PubMed · 4436019
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J F Finucane, M Kaiz. 1974. Adrenal function in autoimmune thyroiditis.. https://doi.org/10.1007/bf03004786
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The present study was conducted to assess the effect of nutritional stress induced by food deprivation on expression of messenger ribonucleic acid (mRNA) for corticotropin-releasing hormone receptor type 2beta (CRH-R2beta) in the rat cardiovascular system in the presence or absence of changes in circulating corticosterone. Food deprivation for 96 h caused a robust increase in plasma corticosterone levels and a significant decrease in CRH-R2beta mRNA expression in the rat heart. Starvation for 48 and 96 h decreased CRH-R2beta mRNA expression in the atria, ventricle as well as aorta of sham-adrenalectomized (sham) rats. Surprisingly, clamping plasma glucocorticoids at low levels by adrenalectomy with corticosterone pellet replacement (ADX+B) did not completely prevent starvation-induced decreases of CRH-R2beta mRNA expression in the rat cardiovascular system. Urocortin (Ucn) mRNA expression was increased significantly by food deprivation in the heart of sham as well as ADX+B rats. We speculate that food deprivation may increase urocortin, which in turn down-regulates CRH-R2beta mRNA expression in cardiovascular system. These data indicate that food deprivation despite the presence or absence of changes in circulating corticosterone may have an inhibitory effect on CRH-R2beta mRNA expression in the rat cardiovascular system.
Adrenomedullin (AM) is hypothesized to be a physiologically relevant regulator in fluid and electrolyte homeostasis. AM acts within the central nervous system to inhibit both water and salt intake. The peptide has direct actions in the hypothalamus to decrease vasopressin secretion and in the pituitary gland to inhibit ACTH release. AM decreases production and release of aldosterone from the adrenal glands and acts directly in the kidneys to increase renal blood flow and cause diuresis and natriuresis. Whether or not these complementary actions in brain, pituitary, adrenal gland, and kidney reflect coordinated regulatory mechanisms is currently unknown. Development of molecular tools to determine the physiologic role of endogenous AM will greatly enhance our understanding of AM and its regulation of fluid and electrolyte homeostasis.
Duodenal infusion of hypertonic solutions elicits osmolality-dependent thermogenesis in urethane-anaesthetized rats. Here we investigated the involvement of the autonomic nervous system, adrenal medulla and brain in the mechanism of this thermogenesis. Bilateral subdiaphragmatic vagotomy greatly attenuated the first hour, but not the later phase, of the thermogenesis induced by 3.6 % NaCl (10 ml kg(-1)). Neither atropine pretreatment (10 mg kg(-1), I.P.) nor capsaicin desensitization had any effect on the osmotically induced thermogenesis, suggesting the involvement of non-nociceptive vagal afferents. Bilateral splanchnic denervation caudal to the suprarenal ganglia also had no effect, suggesting a lack of involvement of spinal afferents and sympathetic efferents to the major upper abdominal organs. Adrenal demedullation greatly attenuated the initial phase, but not the later phase, of thermogenesis. Pretreatment with the beta-blocker propranolol (20 mg kg(-1), I.P.) attenuated the thermogenesis throughout the 3 h observation period. The plasma adrenaline concentration increased significantly 20 min after osmotic stimulation but returned to the basal level after 60 min. The plasma noradrenaline concentration increased 20 min after osmotic stimulation and remained significantly elevated for 120 min. Therefore, adrenaline largely mediated the initial phase of thermogenesis, and noradrenaline was involved in the entire thermogenic response. Moreover, neither decerebration nor pretreatment with the antipyretic indomethacin (10 mg kg(-1), S.C.) had any effect. Accordingly, this thermogenesis did not require the forebrain and was different from that associated with fever. These results show the critical involvement of the vagal afferents, hindbrain and sympathoadrenal system in the thermogenesis induced by osmotic stimulation of the intestines.