Background: Angiotensin II can impair endothelial function, which is mediated by the angiotensin II type 1 receptor subtype.
Objective: To test the hypothesis that treatment with the angiotensin II type 1 receptor antagonist losartan would restore the normal dilation of the left main coronary artery to the cold pressor test in patients with essential hypertension, as assessed by echocardiography.
Patients and methods: The study population included 24 patients with mild to moderate essential hypertension and 24 matched, healthy subjects. The cold pressor test-induced and nitroglycerin-induced changes in the left main coronary artery diameter were measured by echocardiography at the end of the washout period and after 12 weeks of losartan administration.
Results: The percentage change in the left main coronary artery diameter induced by the cold pressor test in patients with hypertension (-4.3 8.7%) was significantly lower than that in control subjects (10.5 3.9%, P<0.0001). The percentage change in the left main coronary artery diameter induced by the cold pressor test in patients with essential hypertension after losartan treatment (13.7 8.0%) was significantly higher than that before losartan treatment (-4.3 8.7%, P<0.0001). The percentage change in the left main coronary artery diameter induced by the cold pressor test after losartan treatment was not significantly different between the 14 patients with hypertension who had satisfactory control of blood pressure (14.1 8.8%) and the 10 patients with hypertension who did not have satisfactory control of blood pressure (13.1 7.0, P=0.8). Losartan treatment in patients with essential hypertension did not modify the percentage change in the left main coronary artery diameter caused by sublingual administration of nitroglycerin (23.2 14.4% versus 27.2 13.5, P=0.2).
Conclusions: The present study demonstrates that treatment with the angiotensin II type 1 receptor antagonist losartan normalized the response of the left main coronary artery to the cold pressor test in patients with mild to moderate essential hypertension, and that this effect is not dependent on the reduction of blood pressure.