Fumio Ida

Exercise Training Increases Baroreceptor Gain Sensitivity in Normal and Hypertensive Rats

Exercise training attenuates arterial hypertension and increases baroreflex sensitivity in spontaneous hypertension. However, no information exists regarding the portion of the baroreflex arch in which this attenuation takes place. We tested the hypothesis that exercise training increases the afferent pathway sensitivity of baroreflex control in both normotensive and spontaneously hypertensive rats (SHR). Arterial pressure and whole-nerve activity of the aortic baroreceptor (multifiber preparation) were evaluated in 30 male rats assigned to 4 groups: sedentary and exercise-trained normotensive rats and sedentary and exercise-trained SHR. Exercise training was performed on a motor treadmill, 5 d/wk for 60 minutes, gradually progressing toward a speed of 26.8 m/min. Exercise training reduced mean arterial pressure in conscious exercise-trained SHR (183±4 versus 165±7 mm Hg). The relation between changes in aortic baroreceptor discharge and changes in systolic arterial pressure increased significantly in exercise-trained normotensive rats (2.09±0.1 versus 1.44±0.1%/mm Hg) and exercise-trained SHR (0.92±0.1 versus 0.71±0.1%/mm Hg) compared with their respective sedentary rats. Likewise, the average aortic baroreceptor gain sensitivity (calculated by logistic equation) was significantly higher in exercise-trained normotensive rats (2.25±0.19 versus 1.77±0.03%/mm Hg) and exercise-trained SHR (1.07±0.04 versus 0.82±0.05%/mm Hg) compared with their respective sedentary control rats. In conclusion, exercise training increases aortic baroreceptor gain sensitivity in normotensive and SHR, thus improving baroreceptor sensitivity, which may result in a more efficient arterial pressure regulation by the baroreflexes.

Changes of Renal Sympathetic Activity in Acute and Chronic Conscious Sinoaortic Denervated Rats

The arterial pressure level attained in sinoaortic denervated rats depends on the net effect of eliminating excitatory and inhibitory influences (chemoreceptor and baroreceptor elimination, respectively). After sinoaortic denervation is completed, the hypertension usually observed within the first few days is followed by normotension at the chronic stages. In this work renal sympathetic nerve activity was measured in conscious, unrestrained rats 6 hours (acute) and 20 days (chronic) after sinoaortic denervation. Increased arterial pressure (154 +/- 10 versus 114 +/- 3 mm Hg in controls) and renal sympathetic nerve activity (32 +/- 5 versus 13 +/- 2 bars per cycle in controls) with no changes in heart rate (404 +/- 17 vs 380 +/- 26 beats per minute) were observed in rats with acute sinoaortic denervation. In rats with chronic sinoaortic denervation, arterial pressure (119 +/- 8 mm Hg) and renal sympathetic nerve activity (13 +/- 6 bars per cycle) returned to control levels. Bradycardiac and tachycardiac responses to changes in blood pressure were reduced to 88% and 89%, respectively, in rats with acute sinoaortic denervation and 76% and 74%, respectively, in rats with chronic sinoaortic denervation. The reflex control of renal sympathetic nerve activity after acute and chronic sinoaortic denervation showed an impairment of sympathoinhibition (0.13 +/- 0.02 and 0.25 +/- 0.1 bars per cycle, respectively, versus 0.9 +/- 0.17 bars per cycle in controls). Sympathoexcitatory responses also were impaired in rats with acute and chronic sinoaortic denervation (0.08 +/- 0.03 and 0.37 +/- 0.1 bars per cycle, respectively, compared with 0.98 +/- 0.2 bars per cycle in controls).(ABSTRACT TRUNCATED AT 250 WORDS)

RESETTING OF AORTIC BARORECEPTORS IN RESPONSE TO HYPOTENSION DOES NOT ALTER GAIN SENSITIVITY

1 In chronic hypertension, the baroreceptors reset to hypertensive levels with a decrease in gain sensitivity, but only a few studies have evaluated baroreceptor resetting during chronic hypotension and, under these conditions, no consistent information is available concerning changes in baroreceptor gain sensitivity. Therefore, in the present study, the aortic baroreceptor function curve and the baroreflex control of heart rate (HR) were evaluated in chronic hypotension produced by myocardial infarction (MI) with no heart failure. 2 Aortic baroreceptor function curves were studied in anaesthetized three groups of rats: (i) MI‐7, six rats 7 days after MI; (ii) MI‐30, nine rats 30 days after MI; and (iii) five control animals (SHAM). The pressure–nerve activity relationship was measured during rapid changes in blood pressure by integrating the whole‐nerve activity of the baroreceptors in a computerized beat‐to‐beat analysis. 3 Both long‐term periods (7 or 30 days) of hypotension were accompanied by complete resetting of the baroreceptor in rats (the leftward displacement of the baroreceptor curve matched the decrease in blood pressure). Moreover, the resetting of the baroreceptor function curve was not accompanied by changes in gain sensitivity (1.47, 1.64 and 1.67%/mmHg for SHAM, MI‐7 and MI‐30 groups, respectively) and the baroreflex control of HR was normal comparing SHAM and MI‐30 groups (bradycardic 1.62 ± 0.18 vs 1.99 ± 0.52 b.p.m./mmHg, respectively; tachycardic 3.6 ± 0.5 vs 4.1 ± 0.4 b.p.m./mmHg for, respectively). 4 The data indicate that the resetting of baroreceptors in chronic hypotension is stable and is not accompanied by changes in gain sensitivity, as observed in hypertension. This may account for the normal baroreflex control of HR observed in non‐anaesthetized rats.

Characteristics and Extent of Rapid Aortic Baroreceptor Resetting in Rat

The characteristics of rapid or acute resetting of the aortic baroreceptors were studied in anesthetized rats during 30 minutes of sustained hypertension produced by phenylephrine infusion. Two minutes after the onset of hypertension, a resetting of 26% (ratio of change in systolic threshold pressure to total change in diastolic pressure) was demonstrable. This represents 60% of the maximal resetting (43%) observed after 20 minutes. Thereafter, the magnitude of resetting remained stable. Pressure-nerve activity showed a parallel shift after 2 and 20 minutes of hypertension, with a slight tendency to increased slope at elevated pressures, especially in the baroreceptor function curve analyzed after 2 minutes. These results suggest that in rats, no significant difference exists in the time course for resetting of baroreceptor fibers with low vs. high thresholds. In contrast to other studies, reversibility of the resetting process was not complete within 30 minutes of pressure normalization, and the extent of reversal was no greater than 60%. The data of the present study, taken together with those obtained previously after 6 hours of hypertension, suggest that during the onset and maintenance of hypertension in rat, acute or rapid resetting of the baroreceptors reaches its maximum in 20 minutes (40%) and remains stable for up to 6 hours, with no apparent change in the baroreceptor gain.