ANGIOTENSIN-CONVERTING ENZYME-INHIBITION, BUT NOT CALCIUM ANTAGONISM,IMPROVES A RESPONSE OF THE RENAL VASCULATURE TO L-ARGININE IN PATIENTS WITH ESSENTIAL-HYPERTENSION

Citation
Y. Higashi et al., ANGIOTENSIN-CONVERTING ENZYME-INHIBITION, BUT NOT CALCIUM ANTAGONISM,IMPROVES A RESPONSE OF THE RENAL VASCULATURE TO L-ARGININE IN PATIENTS WITH ESSENTIAL-HYPERTENSION, Hypertension, 32(1), 1998, pp. 16-24
Citations number
44
Categorie Soggetti
Peripheal Vascular Diseas
Journal title
ISSN journal
0194911X
Volume
32
Issue
1
Year of publication
1998
Pages
16 - 24
Database
ISI
SICI code
0194-911X(1998)32:1<16:AEBNCA>2.0.ZU;2-A
Abstract
Endothelial function has been shown to be impaired in patients with es sential hypertension. The purpose of the present study was to determin e whether antihypertensive drug therapy improves impaired endothelium- dependent renal vasorelaxation in essential hypertensive patients with out atherosclerosis. We evaluated the effects of intravenous infusion of L-arginine (500 mg/kg given over 30 minutes) on systemic and renal hemodynamics in 27 patients with mild to moderate essential hypertensi on who were randomly assigned to treatment with either the angiotensin -converting enzyme inhibitor imidapril or the calcium antagonist amlod ipine for 12 weeks in a double-blind fashion. After the 12 weeks, the decrease in blood pressure was similar in the imidapril (n=14) and aml odipine (n=13) groups. The increase in renal plasma flow was also simi lar in both groups. L-Arginine-induced renovascular relaxation was inc reased by imidapril (renal plasma flow, 9.6+/-5.1% to 14.4+/-7.4%; ren al vascular resistance, -10.4+/-8.1% to -16.7+/-9.2%, P<0.05, respecti vely) but not by amlodipine. Urinary excretion of nitrite/nitrate in r esponse to L-arginine was significantly increased by imidapril (90+/-2 9% to 134+/-63%, P<0.05) but remained unchanged by amlodipine, These f indings suggest that angiotensin-converting enzyme inhibition improves the impaired endothelium-dependent renovascular relaxation in patient s with essential hypertension due to the increase in nitric oxide prod uction and that the reduction in blood pressure with a calcium antagon ist does not play a major role in the potentiation of L-arginine/nitri c oxide-mediated effects.