The present experiments investigated the hypothesis that lactation constitutes a chronic stress to the adrenocortical system. To determine whether the normal circadian control of the adrenocortical system or the ability to mount an adequate ACTH response to stress are modified during lactation, we compared morning and evening basal and stress-induced ACTH, corticosterone (B), and PRL secretion as well as pituitary ACTH content and thymus weight in virgins and lactating females on day 10 of lactation. We also compared the capacity of B to suppress ACTH secretion in adrenalectomized virgin or lactating females, both given various B pellet replacement doses (40-130% B) for 5 days. In addition, we investigated the influence of decreased litter size and increased caloric intake on basal circadian activity in the adrenocortical system. Finally, we measured suckling-induced activation of ACTH and B release and restoration of basal morning ACTH and B levels after pup separation. In all 10-d lactating females, basal PRL levels were elevated compared to virgins and the circadian rhythm observed in virgins (P less than 0.05) was absent in all lactating females. By contrast, diurnal variations in ACTH and B secretion (P less than 0.05 or 0.01) were observed in all females regardless of lactation and changes in caloric intake or litter size. Plasma ACTH and B were elevated during the trough of the diurnal rhythm in mothers, compared to virgins. The amplitude of the increase in ACTH between trough and peak was greater in mothers than virgins; however, the amplitude of the increase in plasma B was greater for virgins than mothers, probably because of the higher levels of corticosteroid binding globulin in the former. Diurnal rhythms in stress responsiveness and sensitivity of ACTH to B feedback were normal in mothers; however, the magnitude of their ACTH, B, and PRL response to ether stress was less in mothers than virgins. Attempts to normalize basal ACTH and B concentrations by increasing calorie consumption were unsuccessful. However, we found that suckling caused marked stimulation of ACTH and B secretion; moreover, within 24 h after pups removal, trough ACTH and B concentrations were restored to normal values.(ABSTRACT TRUNCATED AT 400 WORDS)

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We studied the effects of the estrous cycle, ovariectomy and estrogen replacement on angiotensin-converting enzyme (ACE) (kininase II, EC 3.4.15.1) and angiotensin II (AT) receptors in the pituitary gland of the female rat. Quantitative autoradiography, with the use of consecutive pituitary sections, allowed for simultaneous determination of changes in binding and in the potential AT synthetic ability of individual pituitaries, and for a correlation between these two phenomena. In the anterior pituitary, ACE activity and binding of the ACE inhibitor [¹²⁵I]-351A were not changed during the estrous cycle. Ovariectomy produced a significant increase in ACE activity and binding, and both of these parameters returned to normal after estrogen replacement. There were no changes in ACE activity or binding in the posterior pituitary during the estrous cycle or after ovariectomy or hormone replacement. AT receptors were characterized as of the AT₁ type, since they were displaced by the selective AT₁ antagonist DuP 753 and not by the AT₂ competitor PD 123177. There were marked changes in the concentration of AT₁ receptors during the estrous cycle, with highest numbers in metestrus, lower in estrus and diestrus, and lowest during proestrus. Estrogen replacement in ovariectomized rats decreased AT₁ receptor number in the anterior pituitary. Our results indicate a dual effect of estrogen on anterior pituitary AT, physiologically on AT receptor expression and pharmacologically on ACE activity.

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