DIFFERENT MECHANISMS OF POLYURIA AND NATRIURESIS ASSOCIATED WITH PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA

The mechanism of polyuria associated with paroxysmal supraventricular tachycardia (SVT) was investigated in 8 patients. SVT was induced artificially and sustained for 60 minutes. Urine and blood samples were collected every 30 minutes. During the latter half of SVT, urine flow increased twofold in the control subjects before SVT. Urinary sodium excretion increased significantly ( < 0.01) within 30 minutes after SVT. Urinary excretion of antidiuretic hormone (ADH) decreased (p < 0.01) during the latter half of SVT and increased (p < 0.01) after SVT, respectively. Plasma level of ADH did not change during SVT but increased (p < 0.05) after SVT. The concentration of plasma atrial natriuretic polypeptide (ANP) increased significantly (p < 0.05) before SVT ended. Urinary excretion of prostaglandin E2 increased significantly (p < 0.05) after termination of SVT. The percent changes in the urinary excretion of prostaglandin E2 were correlated (r = 0.713, p < 0.001) with those of ADH. There was also a correlation (r = 0.6, p < 0.001) between the percent changes in the urinary excretion of prostaglandin E2 and those of sodium. Their findings suggest that the polyuria during SVT is attributed mainly to the inhibition of ADH release and that the natriuresis after SVT is due not only to the increased ANP but also to the increased renal prostaglandin E2 probably stimulated by ADH.