Muscarine binding sites in bovine adrenal medulla

Ba, Barron; Lc, Murrin; Td, Hexum

doi:10.1016/0014-2999(86)90112-3

Cited by 8 publications

(7 citation statements)

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“…In addition to cholinergic regulation of catecholamine biosynthesis and release via nicotinic receptors, activation of muscarinic receptors potentiates nicotinic receptor-mediated catecholamine release in bovine adrenomedullary cells (5,42). Pharmacological studies support the expression of multiple muscarinic receptor subtypes in both bovine and rat adrenal medulla, while other studies using RT-PCR indicate that type 3 and 4 muscarinic receptors are expressed in the adrenal medulla (6,17,36). The coincident onset of the increase in expression of TH and PNMT with functional/structural innervation in the late-gestation sheep fetus supports a role for cholinergic mechanisms in the regulation of expression of these key enzymes mediating catecholamine biosynthesis.…”

mentioning

confidence: 81%

Long-term hypoxia modulates expression of key genes regulating adrenomedullary function in the late gestation ovine fetus

Ducsay¹,

Hyatt²,

Młynarczyk³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Ducsay CA, Hyatt K, Mlynarczyk M, Root BK, Kaushal KM, Myers DA. Long-term hypoxia modulates expression of key genes regulating adrenomedullary function in the late gestation ovine fetus. Am J Physiol Regul Integr Comp Physiol 293: R1997-R2005, 2007. First published August 15, 2007; doi:10.1152/ajpregu.00313.2007.-We previously communicated that long-term hypoxia (LTH) resulted in a selective reduction in plasma epinephrine following acute stress in fetal sheep. The present study tested the hypothesis that LTH selectively reduces adrenomedullary expression of phenylethanolamine-N-methyltransferase (PNMT), the rate-limiting enzyme for epinephrine synthesis. We also examined the effect of LTH on adrenomedullary nicotinic, muscarinic, and glucocorticoid receptor (GR) expression. Ewes were maintained at high altitude (3,820 m) from 30 to 138 days gestation (dGA); adrenomedullary tissue was collected from LTH and age-matched, normoxic control fetuses at 139 -141 dGA. Contrary to our hypothesis, in addition to PNMT, adrenomedullary expression (mRNA, protein) of tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH) were reduced in the LTH fetus. Immunocytochemistry indicated that TH and DBH expression was lower throughout the medulla, while PNMT appeared to reflect a reduction in PNMT-expressing cells. Nicotinic receptor alpha 1, 2, 3, 5, 6, 7, beta 1, 2, and 4 subunits were expressed in the medulla of LTH and control fetuses. Messenger RNA for alpha 1 and 7 and beta 1 and 2 subunits was lower in LTH fetuses. Muscarinic receptors M1, M2, and M3 as well as the GR were also expressed, and no differences were noted between groups. In summary, LTH in fetal sheep has a profound effect on expression of key enzymes mediating adrenomedullary catecholamine synthesis. Further, LTH impacts nicotinic receptor subunit expression potentially altering cholinergic neurotransmission within the medulla. These findings have important implications regarding fetal cardiovascular and metabolic responses to stress in the LTH fetus. adrenal; ovine; catecholamine BY LATE GESTATION IN THE DEVELOPING ovine fetus, stress activates the sympathetic nervous system, eliciting the release of both norepinephrine and epinephrine. These catecholamines play an essential role in regulating fetal cardiovascular and metabolic responses to a wide variety of stresses and are fundamental in the adaptation of the neonate to the extrauterine environment postbirth (12,35,36). As observed in the adult, the adrenal medulla is the major source of both basal and stress-induced epinephrine in the circulation and contributes significantly to plasma norepinephrine concentrations in the late-gestation ovine fetus (12,25,34,35). There is evidence that both structural and functional innervation of the adrenal medulla occurs during the final third of gestation as the fetus prepares for birth with synapses between splanchnic cholinergic nerve terminals and adrenal chromaffin cells developing between 100 and 130 days of gestation (dGA; term is ϳ148 dGA) in fetal sheep ...

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mentioning

confidence: 81%

Long-term hypoxia modulates expression of key genes regulating adrenomedullary function in the late gestation ovine fetus

Ducsay¹,

Hyatt²,

Młynarczyk³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The doses of methacholine and pilocarpine infused alone were the same as the dose of ACh, yet had no effect on the basal release of catecholamines and Me-IRM. We have shown that pilocarpine is slightly more potent than ACh in displacing [3H]-QNB from muscarinic binding sites in the bovine adrenal medulla (Barron & Hexum, 1986).…”

Section: Discussionmentioning

confidence: 84%

“…This increase was subthreshold for exocytosis of catecholamines. In conjunction with these findings, muscarinic receptors have been characterized in the bovine adrenal gland (Kayaalp & Neff, 1979; Barron & Hexum, 1986). The action of muscarinic agonists in the bovine adrenal gland may therefore be a modulatory one rather than a direct effect.…”

Section: Discussionmentioning

confidence: 90%

“…Control of catecholamine release from the bovine adrenal gland has been thought to be exclusively via the nicotinic cholinoceptor (Wilson & Kirshner, 1977 Kayaalp & Neff (1979) and Barron & Hexum (1986). Indirect evidence for the existence of muscarinic receptors was shown by examining changes in phosphatidylinositol labelling (Mohd.…”

Section: Introductionmentioning

confidence: 99%

“…[3H]-quinuclidinyl benzilate ([3H]-QNB) binding to muscarinic receptors was demonstrated by Kayaalp & Neff (1979) and Barron & Hexum (1986). Indirect evidence for the existence of muscarinic receptors was shown by examining changes in phosphatidylinositol labelling (Mohd.…”

Section: Introductionmentioning

confidence: 99%

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Muscarinic receptor modulation of release of [Met⁵]enkephalin immunoreactive material and catecholamines from the bovine adrenal gland

Barron

Hexum

1986

British J Pharmacology

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Muscarinic receptor modulation of secretion from the adrenal medulla was studied using retrogradely perfused bovine tissue. Atropine, at a dose not affecting 1,1 dimethyl‐4‐phenylpiperizinium (DMPP)‐stimulated release, inhibitied the acetylcholine (ACh)‐stimulated release of noradrenaline and [Met5]enkephalin‐immunoreactive material (ME‐IRM). DMPP‐stimulated release of catecholamines and ME‐IRM was potentiated by the addition of methacholine. Pilocarpine significantly potentiated the release of noradrenaline only. Methacholine, pilocarpine or muscarine, when infused alone, had no stimulatory affect on the basal release of ME‐IRM. These findings suggest that the muscarinic receptors in the bovine adrenal medulla function by potentiating the release of ME‐IRM and catecholamines induced by nicotinic receptor stimulation.

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Cholinoceptor-mediated control of catecholamine release from chromaffin cells in the American eel, Anguilla rostrata

Reid

Perry

1995

J Comp Physiol B

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The cholinergic agonist-induced secretion of catecholamines from chromaffin cells in the American eel, Anguilla rostrata, was assessed using a saline-perfused posterior cardinal vein preparation. Direct membrane depolarization with 60 mmol.l-1 K+ caused a significant release of catecholamines (adrenaline+noradrenaline) into the perfusate which was unaffected by pre-treatment with the ganglion blocker, hexamethonium (final concentration = 10(-3) mol.l-1). The nicotinic receptor agonist, 1,1-dimethyl-4-phenyl-piperazinium iodide, evoked catecholamine release in response to several doses exceeding 10(-7) mol; at 10(-5) mol the response was abolished by pre-treatment with the ganglion blocker, hexamethonium (final concentration = 10(-3) mol.l-1). The muscarinic receptor agonist, pilocarpine, did not elicit catecholamine release in response to any of the doses administered (10(-8)-10(-4) mol). A single injection of the mixed nicotinic/muscarinic cholinoceptor agonist, carbachol (10(-5) mol), caused the release of catecholamines which was abolished by pre-treatment with hexamethonium but which was unaffected by pre-treatment with the muscarinic receptor antagonist atropine (final concentration = 10(-5) mol.l-1). The results of this study indicate that the process of cholinergic agonist-induced catecholamine secretion from the chromaffin cells in the American eel is mediated exclusively by activation of nicotinic receptors with no involvement of the muscarinic receptor.

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Muscarine binding sites in bovine adrenal medulla

Cited by 8 publications

References 9 publications

Long-term hypoxia modulates expression of key genes regulating adrenomedullary function in the late gestation ovine fetus

Long-term hypoxia modulates expression of key genes regulating adrenomedullary function in the late gestation ovine fetus

Muscarinic receptor modulation of release of [Met⁵]enkephalin immunoreactive material and catecholamines from the bovine adrenal gland

Cholinoceptor-mediated control of catecholamine release from chromaffin cells in the American eel, Anguilla rostrata

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Muscarine binding sites in bovine adrenal medulla

Cited by 8 publications

References 9 publications

Long-term hypoxia modulates expression of key genes regulating adrenomedullary function in the late gestation ovine fetus

Long-term hypoxia modulates expression of key genes regulating adrenomedullary function in the late gestation ovine fetus

Muscarinic receptor modulation of release of [Met5]enkephalin immunoreactive material and catecholamines from the bovine adrenal gland

Cholinoceptor-mediated control of catecholamine release from chromaffin cells in the American eel, Anguilla rostrata

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Muscarinic receptor modulation of release of [Met⁵]enkephalin immunoreactive material and catecholamines from the bovine adrenal gland