Plasma Kinin Levels in Acute Renovascular Hypertension in Dogs

Publisher Website
Google Scholar
Abstract
The role of kinins in the hypertensive response to acute renal artery constriction (RAC) was examined in the dog. RAC resulted in an increase in systemic arterial pressure (SAP) from 144 ± 6 to 155 ± 4 mm HG (p < 0.05). Simultaneously, arterial plasma bradykinin decreased from 2.3 ± 0.2 to 1.4 ± 0.1 ng/ml (p < 0.01), while renal venous bradykinin remained unchanged (2.3 + 0.2 to 2.0 + 0.4 ng/ml, p > 0.05). At the same time urinary kallikrein decreased from 55 ± 6 to 33 + 4 milliesterase units (mEU)/min (p < 0.05), while urinary kinin decreased from 3.2 + 0.4 to 1.9 + 0.3 ng/min (p < 0.05). There was a significant correlation between the decrease in arterial bradykinin and the rise in SAP induced by RAC (p < 0.01). Administration of the dipeptidyl hydrolase inhibitor SQ20881 during RAC reduced angiotensin-converting enzyme levels from 578 + 86 to 10 + 0.0 mU/ml (p < 0.005). There was an associated increase in arterial bradykinin (1.4 + 0.1 to 5.8 ± 0.8 ng/ml, p < 0.001), renal venous bradykinin (2.0 + 0.4 to 5.7 ± 0.5 ng/ml, p < 0.005), and urinary kinin (1.9 ± 0.3 to 5.0 ± 0.7 ng/min, p < 0.01) in conjunction with return of SAP to control levels. Urinary kallikrein, however, remained depressed following SQ20881 (33 ± 4 to 30 ± 5 mEU/min, p > 0.05). These results suggest that (1) decreases in circulating BK may potentiate the vasoconstrictor effect of angiotensin II and contribute to the hypertension induced by RAC, and (2) urinary kallikrein is an unreliable marker of changes in plasma bradykinin in this model of hypertension.