A KALLIKREIN-LIKE ENZYME IN THE AORTA OF NORMOTENSIVE AND HYPERTENSIVE RATS

We evaluated whether vascular kallikrein is altered in rats with genet ic or experimental hypertension. Group 1 was infused intraperitoneally with angiotensin II (Ang II) or vehicle for 4 weeks; group 2 was inje cted subcutaneously with deoxycorticosterone (75 mu mol/kg once a week ) or vehicle for 4 weeks; group 3 consisted of uninephrectomized rats on high sodium intake given deoxycorticosterone or vehicle; and group 4 consisted of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Active and total kallikrein activity was measured in abdom inal aortic homogenates using an amidolytic assay. Ang II increased sy stolic blood pressure at a dose of 400 nmol/kg per day (146+/-6 versus 123+/-3 mm Hg in controls, P<.01) but not at 80 nmol/kg per day. Deox ycorticosterone did not increase blood pressure except in uninephrecto mized rats on high salt (173+/-6 versus 135+/-4 mm Hg in controls, P<. 01). Blood pressure averaged 194+/-2 mm Hg in SHR and 123+/-3 mm Hg in WKY rats. Vascular kallikrein was similar in rats given Ang II or veh icle. In deoxycorticosterone-treated rats total kallikrein was higher than in controls (9.2+/-0.8 versus 3.5+/-0.1 pkat/mg protein, P<.05), whereas active kallikrein did not differ (0.09+/-0.04 versus 0.09+/-0. 03 pkat/mg protein, P=NS). A similar pattern was observed in uninephre ctomized deoxycorticosterone-treated rats (active, 0.09+/-0.03 versus 0.10+/-0.04, P=NS; total, 7.4+/-0.7 versus 4.1+/-0.2 pkat/mg protein, P<.05). Kallikrein activity was higher in SHR compared with WKY rats ( active, 0.34+/-0.04 versus 0.10+/-0.03; total, 9.5+/-1.2 versus 4.6+/- 0.3 pkat/mg protein, P<.05). In conclusion, a kallikrein-like enzyme i s present in rat aorta. The activity of this enzyme is elevated in rat s with genetic hypertension, and it may be regulated by mineralocortic oids.