Conivaptan HCl Vasopressin Receptor antagonist

Conivaptan (0.03, 0.1 and 0.3 mg/kg i.v.) dose-dependently increases urine volume and reduces urine osmolality in both myocardial infarction and sham-operated rats. Conivaptan (0.3 mg/kg i.v.) significantly reduces right ventricular systolic pressure, left ventricular end-diastolic pressure, lung/body weight and right atrial pressure in myocardial infarction rats. Conivaptan (0.3 mg/kg i.v.) significantly increases dP/dt(max)/left ventricular pressure in myocardial infarction rats. [1] Conivaptan produces an acute increase in urine volume (UV), a reduction in osmolality (UOsm) and, at the end of the investigation, cirrhotic rats receiving the V(1a)/V(2)-AVP receptor antagonist does not show hyponatremia or hypoosmolality. Conivaptan also normalizes U(Na)V without affecting creatinine clearance and arterial pressure. [2] Conivaptan (0.01 to 0.1 mg/kg i.v.) exerts a dose-dependent diuretic effect in dogs without an increase in the urinary excretion of electrolytes, inhibits the pressor effect of exogenous vasopressin in a dose-dependent manner (0.003 to 0.1 mg/kg i.v.) and, at the highest dose (0.1 mg/kg i.v.), almost completely blocks vasoconstriction caused by exogenous vasopressin. Conivaptan (0.1 mg/kg i.v.) improves cardiac function, as evidenced by significant increases in left ventricular dP/dtmax, cardiac output and stroke volume, and reduces preload and afterload, as evidenced by significant decreases in left ventricular end-diastolic pressure and total peripheral vascular resistance in dogs with congestive heart failure. [3]