Circulatory Response to Oral Furosemide Administration in Patient with Unmedicated Essential Hypertension

Abstract

Circulatory dynamics at rest and after the oral administration of 80 mg furosemide were evaluated in 46 patients with normal-renin hypertension,34 patients with low-renin hypertension and 28 normal subjects. The normal-renin hypertensives were comprised of 29 men and 17women, and the low-renin hypertensives of 13 men and 21 women. Cases with severe staged hypertension were excluded from this study.
Hemodynamic parameters were determined by Impedance Cardiography at rest and three hours after administration of furosemide in supine position.
At rest, the normal and the low-renin hypertensives showed smaller stroke index than the normal subjects, but cardiac index did not differ significantly among three groups. In the lowrenin hypertensives, mean and diastolic blood pressure and total peripheral resistance were higher than the normal-renin hypertensives.Hematocrit was significantly lower in the low-renin group than the other two groups.
Urine volume following three hours of furosemide administration was smaller in the hypertensive group than the normals, but no difference was found between the normal-renin and the low-renin groups. Hematocrit increased indentically in all three groups.
The normal subjects responded to the provocation of furosem ide by significant reduction of cardiac output and elevation of total peripheral resistance without any significant changes in heart rate and mean blood pressure. These observations indicate that the blood pressure was maintained by the elevation of total peripheral resistance in response to the reduction of circulatory blood volume and cardiac output induced by the diuretic effect of furosemide. The normal-renin hypertensives responded to furosemide by significant reduction of blood pressure and stroke index with significant increase in heart rate and total peripheral resistance. This group showed greater reduction of stroke index and increase of heart rate compared to lowrenin group. These findings suggest that in addition to the effect of angiotensin II, the increased sympathetic activity was one of the major compensatory mechanism following the provocation of furosemide. On the other hand, low-renin hypertensives responded to furosemide by significant reduction of cardiac output and marked reduction of blood pressure. There were no significant changes in heart rate and total peripheral resistance in low-renin hypertensives. In low-renin hypertension, it is assumed that hypervolemia is one of the most important factor to maintain the high blood pressure. Therefore, it is suggested that the reductin of blood pressure and cardiac output following furosemide were observed without compensatory sympathetic activity.