INTRODUCTION:
Ovarian hormone deprivation associated with systemic arterial hypertension can synergistically compromise cardiac morphology and function. This scenario is particularly relevant for women with premature ovarian failure, increasing cardiovascular risk. In turn, aerobic physical training (APT) is widely recognized as a therapeutic tool that promotes beneficial effects on cardiac morphology and function under different disease conditions. Therefore, we investigated the application of APT as a countermeasure to the impairments induced by early ovarian hormone deprivation in hypertensive rats.
METHODS:
The experimental protocols were conducted on spontaneously hypertensive rats (SHR, N=32) and normotensive Wistar Kyoto rats (WKY, n=32). At the eighteenth week of life, half of the rats in each group underwent ovariectomy (OVX; N=16), and the other half underwent sham surgery (SHAM; N=16). After two weeks, the animals were again divided into two new groups (N=08): trained groups (SHAM and OVX) and groups subjected to aerobic physical training through swimming for 14 weeks, five days a week (SHAM-T and OVX-T). Before (twentieth week of life) and after 14 weeks (thirty-fourth week of life), all rats had their cardiac morphology and function analyzed by means of two-dimensional echocardiography. Finally, all the rats were euthanized, and their hearts were removed for analysis of coronary bed reactivity and left ventricular contractility using the Langendorff technique.
RESULTS:
Cardiac morphology and function analysis show that ovariectomy independently reduced systolic volume, ejection fraction, and shortening fraction. It also increased left ventricular (LV) diastolic and systolic diameter and volume in SHR. In turn, APT promoted opposite effects on LV dimensions depending on hormonal status. Whereas in SHAM rats APT reduced LV end-diastolic diameter and volume, in OVX rats APT increased these parameters. Isolated LV contractility evaluation showed that ovariectomy reduced dP/dtmax and dP/dtmin values independently, and LV pressure in SHR. In turn, APT increased dP/dtmin values in SHR. Finally, β-adrenergic sensitivity evaluation showed that ovariectomy independently increased the LV pressure response to salbutamol, whereas APT reduced it. Also, APT suppressed the increase in LV dobutamine response secondary to ovariectomy.
CONCLUSION:
The ovariectomy-induced cardiac morphology and functional impairments observed on hypertensive rats were accompanied by a compensatory increase in β-adrenergic responsiveness. Although the APT protocol did not alter the ovariectomy-induced dilated cardiac phenotype observed in vivo, it independently increased dP/dtmin and normalized the β-adrenergic responsiveness secondary to hormone deprivation. These results suggest that APT may normalize the ovariectomy-induced increase in β-adrenergic responsiveness. Furthermore, the increase in dP/dtmin appears to be independent of hormonal status or morphological remodeling.