Vasodepressor effects of prazosin during insulin-induced hypoglycemia in hypertensive patients.

As both hormonal and hemodynamic alterations similar to those occurring during exercise can also be produced in humans by hypoglycemia, the present study explored changes in hemodynamic parameters during hypoglycemia and the effects of the alpha 1-adrenergic blocker, prazosin, on those responses in hypertensive patients. In the control group, which did not receive prazosin, plasma epinephrine, plasma norepinephrine and plasma renin activity (PRA) all increased along with a rise in blood pressure during hypoglycemia. On the other hand, the blood pressure decreased despite similar increases in plasma catecholamine levels and PRA in the prazosin treated group. The hemodynamic parameters, analyzed using M-mode echocardiography, changed in both the control and prazosin groups during hypoglycemia; stroke volume and cardiac output showed similar increases. However, while the total peripheral resistance did not change significantly in the control group, it decreased in the prazosin group during hypoglycemia. In accord with the changes in total peripheral resistance, the increment in mean-velocity of circumferential fiber shortening (m-Vcf) during hypoglycemia was greater in the prazosin group than in the control. These results suggest that: hypoglycemia stimulates the sympatho-adrenal axis which then releases catecholamines leading to a rise in blood pressure and tachycardia; In contrast, the blood pressure decreases during hypoglycemia in the prazosin group despite an increase in plasma catecholamines, because the alpha-receptors are blocked by prazosin and the unopposed beta-adrenergic effects of the catecholamines are pronounced enough to reduce the total vascular resistance.