Effects of adrenalectomy and thyroidectomy on postnatal rat lung development and cytoplasmic factors modulating adenylate cyclase activity

Abstract

Effects of adrenalectomy (ADX) and thyroidectomy (THX) on postnatal rat lung growth and development were investigated in relation to the cytoplasmic factors modulating adenylate cyclase activity. On day 21 ADX and THX in rats reduced body and lung weights on days 31 and 43. However, lung weight/body weight was not affected by ADX or THX. Treatment of ADX and THX rats with dexamethasone and thyroxine (T4), respectively, for 10 days neither restored body growth to the control level nor had any effect on lung growth. Neither protein, DNA, or protein/DNA showed any significant changes in lungs of ADX and THX rats. However, lung glycogen increased in ADX rats and decreased on treatment with dexamethasone. On the other hand, THX and treatment of THX rats with T4 essentially had no effect on lung glycogen level. ADX resulted in lower adenylate cyclase activity and its stimulation by the cytoplasmic factors in ADX rat lungs. Dexamethasone treatment of ADX rats restored the basal adenylate cyclase activity to the control level, but potentiated the cytoplasmic activation of adenylate cyclase much more than the control lung supernatant. THX, on the other hand, increased the basal adenylase cyclase activity, but its stimulation by the lung supernatant was diminished. Treatment of THX rats with T4 did not alter the basal adenylate cyclase activity compared with THX rats, but the cytoplasmic activation of adenylate cyclase was restored to the control level. Alterations in adenylate cyclase activation by the lung supernatant from ADX and THX rats did not appear to be due to changes in either the amount of enzyme in membranes or its sensitivity to the cytoplasmic factors. While ADX did not alter cyclic AMP-phosphodiesterase activity in rat lung, THX reduced this enzyme activity, which was restored to the control level on treatment of THX rats with T4. These data suggest that hormones such as glucocorticoids and thyroxine may influence lung growth and development by inducing alterations in the cytoplasmic factors activating adenylate cyclase, cyclic AMP, and glycogen metabolism.