Immunoreactive bradykinin and [des-Arg9]-bradykinin in low-renin essential hypertension--before and after treatment with enalapril (MK 421)

• Published in: The Journal of laboratory and clinical medicine Vol. 102; no. 5; p. 714
• Main Authors: Odya, C E, Wilgis, F P, Walker, J F, Oparil, S
• Format: Journal Article
• Language: English
• Published: United States 01-11-1983
• Subjects: Adult; African Continental Ancestry Group; Aged; Animals; Bradykinin - analogs & derivatives; Bradykinin - blood; Bradykinin - urine; Dipeptides - administration & dosage; Enalapril; European Continental Ancestry Group; Female; Humans; Hypertension - drug therapy; Hypertension - physiopathology; Male; Middle Aged; Rabbits; Radioimmunoassay; Renin - blood; Time Factors
• ISSN: 0022-2143

Bradykinin (BK) and [des-Arg9]-bradykinin (-9BK) concentrations in blood and urine samples from 18 normotensive subjects and 23 patients with low-renin essential hypertension were determined by radioimmunoassay. BK and -9BK levels in venous blood from normotensive subjects were 67.1 +/- 60.8 pg/ml and 204.1 +/- 44.5 (mean +/- S.D.), respectively, and levels in urine from normotensive subjects were 5.3 +/- 5.3 ng/ml and 1.6 +/- 1.2, respectively. The blood and urinary levels of BK and -9BK in low-renin essential hypertensives were not significantly different from those of normotensives and did not change when the hypertensives were treated with the new orally active angiotensin I-converting enzyme (ACE) inhibitor, enalapril (MK421). It has been proposed that BK levels do not change with ACE inhibition because under these conditions BK might be metabolized to -9BK by kininase I. Since -9BK levels did not increase with MK421 treatment, this possibility can be excluded. The absence of elevations in blood and urine BK and -9BK after administration of MK421 does not support an involvement of kinins in the mechanism of antihypertensive action of MK421 in these patients. On the basis of the data, it is not possible to exclude such an involvement, however, because local changes in kinin concentrations could occur that are not reflected by changes in circulating or urinary kinin levels.