Influence of the estrous cycle on the sensitivity to catecholamines in right atria from rats submitted to foot-shock stress

Abstract

We investigated the mechanisms of the alterations in sensitivity to catecholamines in right atria from female rats exhibiting regular 4-day estrous cycles after three foot-shock sessions at estrus, metestrus, and diestrus or at diestrus, proestrus, and estrus. Right atria from stressed rats sacrificed at diestrus showed subsensitivity to noradrenaline and adrenaline. After in vitro sympathetic denervation (38 microM 6-hydroxydopamine) plus inhibition of neuronal reuptake (0.1 microM desipramine) subsensitivity to noradrenaline was abolished, but it was again evident when extraneuronal uptake was also inhibited (10 microM phenoxybenzamine and 30 microM corticosterone). The same pretreatment abolished the subsensitivity to adrenaline. After addition of 1 microM butoxamine, a beta 2-adrenoceptor antagonist, the tissues from stressed rats were subsensitive to adrenaline. Right atria from stressed rats sacrificed at estrus did not show any alteration in sensitivity to catecholamines. We conclude that after foot-shock stress, right atria from female rats sacrificed at diestrus showed subsensitivity of the chronotropic response to catecholamines as a result of a conformational alteration of beta 1-adrenoceptors, simultaneously with an increase in beta 2-adrenoceptor-mediated response. The mechanisms seem to be similar to those which underlie stress-induced alterations in catecholamine sensitivity in right atria from male rats. However, during estrus there are some protective factors that prevent the effects of stress on right atria.

Metabolic markers following beta-adrenoceptor agonist infusion in footshock-stressed rats

“…Because we have previously shown that after this same stress protocol cardiac tissue and adipocytes are supersensitive to isoproterenol and subsensitive to noradrenaline (7,8) and to BRL 37344 (8), we examined the effect of an infusion of these compounds on plasma glucose, glycerol and triacylglycerol levels in stressed rats.…”

“…Tissues from stressed rats are supersensitive to adrenaline (2,7), which is elevated in stressed rats, and to isoproterenol (7). However, subsensitivity to noradrenaline has been reported in cardiac tissue and adipocytes from stressed rats (7,8).…”

“…However, subsensitivity to noradrenaline has been reported in cardiac tissue and adipocytes from stressed rats (7,8). In vivo conditions are much more complex and involve several factors which are difficult to control.…”

“…Several experimental models have been used to elucidate stress mechanisms, including novelty, water immersion (3), immobilization (4,5), swimming (6), and footshock (7)(8)(9). Using a footshock stress paradigm (7), we demonstrated that ß-adrenergic receptor signaling was altered in cardiac and adipose tissues of stressed rats (6)(7)(8)(9)(10).…”

“…Using a footshock stress paradigm (7), we demonstrated that ß-adrenergic receptor signaling was altered in cardiac and adipose tissues of stressed rats (6)(7)(8)(9)(10). Altered myocardial adrenergic receptor signaling has been demonstrated in several models of cardiac disease such as heart failure (11,12) and ischemic heart disease (12), and these pathologies had been associated with stress (13).…”