We examined the contribution of endogenous prostanoids to baroreceptor activation in chronic renal hypertension. Baroreceptor activity was recorded from the vascularly isolated carotid sinus during slow ramp increases in pressure in rabbits anesthetized with pentothal and chloralose. Mean arterial pressure averaged 133±4 mmHg in hypertensive rabbits (one kidney, one wrap, n = 12) and 85±3 mmHg in normotensive rabbits (one kidney, no wrap, n = 13). Baroreceptor activity was decreased significantly (P < 0.05) in the hypertensive compared with the normotensive rabbits. The decreased baroreceptor activity could not be explained by decreased distensibility of the carotid sinus (sonomicrometers). Inhibition of the endogenous formation of prostanoids with intrasinus administration of indomethacin (50 .M) decreased baroreceptor activity in normotensive (P < 0.05) but not in hypertensive rabbits over a wide range of pressures. At a pressure of 120 mmHg, activity declined from 61±14 spikes/s before indomethacin to 47±12 spikes/s with indomethacin, i.e., a drop of 24±4%. In contrast, corresponding values in hypertensive rabbits averaged 41±13 and 40±12 spikes/s (-1±2%). Intrasinus prostacyclin, on the other hand, increased activity in both groups: at 120 mmHg activity increased from 62±9 to 92±15 spikes/s (51±17%) in normotensive rabbits and from 29±7 to 47±14 spikes/s (68±23%) in hypertensive rabbits. Neither indomethacin nor prostacyclin (n = 5) influenced the pressure-diameter relation of the carotid sinus. The increase in prostacyclin (6-keto-PGFI.) formation by the sinus in response to its exposure to arachidonic acid (10 AM) was significant (P < 0.05) in the normotensives (1,627±344%; n = 5) but not in the hypertensives (583±353%; n = 5). We conclude that the decreased baroreceptor activity in chronic hypertension may not be caused by decreased distensibility of the vascular wall of the sinus and that endogenous prostanoids that contribute to baroreceptor activation in normotensive rabbits fail to do so in hypertensive rabbits. This appears to be due to decreased formation of prostacyclin rather than decreased sensitivity of the

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 (PtJ 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 (A P^/A holding pressure x 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 Pa, 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. (Hypertension 1991;17:72-79) B aroreceptors buffer fluctuations in arterial pressure by causing reflexly mediated reciprocal changes in both heart rate and sympathetic nerve activity. 1 These changes keep the level of arterial pressure at a predetermined operating level or set point. When changes in pressure are sustained for several minutes, however, baroreceptors are reset rapidly and the baroreceptor pressure-activity curve shifts in the direction of pressure change to function at a new set point. 2 -5 This allows baroreceptors to buffer fluctuations of arterial pressure effectively because the new pressure set point remains on the steep portion of the reset pressure-activity curve. However, resetting provides positive feedback in the control of arterial pressure. During acute hypotension, baroreceptor activity increase...

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