Failure of L-arginine to induce hypotension in patients with a history of accelerated-malignant hypertension

Abstract

A profound elevation of blood pressure on exercises or after withdrawal of antihypertensive drugs has been reported in patients with a history of accelerated-malignant hypertension. We tested the hypothesis that severe endothelial dysfunction is responsible for the profound hypertensive response in these patients. Responses of blood pressure, heart rate and plasma cyclic guanosine monophosphate to intravenously infused L-arginine, a precursor of nitric oxide, was investigated in hypertensive patients with (group A) or without any history of accelerated-malignant hypertension (group B) in order to evaluate endothelial function. Casual blood pressure or severity of hypertension was not different between group A and B. Infusion of L-arginine decreased mean blood pressure in group B (97.4 ± 8.7 to 81.7 ± 6.9 mm Hg), but not in group A (99.0 ± 10.2 to 101.5 ± 8.7 mm Hg). Plasma levels of cyclic guanosine monophosphate were increased after infusion of L-arginine in group B (5.4 ± 2.0 to 7.7 ± 1.7 pmol/ml, P< 0.01), while no significant changes were observed in group a (5.4 ± 2.1 to 5.9 ± 2.1 pmol/ml). there was a significant correlation between decrease in mean blood pressure and increase in plasma levels of cyclic guanosine monophosphate (r = 0.83, P < 0.001). the results indicated that much more severe endothelial dysfunction is present in hypertensive patients with a history of accelerated-malignant hypertension as compared to those without the history. the difference in the endothelial function may account for the different pressor responses to exercises or other stimuli observed in hypertensive patients with and without a history of accelerated-malignant hypertension.