TY - JOUR
T1 - Renal denervation prevents sodium retention and hypertension in salt-sensitive rabbits with genetic baroreflex impairment
AU - Weinstock, Marta
AU - Gorodetsky, Elena
AU - Kalman, Ronald
PY - 1996
Y1 - 1996
N2 - 1. Rabbits with a genetic impairment in baroreflex control of heart rate become hypertensive on a high salt diet. The present study determined the effect of bilateral renal denervation on blood pressure and sodium balance after salt loading (four times normal intake; 28-36 mEq NaCl/day) in normotensive rabbits with high (Group I) and low (Group II) baroreflex sensitivity, respectively. 2. Eight rabbits in each group were denervated or sham-denervated 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 ± 0.15 beats min-1 mmHg-1). 3. In Group I sham-denervated rabbits, mean arterial pressure remained unchanged, and plasma renin activity and heart rate fell significantly in response to the high salt. In Group II sham-denervated rabbits, mean arterial pressure increased by 10.6 ± 1.2 mmHg, and heart rate and plasma renin activity remained unchanged. Their cumulative Na+ retention and weight gain was more than twice that of Group I sham-denervated rabbits. 4. Renal denervation decreased 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 < 0.01) and completely prevented the increase in mean arterial pressure in response to high salt in Group II. 5. The results suggest that Group II rabbits retain salt and fluid in response to their diet because of an abnormality in their control of renal nerve activity, possibly via vagal afferents. This results in blood pressure elevation because of an inability to lower peripheral resistance and heart rate in response to the increase in cardiac output. 6. Since they display several of the characteristics of salt-sensitive hypertensive humans, i.e. salt retention, normal plasma renin activity, but abnormal regulation of plasma renin activity and blood flow in response to salt loading, Group II are an appropriate model of human salt-induced hypertension.
AB - 1. Rabbits with a genetic impairment in baroreflex control of heart rate become hypertensive on a high salt diet. The present study determined the effect of bilateral renal denervation on blood pressure and sodium balance after salt loading (four times normal intake; 28-36 mEq NaCl/day) in normotensive rabbits with high (Group I) and low (Group II) baroreflex sensitivity, respectively. 2. Eight rabbits in each group were denervated or sham-denervated 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 ± 0.15 beats min-1 mmHg-1). 3. In Group I sham-denervated rabbits, mean arterial pressure remained unchanged, and plasma renin activity and heart rate fell significantly in response to the high salt. In Group II sham-denervated rabbits, mean arterial pressure increased by 10.6 ± 1.2 mmHg, and heart rate and plasma renin activity remained unchanged. Their cumulative Na+ retention and weight gain was more than twice that of Group I sham-denervated rabbits. 4. Renal denervation decreased 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 < 0.01) and completely prevented the increase in mean arterial pressure in response to high salt in Group II. 5. The results suggest that Group II rabbits retain salt and fluid in response to their diet because of an abnormality in their control of renal nerve activity, possibly via vagal afferents. This results in blood pressure elevation because of an inability to lower peripheral resistance and heart rate in response to the increase in cardiac output. 6. Since they display several of the characteristics of salt-sensitive hypertensive humans, i.e. salt retention, normal plasma renin activity, but abnormal regulation of plasma renin activity and blood flow in response to salt loading, Group II are an appropriate model of human salt-induced hypertension.
KW - Cardiopulmonary baroreceptors
KW - Conscious rabbits
KW - High salt intake
KW - Plasma renin activity
KW - Renal sympathetic nerves
KW - Sodium excretion
UR - http://www.scopus.com/inward/record.url?scp=0029922041&partnerID=8YFLogxK
U2 - 10.1042/cs0900287
DO - 10.1042/cs0900287
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C2 - 8777835
AN - SCOPUS:0029922041
SN - 0143-5221
VL - 90
SP - 287
EP - 293
JO - Clinical Science
JF - Clinical Science
IS - 4
ER -