Teunissen K E, Postma C T, van Jaarsveld B C, Derkx F H, Thien T
Department of Medicine of the University Hospital Nijmegen, The Netherlands.
J Hypertens. 1997 Dec;15(12 Pt 2):1791-6. doi: 10.1097/00004872-199715120-00091.
To determine whether active renin and endothelin levels in venous plasma differ between patients with renal artery stenosis and patients with primary hypertension. Among the patients with renal artery stenosis we also compared active renin and endothelin levels between subjects who had been cured or whose blood pressure had improved after treatment of the stenosis and those without a beneficial reaction after such treatment.
We measured immunoreactive endothelin and active renin levels in peripheral venous plasma before and 1 h after angiotensin converting enzyme inhibition in 25 patients with primary hypertension and in 27 patients with hypertension and renal artery stenosis. Percutaneous transluminal angioplasty was performed in 21 patients of the latter group. For 11 patients of this group, hypertension was cured or there was an improvement, whereas 10 other patients did not respond to this treatment. Baseline active renin and endothelin levels were compared between these groups, as were the clinical characteristics of the patients.
Baseline endothelin levels were similar in members of the renal artery stenosis [median 3.6 pg/ml (range 1.4-11.7)] and in members of the no stenosis group [5.0 pg/ml (1.5-8.0)]. Also baseline endothelin levels did not differ between members of the successfully treated [3.6 pg/ml (1.8-8.9)] and unsuccessfully treated groups [3.75 pg/ml (1.4-8.3)]. Angiotensin converting enzyme (ACE) inhibition failed to cause a significant change in endothelin level in members of any of the patient groups. Although baseline renin levels differed significantly between members of the renal artery stenosis and no stenosis groups [40.2 microu/ml (0.9-543) versus 13.4 microu/ml (2.5-931), (P< 0.05)], there was no difference in baseline renin levels between the members of successful and unsuccessful groups [25.7 microu/ml (9.2-475.6) versus 65.3 microu/ml (12.3-542.6)]. ACE inhibition caused a significant increase in renin level in members of all groups except the unsuccessfully treated group.
Circulating endothelin levels did not differ significantly among patients with essential hypertension, hypertension with renal artery stenosis and proven renovascular hypertension and, although the renin-angiotensin system was clearly activated in members of the renovascular hypertension group, ACE inhibition did not affect their endothelin levels. These results suggest that endothelin does not play a direct role in the pathophysiology of renovascular hypertension.
