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Background and aim: The goal of this study was to investigate whether physical stress is able to modulate apoptotic response in rat myocardial tissue. The effects of foot shock stress on the histopatological changes and immunohistochemistry for p53, bcl-2 and bax were evaluated. Methods: Male Wistar rats (n= 10) were distributed into two groups: group 1, control and group 2, stress. The stress protocol consisted of one daily foot-shock session applied on three consecutive days. Results: The results pointed out no remarkable changes of myocardial tissue between groups. Also, the foot shock stress was not able to modulate p53, bcl-2 or bax expression, as depicted by no significant statistically differences (P > 0.05) between groups for all immunomarkers evaluated. Conclusions: Taken together, our results suggest that foot shock stress did not induce histopathological changes in rat myocardial tissue. It seems that physical stress is not able to modulate apoptotic response in rats. Certainly, this finding offers new insights into the mechanisms underlying the relation between apoptosis and cardiac injury after stress.

Several cardiovascular disorders have been related to alterations in beta-adrenoceptor (beta-AR) signaling at or beyond the receptor level. During the stress reaction, the sympathetic-adrenal medullary system and the hypothalamus-pituitary-adrenal cortex axis are activated, causing beta-AR overstimulation and remodeling of the beta(1)/beta(2)/beta(3)-AR ratio in cardiomyocytes. In a model of foot-shock stress, we described decreased beta(1)-AR signaling occurring simultaneously with increased beta(2)-AR signaling, whereas the response to the nonconventional agonist, CGP12177, was not altered. These alterations may play an adaptive role to the increased sympathetic drive to the heart, protecting the cardiac tissue from the cardiotoxic effects mediated by beta(1)-ARs overstimulation without altering cardiac output, since this would be sustained by the beta(2)-AR, which would also protect myocytes from apoptosis. Moreover, the selective enhancement of the beta(2)-AR population might help to diminish the risk of overstimulation since this adrenoceptor subtype couples to both, stimulatory G (Gs) and inhibitory G (Gi) proteins. On the other hand, in the model of neurogenic hypertension, the decrease in beta(1)-AR-mediated response is not followed by increase in the beta(2)-AR-mediated response. However, the response to CGP12177, which was desensitized 48 h after the surgery, was normalized 7 days after that, when beta(1)-AR were downregulated. Therefore, both experimental models provided evidence that the classical isoform of beta(1)-AR and the recently described low-affinity isoform of beta(1)-AR show independent behavior and provide the heart with adaptive mechanisms to increased sympathetic stimulation during stress.

Adipocytes isolated from epididymal adipose tissue of foot-shock stressed rats are supersensitive to isoprenaline and subsensitive to norepinephrine. These alterations are probably mediated by a stress-induced increase in plasma corticosterone levels. We investigated whether foot-shock stress modifies the expression of glucocorticoid receptors (GRs) and beta-adrenergic protein receptors (beta-ARs) in epididymal adipose tissue from rats submitted to one daily foot-shock session on three consecutive days. This stress protocol caused decreases in GR, beta(1)-AR, and beta(3)-AR protein levels, but caused an increase in beta(2)-AR. These results confirm and support previous functional studies. The alterations in protein expression may be modulated by the high corticosterone levels that downregulate the glucocorticoid receptor.