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Swimming exercise changes hemodynamic responses evoked by blockade of excitatory amino receptors in the rostral ventrolateral medulla (RVLM) in spontaneously hypertensive rats (SHR)

Abstract

Exercise training reduces sympathetic activity in hypertensive humans and rats. We hypothesized the swimming exercise would change the neurotransmission into the RVLM, a key region involved in sympathetic outflow, and hemodynamic control in SHR and Wistar-Kyoto (WKY) rats. Bilateral injections of kynurenic acid (KYN) were carried out into the RVLM in sedentary (S) or exercised (E) SHR and WKY rats submitted to swimming for 6 wks. Rats were alpha-chloralose anesthetized, artificially ventilated, with Doppler flow probes around the lower abdominal aorta and superior mesenteric artery. Injections into the RVLM were made prior and after i. v. L-NAME (nitric oxide synthase, NOS, inhibitor). Injections of KYN into the RVLM elicited a major vasodilation in the hind limb than in the mesenteric artery in E-SHR compared to S-SHR, but similar decrease in arterial pressure was observed in both groups. Injections of KYN into the RVLM elicited L-NAME attenuated the hind limb vasodilation evoked by KYN and increased the mesenteric vasodilation in E-SHR. Swimming exercise can enhance the hind limb vasodilation mediated by peripheral NO release, reducing the activation of neurons with EAA receptors in the RVLM in SHR. (AU)