[The effect of alterations of the renin-angiotensin system and the sympathetic nervous system on plasma bradykinin concentration in patients with essential hypertension].
We studied the possible interplay between plasma bradykinin (P-BK) and the renin-angiotensin axis in essential hypertension, the effect of catecholamine on P-BK by standing and norepinephrine (NE) infusion, and the possible role of bradykinin in the hypotensive mechanism of angiotensin I converting enzyme inhibitor (captopril) in renin-independent essential hypertension. Plasma bradykinin was measured by sensitive radioimmunoassay in 44 hypertensive patients and compared with that of 24 normotensive subjects. P-BK was not significantly reduced in hypertensive patients, and when subjects were divided by age range, the P-BK was reduced by aging in normotensive subjects but not in hypertensive patients, and the elder (60 approximately 80 yr) age normotensive group showed significantly (p less than 0.05) lower P-BK compared with the elder hypertensive group. 28 essential hypertensive patients (EHT) who were classified as WHO stageI (n=15) and WHO stageII (n=13) were given 80 mg of furosemide orally and kept upright for 4 hours. Plasma renin activity (PRA), P-BK, plasma aldosterone (P-Ald) and serum angiotensin converting enzyme activity (ACEA) were measured before and after furosemide administration. Twelve normotensive subjects served as controls. PRA, P-Ald and ACEA showed a significant increase (p less than 0.05) in all groups in response to furosemide. In normotensives, basal P-BK was 11.1 +/- 1.3 pg/ml which increased to 15.6 +/- 1.8 pg/ml (p less than 0.02) after furosemide. These changes of P-BK were in parallel with PRA, P-Ald and ACEA. In the WHO stageI EHT group, baseline P-BK was 9.7 +/- 1.3 pg/ml which increased to 15.6 +/- 1.8 pg/ml (p less than 0.02) and PRA, P-Ald and ACEA showed a similar increase as in normotensives. In the WHO stageII EHT patients, however, P-BK showed only a slight increase from 9.8 +/- 1.0 pg/ml to 12.0 +/- 1.1 pg/ml after furosemide. These changes were smaller either than normotensives or the WHO stageI EHT group. There was a slight but significant correlation between PRA and P-BK in normotensives and in the WHO stageI EHT. There was no correlation between PRA and P-BK in the WHO stageII EHT. The present results do not support the view that there may be a direct linkage between the kallikrein kinin system and the renin angiotensin axis mediated by kininase II or angiotensin converting enzyme in human peripheral blood.(ABSTRACT TRUNCATED AT 400 WORDS)
D000328:Adult; D000367:Age Factors; D001794:Blood Pressure / Q000187:drug effects; D001920:Bradykinin / Q000097:blood*; D002216:Captopril / Q000494:pharmacology; D005665:Furosemide / Q000494:pharmacology; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000503:physiopathology; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood; D007703:Peptidyl-Dipeptidase A / Q000097:blood; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System; D013564:Sympathetic Nervous System / Q000503:physiopathology*
D005665:Furosemide; D002216:Captopril; D007703:Peptidyl-Dipeptidase A; D012083:Renin; D001920:Bradykinin; D009638:Norepinephrine