Myocardial sensitivity to catecholamines following exposure of rats to irregular, signalled footshock.

Emotional stress is associated with an increased activity of both the pituitary-adrenal cortical system and the sympathetic-adrenal medullary systems resulting in raised plasma levels of glucocorticoids and catecholamines. There is evidence to suggest that prolonged stress induced adrenergic hyperactivity initiated myocardial pathogenesis and that this may relate to a corticosteroid catecholamine interaction. In the present study driven atrial strips removed from stressed male CSF rats were found to exhibit an enhanced sensitivity to both norepinephrine and epinephrine. These animals had previously been subjected to irregular foot shock associated with a warning signal; a situation producing a high plasma steroid level. The enhanced myocardial sensitivity to both catecholamines was observed in naive animals subjected to a single period, and persisted unchanged in animals stressed daily over a 28 day period. The hypersensitivity of the myocardium observed immediately after stress was maintained for at least 24 hr, whereas the circulating steroid level had returned to control values within 3 hr. In animals subjected to regular stress without a warning signal, a situation producing a much lower steroid level, no enhanced myocardial sensitivity was observed. While the aetiology of the phenomenon of enhanced myocardial sensitivity to catecholamines is not entirely understood, the evidence presented suggests that it may be related to the extreme elevation of circulating glucocorticoids. The sensitivity of the vas deferens however, was unaltered even though the animals were subjected to the stressor producing a high plasma steroid level. This apparent specifcity of the stress induced sensitivity change is discussed on the basis of receptor differences.