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

A profound elevation of blood pressure on exercises or after withdrawal of antihypertensive drugs has been reported in patients with a history of acce lerated-malignant hypertension. We tested the hypothesis that severe endoth elial dysfunction is responsible for the profound hypertensive response in these patients. Responses of blood pressure, heart rate and plasma cyclic g uanosine monophosphate to intravenously infused L-arginine, a precursor of nitric oxide, was investigated in hypertensive patients with (group A) or w ithout any history of accelerated-malignant hypertension (group B) in order to evaluate endothelial function. Casual blood pressure or severity of hyp ertension was not different between group A and B. Infusion of L-arginine d ecreased 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-argin ine in group B (5.4 +/- 2.0 to 7.7 +/- 1.7 pmol/ml, P < 0.01), while no sig nificant 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 pre ssure and increase in plasma levels of cyclic guanosine monophosphate (r = 0.83, P < 0.001). The results indicated that much more severe endothelial d ysfunction is present in hypertensive patients with a history of accelerate d-malignant hypertension as compared to those without the history. The diff erence in the endothelial function may account for the different presser re sponses to exercises or other stimuli observed in hypertensive patients wit h and without a history of accelerated-malignant hypertension.