antagonists were synthesized, however, the effect of vasopressin V1 and V2 receptor antagonists on heart failure is still unclear. We examined the effect of vasopressin Vl receptor antagonist and vasopressin V2 receptor antagonist on heart failure after acute and chronic myocardial infarction. Myocardial infarction was made to the rats by ligation of left anterior descending coronary artery. On one day (acute) and two months (chronic) after the surgery, we orally administered V1 receptor antagonist at 60 mg/kg/day or V2 receptor antagonist at 30 mg/kg/day to myocardial infarcted rats. After one week of treatment, we measured the hemodynamics and electrolytes in the blood. In the acute and chronic myocardial infarcted rats, the left ventricular endodiastolic pressure (LVEDP) increased to 16 ± 3 and 20 ± 4 mmHg, respectively, and V2-ant decreased LVEDP to 6 ± 4(p < 0,01) and 5 ± 3 mmHg (p < 0.011, respectively. V2-ant decreased significantly the left ventricular endodiastolic volume (LVEDV) in chronic myocardial infarction (non-treated rats; 2.31 ± 0.18, V2-ant treated vats; 1,76 ± 0.10 ml/kg)(p < 0,01). In the chronic myocardial infarcted rats, abdominal ascites appeared, and the weight of lung or liver increased. V2 receptor antagonist decreased them. V2 receptor antagonist improved hemodynamics and the signs of heart failure in myocardial infarcted rats. V1 receptor antagonist tended to decrease LVEDP in the acute and chronic myocardial infarcted rats. V1 and V2 receptor antagonists did not change the electrolytes in the blood, Vasopressin antagonist, especially V2 receptor antagonist, is a useful drug for heart failure after myocardial infarction.
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