RENAL DENERVATION PREVENTS SODIUM RETENTION AND HYPERTENSION IN SALT-SENSITIVE RABBITS WITH GENETIC BAROREFLEX IMPAIRMENT

1. Rabbits with a genetic impairment in baroreflex control of heart ra te become hypertensive on a high salt diet, The present study determin ed the effect of bilateral renal denervation on blood pressure and sod ium balance after salt loading (four times normal intake; 28-36 mEq Na Cl/day) rabbits with high (Group I) and baroreflex sensitivity, respec tively, 2. Eight rabbits in each group were denervated or sham-denerva ted 1 week before commencement of the high salt diet, Before operation , the two groups differed only in the gain of their cardiac baroreflex (Group I, -6.4 +/- 0.4 beats min(-1) mmHg(-1); Group II, -3.2 +/- 0.1 5 beats min(-1) mmHg(-1)). 3. In Group I sham-denervated rabbits, mean arterial pressure remained unchanged, and plasma renin activity and h eart rate fell significantly in response rep the high salt, In Group I I sham-denervated rabbits, mean arterial pressure increased by 10.6 +/ - 1.2 mmHg, and heart rate and plasma renin activity remained unchange d, Their cumulative Na+ retention and weight gain was more than twice that of Group 1 sham-denervated rabbits, 4. Renal denervation decrease d plasma renin activity in both groups to <1 pmol Ang I h(-1) ml(-1), lowered cumulative Na+ retention from 102 +/- 4 to 35 +/- 5 mEq (P<0.0 1) and completely prevented the increase in mean arterial pressure in response to high salt in Group II, 5. The results suggest that Group I I rabbits retain salt and fluid in response to their diet because of a n abnormality in their control of renal nerve activity, possibly via b lood vagal afferents, This results in elevation because of an inabilit y to pressure lower peripheral resistance and heart rate in response t o the increase in cardiac output, 6. Since they display several of the characteristics of salt-sensitive hypertensive humans, i,e, salt rete ntion, normal plasma renin activity, but abnormal regulation of plasma renin activity and blood flow in response to salt loading, Group II a re an appropriate model of human salt-induced hypertension.