Abstract:SUMMARY1. Adrenal responses to intra-aortic infusions of acetylcholine (4-5 nmol min-' kg-' for 10 min) have been investigated in hypophysectomized conscious calves given exogenous adrenocorticotrophic hormone (ACTH) (2 ng min-' kg-' i.v.) in the presence and absence of hexamethonium.2. Acetylcholine produced a significant increase in adrenal cortisol output and plasma cortisol concentration. In the absence of nicotinic blockade with hexamethonium this was apparently accounted for by an increase in adrenal ACT… Show more
“…This species difference in expression incidence and amount of GABA A receptors in AMC cells may be ascribed to glucocorticoids produced in adrenal cortical cells. The major glucocorticoid in guinea‐pig (Malinowska & Nathanielsz, 1974) and bovine adrenal cortical cells (Bloom et al., 1977; Jones & Edwards, 1991) is cortisol, whereas that in mice (Taves et al., 2015) and rats (Bernardi et al., 1998; Hashimoto et al., 1989; Zoccal et al., 2007) is corticosterone. Hamster adrenal cortical cells are a dual secretor, mainly secreting corticosterone under basal and cortisol under stressful conditions (Ottenweller et al., 1985).…”
Section: Discussionmentioning
confidence: 99%
“…The fact that GABA A receptors already develop at birth raises the possibility that the development of GABA A receptors in AMC cells (Malinowska & Nathanielsz, 1974) and cattle (Bloom et al, 1977;Jones & Edwards, 1991) is cortisol, whereas that in mice (Taves et al, 2015) and rats (Bernardi et al, 1998;Hashimoto et al, 1989;Zoccal et al, 2007) is corticosterone. Because the potency of corticosterone in lowering serum Ca 2+ in rats was reported to be one-eighth that of cortisol (Mahgoub et al, 1997), the low glucocorticoid activity of corticosterone might explain low expression levels of GABA A receptors in rodent AMC cells (Inoue et al, 2013).…”
γ-Aminobutyric acid (GABA) is thought to play a paracrine role in adrenal medullary chromaffin (AMC) cells. Comparative physiological and immunocytochemical approaches were used to address the issue of how the paracrine function of GABA in AMC cells is established. GABA A receptor Clchannel activities in AMC cells of rats and mice, where corticosterone is the major glucocorticoid, were much smaller than those in AMC cells of guinea-pigs and cattle, where cortisol is the major. The extent of enhancement of GABA A receptor α3 subunit expression in rat pheochromocytoma (PC12) cells by cortisol was larger than that by corticosterone in parallel with their glucocorticoid activities. Thus, the species difference in GABA A receptor expression may be ascribed to a difference in glucocorticoid activity between corticosterone and cortisol. GABA A receptor Clchannel activity in mouse AMC cells was enhanced by allopregnanolone, as noted with that in guinea-pig AMC cells, and the enzymes involved in allopregnanolone production were immunohistochemically detected in the zona fasciculata in both mice and guinea pigs. The expression of glutamic acid decarboxylase 67 (GAD67), one of the GABA synthesizing enzymes, increased after birth, whereas GABA A receptors already developed at birth. Stimulation of pituitary adenylate cyclase-activating polypeptide (PACAP) receptors, but not nicotinic or muscarinic receptors, in PC12 cells, resulted in an increase in GAD67 expression in a protein-kinase A-dependent manner. The results indicate that glucocorticoid and PACAP are mainly responsible for the expressions of GABA A receptors and GAD67 involved in GABA signaling in AMC cells, respectively.
“…This species difference in expression incidence and amount of GABA A receptors in AMC cells may be ascribed to glucocorticoids produced in adrenal cortical cells. The major glucocorticoid in guinea‐pig (Malinowska & Nathanielsz, 1974) and bovine adrenal cortical cells (Bloom et al., 1977; Jones & Edwards, 1991) is cortisol, whereas that in mice (Taves et al., 2015) and rats (Bernardi et al., 1998; Hashimoto et al., 1989; Zoccal et al., 2007) is corticosterone. Hamster adrenal cortical cells are a dual secretor, mainly secreting corticosterone under basal and cortisol under stressful conditions (Ottenweller et al., 1985).…”
Section: Discussionmentioning
confidence: 99%
“…The fact that GABA A receptors already develop at birth raises the possibility that the development of GABA A receptors in AMC cells (Malinowska & Nathanielsz, 1974) and cattle (Bloom et al, 1977;Jones & Edwards, 1991) is cortisol, whereas that in mice (Taves et al, 2015) and rats (Bernardi et al, 1998;Hashimoto et al, 1989;Zoccal et al, 2007) is corticosterone. Because the potency of corticosterone in lowering serum Ca 2+ in rats was reported to be one-eighth that of cortisol (Mahgoub et al, 1997), the low glucocorticoid activity of corticosterone might explain low expression levels of GABA A receptors in rodent AMC cells (Inoue et al, 2013).…”
γ-Aminobutyric acid (GABA) is thought to play a paracrine role in adrenal medullary chromaffin (AMC) cells. Comparative physiological and immunocytochemical approaches were used to address the issue of how the paracrine function of GABA in AMC cells is established. GABA A receptor Clchannel activities in AMC cells of rats and mice, where corticosterone is the major glucocorticoid, were much smaller than those in AMC cells of guinea-pigs and cattle, where cortisol is the major. The extent of enhancement of GABA A receptor α3 subunit expression in rat pheochromocytoma (PC12) cells by cortisol was larger than that by corticosterone in parallel with their glucocorticoid activities. Thus, the species difference in GABA A receptor expression may be ascribed to a difference in glucocorticoid activity between corticosterone and cortisol. GABA A receptor Clchannel activity in mouse AMC cells was enhanced by allopregnanolone, as noted with that in guinea-pig AMC cells, and the enzymes involved in allopregnanolone production were immunohistochemically detected in the zona fasciculata in both mice and guinea pigs. The expression of glutamic acid decarboxylase 67 (GAD67), one of the GABA synthesizing enzymes, increased after birth, whereas GABA A receptors already developed at birth. Stimulation of pituitary adenylate cyclase-activating polypeptide (PACAP) receptors, but not nicotinic or muscarinic receptors, in PC12 cells, resulted in an increase in GAD67 expression in a protein-kinase A-dependent manner. The results indicate that glucocorticoid and PACAP are mainly responsible for the expressions of GABA A receptors and GAD67 involved in GABA signaling in AMC cells, respectively.
“…In addition to the well documented effects on the medulla, which are mediated by acetylcholine acting on nicotinic receptors, it has been established in the conscious calf model that adrenal medullary and cortical responses to low doses of acetylcholine infused intra-aortically (4.5 nmol mm-1 kg-1) are mediated via muscarinic receptors (110,111). These include the release of catecholamines, enkephalins and CRH, together with cortisol and aldosterone.…”
“…The output of cortisol from the adrenal gland in response to adrenocorticotrophic hormone (ACTH) is potentiated by intra-aortic infusions of small amounts of both acetylcholine and of vasoactive intestinal peptide (VIP) in the conscious calf (Bloom, Edwards & Jones, 1987;Jones, Edwards & Bloom, 1991). The response to acetylcholine is attributable to activation of muscarinic receptors (Jones & Edwards, 1992). Release of VIP is thought to be implicated in the potentiation of the steroidogenic response to ACTH during splanchnic nerve stimulation, both in the conscious calf (Bloom et al 1987) and the perfused adrenal gland of the pig, MS 1756 A. V. EDWARDS AND C. T. JONES when the nerve supply is preserved (Erhart-Bornstein, Bornstein, Scherbaum, Pfeiffer & Holst, 1991).…”
SUMMARY1. Adrenal responses to intra-aortic infusions of acetylcholine and vasoactive intestinal peptide (VIP) have been investigated in functionally hypophysectomized calves given exogenous adrenocorticotrophic hormone (ACTH, 2 ng min-' kg-' i.v.).2. Infusions of VIP at a dose of 0 13 #sg min-' kg-' caused a small, but significant increase in adrenaline and noradrenaline output which was, however, far below the level recorded previously in response to acetylcholine (07 ,ug min' kg-'). In contrast, these doses of the two agonists produced closely similar rises in adrenal cortisol output.3. The steroidogenic effects of acetylcholine and VIP were found to be strictly additive and no evidence of potentiation was obtained in relation to either cortical or medullary responses or in the case of any of the cardiovascular responses which were monitored.4. Intra-aortic infusions of VIP, at a dose which produced a substantial increase in adrenal steroidogenesis (0065,ug min-' kg-'), had no effect on the output of catecholamines, enkephalin-like immunoreactivity or corticotrophin-releasing factor, either in the presence or absence of acetylcholine. 5. It is concluded that VIP is unlikely to modulate adrenal medullary responses to muscarinic stimulation in this species as it has been claimed to do in the rat and does not potentiate adrenal steroidogenesis in response to acetylcholine as it does to ACTH.
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