Estudo do efeito do estresse crônico sobre a função cardiovascular em ratas normotensas e espontaneamente hipertensas (SHR)

Abstract

The aim of the present study was to investigate the physiological and somatic changes, with emphasis on the analysis of effects on cardiovascular function, induced by exposure to chronic stress in normotensive male and female rats. We also investigated the possible vulnerability of spontaneously hypertensive females rats (SHR) to physiological and somatic effects induced by stress protocols. The animals were exposed to 10 days protocols of repeated restraint stress (RRS) and chronic variable stress (CVS) protocols. We observed that control females presented basal HR values higher than males, and this effect was related to higher cardiac sympathetic activity and lower cardiac parasympathetic activity, when compared to males. In addition, both RRS and CVS caused HR increase in males, in which it was related to an increase in cardiac sympathetic activity. However, only RRS increased basal HR in females, in which it was also accompanied by an increase in cardiac sympathetic activity. Both RRS and CVS increased plasma corticosterone levels in females. We observed that both stress protocols decreased body weight gain only in males. In addition, CVS caused adrenal hypertrophy in males. Both RRS and CVS reduced the reflex bradycardia response triggered by increased blood pressure in males. In addition, CVS increased the reflex tachycardiac response triggered by decreases of blood pressure in males. Neither of the chronic stress protocols influenced baroreflex activity in females. Regarding the blood pressure response to vasoactive agents, we observed that the pressor response due to the intravenous administration of phenylephrine was not altered by neither of the chronic stress protocols in both genders. The response of acetylcholine was reduced only by CVS in males and increased by both stress protocols in females. The RRS also increased the SNP response in males, but in females both protocols decreased the response to SNP. As expected, we observed that SHR females had higher baseline blood pressure values than normotensive females. RRS caused an increase in basal heart rate in both normotensive and SHR female rats, in which it was related to an increase in cardiac sympathetic activity. Both chronic stress protocols increased baseline plasma corticosterone levels and reduced body weight gain in both SHR and normotensive females. In addition, CVS and RRS caused hypertrophy of the adrenal glands in normotensive rats and increased thymus weight in SHR rats. In summary, concerning to the influence of sexual dimorphisms, the results indicate that, regardless of the type of stress, males are vulnerable to somatic effects and on body weight, while females appear to be more susceptible to the effects of chronic stress on baseline HPA axis activity. In addition, present findings indicate that females are selectively vulnerable to cardiovascular and autonomic changes evoked by homotypic stressors, whereas homotypic and heterotypic stressors similarly affect cardiovascular function and autonomic activity in males. Regarding an influence of hypertension, the findings did not indicate differences in cardiovascular, somatic and neuroendocrine responses induced by stress protocols in normotensive and SHR female rats.