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

• Grant number: 14/50141-2
• Support Opportunities: Regular Research Grants - Publications - Scientific article
• Start date: April 01, 2014
• End date: September 30, 2014
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: Monica Akemi Sato
• Grantee: Monica Akemi Sato
• Host Institution: Faculdade de Medicina do ABC (FMABC). Santo André , SP, Brazil
• City of the host institution: Santo André

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)