Acute and chronic effects of exercise on baroreflexes in spontaneously hypertensive rats.

We studied the effects of acute and chronic exercise on the arterial baroreflex and chemosensitive cardiopulmonary baroreflex (CCB) in spontaneously hypertensive rats (SHR). Arterial baroreflex and CCB were evaluated in normotensive rats (NR, n=11) and SHR (n=5) at rest and after 30 minutes of an acute bout of exercise (45 minutes at 50% of VO2max). In addition, these baroreflexes were evaluated in sedentary (n=5) and exercise-trained (n=9) SHR. Exercise training was performed on a motor treadmill, 5 days/week, during 60 minutes, at 50% of VO2max. Baroreflex bradycardia and tachycardia, analyzed by baroreflex sensitivity index (delta heart rate/delta mean arterial pressure), were significantly lower in SHR than in NR (0.7+/-0.1 versus 2.0+/-0.1 and 1.8+/-0.2 versus 3.4+/-0.1 beats per minute [bpm]/mm Hg, respectively). During the recovery period from acute exercise, baroreflex bradycardia was significantly higher than at rest only in SHR (1.7+/-0.1 versus 0.7+/-0.1 bpm/mm Hg). Hypotension and bradycardia induced by CCB stimulation (5-hydroxytryptamine, I.V.) were similar between SHR and NR, and an acute exercise bout did not change these responses. Exercise training markedly improved baroreflex bradycardia and tachycardia in SHR (1.9+/-0.1 versus 0.7+/-0.1 and 2.9+/-0.1 versus 1.8+/-0.2 bpm/mm Hg, respectively). Exercise-trained rats had greater bradycardiac (118+/-26 versus 14+/-2 and 209+/-30 versus 19+/-5 bpm to 1 and 2 microg/kg 5-HT, respectively) and hypotensive (30+/-6 versus 15+/-3 and 45+/-7 versus 17+/-2 mm Hg to 1 and 2 microg/kg 5-hydroxytryptamine, respectively) responses to CCB stimulation. In conclusion, an acute bout of exercise increases baroreflex bradycardia in SHR, and exercise training attenuates hypertension concomitant with improved arterial baroreflex and CCB sensitivity in SHR.