Rapid baroreceptor resetting in chronic hypertension: Implications for normalization of arterial pressure

Abstract

The purpose of this study was to examine the ability of baroreceptors of renal hypertensive rabbits to reset rapidly during acute changes in arterial pressure. The carotid sinus (CS) was vascularly isolated and baroreceptor activity was recorded during slow ramp increases in CS pressure in hypertensive (one-kidney, one wrap; 127±3 mm Hg) and normotensive (one-kidney, no wrap; 85 ±3 mm Hg) rabbits anesthetized with chloralose. Control measurements were made after holding pressure for 10-15 minutes at the level of arterial pressure recorded before each experiment. Baroreceptor threshold pressure (Pth) was higher in hypertensives (78±4 mm Hg) compared with normotensives (55±3 mm Hg, p<0.05), and nerve activity was less in hypertensives over a wide range of pressure. CS distensibility (sonomicrometers) was not significantly different in the two groups. After increasing holding pressure from control by 30 and 60 mm Hg for 10-15 minutes, the extent of baroreceptor resetting (Δ Pth/Δ holding pressure×100%) in normotensives was 39±6% and 33±2%, respectively, but only 14±5% and 9±3% in hypertensives (p<0.05). After decreasing holding pressure by 30 and 60 mm Hg, resetting was similar in normotensives (32±6% and 28±3%) and hypertensives (34±3% and 30±4%). In hypertensive rabbits, acute (10-15 minutes) exposure of baroreceptors to normotension (71±4 mm Hg) decreased Pth to 62±4 mm Hg and increased nerve activity to levels not significantly different from those of normotensive animals without altering CS distensibility. The results indicate that in chronic renal hypertension: 1) further upward resetting of baroreceptors during acute increases in pressure is suppressed; 2) in contrast, downward resetting during acute decreases in pressure is preserved; 3) baroreceptor activity is restored rapidly after brief exposure of the CS to normal pressure; and 4) changes in CS distensibility do not explain decreased baroreceptor activity in chronic hypertension nor restoration of activity after acute normalization of pressure. Impairment of acute upward resetting and preservation of downward resetting should be beneficial since they would oppose further increases in pressure and facilitate lowering of pressure.