title: Baroreflex deficit blunts exercise training-induced cardiovascular and autonomic adaptations in hypertensive rats.
abstract: 1. Baroreceptors regulate moment-to-moment blood pressure (BP) variations, but their long-term effect on the cardiovascular system remains unclear. Baroreceptor deficit accompanying hypertension contributes to increased BP variability (BPV) and sympathetic activity, whereas exercise training has been associated with an improvement in these baroreflex-mediated changes. The aim of the present study was to evaluate the autonomic, haemodynamic and cardiac morphofunctional effects of long-term sinoaortic baroreceptor denervation (SAD) in trained and sedentary spontaneously hypertensive rats (SHR). 2. Rats were subjected to SAD or sham surgery and were then further divided into sedentary and trained groups. Exercise training was performed on a treadmill (five times per week, 50-70% maximal running speed). All groups were studied after 10 weeks. 3. Sinoaortic baroreceptor denervation in SHR had no effect on basal heart rate (HR) or BP, but did augment BPV, impairing the cardiac function associated with increased cardiac hypertrophy and collagen deposition. Exercise training reduced BP and HR, re-established baroreflex sensitivity and improved both HR variability and BPV. However, SAD in trained SHR blunted all these improvements. Moreover, the systolic and diastolic hypertensive dysfunction, reduced left ventricular chamber diameter and increased cardiac collagen deposition seen in SHR were improved after the training protocol. These benefits were attenuated in trained SAD SHR. 4. In conclusion, the present study has demonstrated that the arterial baroreflex mediates cardiac disturbances associated with hypertension and is crucial for the beneficial cardiovascular morphofunctional and autonomic adaptations induced by chronic exercise in hypertension.
authors.affiliation: Experimental Hypertension Laboratory, Hypertension Unit, Heart Institute, Sao Paulo, Brazil.
authors.forename: I C
authors.initials: IC
authors.lastname: Moraes-Silva
authors.forename: R N
authors.initials: RN
authors.lastname: De La Fuente
authors.forename: C
authors.initials: C
authors.lastname: Mostarda
authors.forename: K
authors.initials: K
authors.lastname: Rosa
authors.forename: K
authors.initials: K
authors.lastname: Flues
authors.forename: N R
authors.initials: NR
authors.lastname: Damaceno-Rodrigues
authors.forename: E G
authors.initials: EG
authors.lastname: Caldini
authors.forename: K
authors.initials: K
authors.lastname: De Angelis
authors.forename: E M
authors.initials: EM
authors.lastname: Krieger
authors.forename: M C
authors.initials: MC
authors.lastname: Irigoyen
mesh_terms: D000222:Adaptation, Physiological / Q000502:physiology*; D000818:Animals; D017763:Autonomic Denervation; D017704:Baroreflex / Q000502:physiology*; D006339:Heart Rate / Q000502:physiology; D006973:Hypertension / Q000503:physiopathology / Q000628:therapy*; D008297:Male; D009200:Myocardial Contraction; D010805:Physical Conditioning, Animal / Q000379:methods; D011311:Pressoreceptors / Q000502:physiology* / Q000601:surgery; D051381:Rats; D011918:Rats, Inbred SHR