Análise da resposta de parâmetros hemodinâmicos à infusão de tiramina pós-treinamento físico em ratos epontaneamente hipertensos

Abstract

Overactivity of the sympathetic nervous system and increased peripheral vascular resistance are crucial features that promote and sustain arterial hypertension. Exercise training is an important tool in the control of blood level, nevertheless its direct influence on peripheral vascular control is still under explored. The aim of the present study was to assess the effects of exercise training by swimming in the vascular control after sympathetic stimulation mimicked by tyramine infusion in spontaneously hypertensive rats (SHR) and theirs normotensive controls (Wistar-Kyoto rats - WKY). Thirty three male rats (48-50 weeks-old) were submitted or not to swimming protocol during 8 weeks, resulting in four experimental groups: sedentary normotensive (SN, n=7), trained normotensive (TN, n=8), sedentary hypertensive (SH, n=9) and trained hypertensive (TH, n=10) rats. Arterial pressure (AP), heart rate (HR), heart rate variability (HRV) in time domain and frequency and AP variability (APV) were recorded in baseline conditions. Following, the infusion of tyramine in three doses (75, 150 and 300 μL/Kg) was administrated. Resting bradycardia was observed in both TN and TH rats compared with their respective sedentary animals (p<0.005). Exercise training attenuated AP in TH vs. SH (p<0.001). The variance of HRV was lower in SH vs. TH (p=0.018). The other hand, the variance of SAPV and DAPV were higher in SH vs. TH (p=0.05). The TN and TH presented an increased parasympathetic modulation compared with their respective sedentary groups (p<0.05). The pressor response to tyramine was enhanced in trained SHR, but not in sedentary SHRs. This fact suggests that physical training promotes a reduction in norepinephrine release, which can be also associated with a smaller sympathetic tonus and a reduction in the vascular peripherical resistance. In conclusion, exercise training is able to attenuate the damage causade by arterial hypertension, acting both on the adequacy of cardiovascular autonomic balance as decreasing peripherical vascular resistance, probably by stimulating a lower release of norepinhephrine to sympathetic stimulation.