The calcium antagonist nimodipine increases β-endorphin release from rat hypophysis through an action on adrenal glands. An “in vivo” and “in vitro” study

Costa, Giovanni; Saija, Antonella; Padovano, I.; Trimarchi, Giancarlo; Pasquale, R. De; Caputi, A.P.

doi:10.1016/s0031-6989(84)80060-0

Cited by 8 publications

(4 citation statements)

References 15 publications

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“…It was observed that the calcium antagonist, nimodipine, increased β-endorphin secretion through an action on the adrenal glands. It was proposed that, since glucocorticoids exhibit feedback inhibition on the regulation of biosynthesis and secretion of POMC, nimodipine, which reduced adrenal gland responsiveness to ACTH, might increase β-endorphin release from the anterior pituitary gland by reducing glucocorticoid secretion from the adrenal cortex (Costa, et al 1984). Hence, regulation of adrenal responsiveness to ACTH affects corticotroph behavior.…”

Section: Processing Of Pomcmentioning

confidence: 99%

60 YEARS OF POMC: Biosynthesis, trafficking, and secretion of pro-opiomelanocortin-derived peptides

Cawley

Loh

2016

Journal of Molecular Endocrinology

147

127

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Pro-opiomelanocortin (POMC) is a prohormone that encodes multiple smaller peptide hormones within its structure. These peptide hormones can be generated by cleavage of POMC at basic-residue cleavage sites by prohormone converting enzymes in the regulated secretory pathway of POMC synthesizing endocrine cells and neurons. The peptides are stored inside the cells in dense core secretory granules until released in a stimulus dependent manner. The complexity of the regulation of the biosynthesis, trafficking and secretion of POMC and its peptides reflect an impressive level of control over many factors involved in the ultimate role of POMC expressing cells, i.e. to produce a range of different biologically active peptide hormones ready for action when signaled by the body. From the discovery of POMC as the precursor to ACTH and β-Lipotropin in the late 1970s to our current knowledge, the understanding of POMC physiology remains a monumental body of work that has provided insight into many aspects of molecular endocrinology. In this chapter, we describe the intracellular trafficking of POMC in endocrine cells, its sorting into dense core secretory granules and transport of these granules to the regulated secretory pathway. Additionally, we review the enzymes involved in the maturation of POMC to its various peptides and the mechanisms involved in the differential processing of POMC in different cell types. Finally, we highlight studies pertaining to the regulation of ACTH secretion in the anterior and intermediate pituitary and POMC neurons of the hypothalamus.

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Section: Processing Of Pomcmentioning

confidence: 99%

60 YEARS OF POMC: Biosynthesis, trafficking, and secretion of pro-opiomelanocortin-derived peptides

Cawley

Loh

2016

Journal of Molecular Endocrinology

147

127

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“…However, it is likely that the role of L-type calcium channels is only secondary to that of dihydropyridine insensitive T-, N or P-type calcium channels [7] since even at very high doses, calcium channel blocking drugs do not produce anaesthesia [8]. Calcium channel blocking drugs have also been shown to increase plasma b-endorphin levels in rats [9]. Consequently, their effect on MAC of volatile anaesthetics may also be mediated by an opioid-receptor mechanism.…”

Section: Discussionmentioning

confidence: 99%

Effect of clevidipine, an ultra-short acting 1,4-dihydropyridine calcium channel blocking drug, on the potency of isoflurane in rats and dogs

Wolff

Leather

Wouters

2000

European Journal of Anaesthesiology

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Clevidipine is a new lipophilic, ultra-short acting 1,4dihydropyridine calcium channel antagonist for intraoperative use. Because sarcolemnal calcium currents are involved in the mechanism of action of anaesthetics we questioned whether clevidipine alters the potency of volatile anaesthetics. We studied the effects of clevidipine on minimal alveolar concentration and the time to awaken from iso¯urane anaesthesia. Sprague-Dawley rats were anaesthetized with iso¯urane, and were allocated to one of four treatments prior to minimal alveolar concentration determination: (a) saline control; (b) clevidipine 20 nmol kg À1 min À1 ; (c) clevidipine 40 nmol kg À1 min À1 ; (d) clonidine 1 mg kg À1 ± positive control. Ten mongrel dogs were anaesthetized with iso¯urane and received a continuous infusion of clevidipine 6 nmol kg À1 min À1 or the solvent (Intralipid 20% ± control). After 2 h of steady-state anaesthesia, minimal alveolar concentration awake and the time to awakening were recorded.Clevidipine reduced minimal alveolar concentration to a small but statistically signi®cant extent (from 1.40 0.16 control to 1.23 0.13 vol % with 20 nmol kg À1 min À1 and to 1.27 0.12 vol % with 40 nmol kg À1 min À1; mean SD; P < 0.05) in rats. Clonidine reduced minimal alveolar concentration to 0.90 0.17 vol % (mean SD; P < 0.05). Minimal alveolar concentration awake and the duration of sleep were not affected by clevidipine in dogs. Clevidipine mildly reduces miinimal alveolar concentration of iso¯urane but does not prolong the duration of sleep and does not affect minimal alveolar concentration awake after a 2-h steady-state iso¯urane anaesthesia.

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“…However, it is likely that the role of l ‐type calcium channels is only secondary to that of dihydropyridine insensitive T‐, N or P‐type calcium channels [7] since even at very high doses, calcium channel blocking drugs do not produce anaesthesia [8]. Calcium channel blocking drugs have also been shown to increase plasma β‐endorphin levels in rats [9]. Consequently, their effect on MAC of volatile anaesthetics may also be mediated by an opioid‐receptor mechanism.…”

Section: Discussionmentioning

confidence: 99%

Effect of clevidipine, an ultra-short acting 1,4-dihydropyridine calcium channel blocking drug, on the potency of isoflurane in rats and dogs

2000

View full text Add to dashboard Cite

Clevidipine is a new lipophilic, ultra-short acting 1, 4-dihydropyridine calcium channel antagonist for intraoperative use. Because sarcolemnal calcium currents are involved in the mechanism of action of anaesthetics we questioned whether clevidipine alters the potency of volatile anaesthetics. We studied the effects of clevidipine on minimal alveolar concentration and the time to awaken from isoflurane anaesthesia. Sprague-Dawley rats were anaesthetized with isoflurane, and were allocated to one of four treatments prior to minimal alveolar concentration determination: (a) saline control; (b) clevidipine 20 nmol kg-1 min-1; (c) clevidipine 40 nmol kg-1 min-1; (d) clonidine 1 microg kg-1 - positive control. Ten mongrel dogs were anaesthetized with isoflurane and received a continuous infusion of clevidipine 6 nmol kg-1 min-1 or the solvent (Intralipid 20% - control). After 2 h of steady-state anaesthesia, minimal alveolar concentration awake and the time to awakening were recorded. Clevidipine reduced minimal alveolar concentration to a small but statistically significant extent (from 1.40 +/- 0.16 control to 1.23 +/- 0.13 vol % with 20 nmol kg-1 min-1 and to 1.27 +/- 0.12 vol % with 40 nmol kg-1 min-1; mean +/- SD; P < 0.05) in rats. Clonidine reduced minimal alveolar concentration to 0.90 +/- 0.17 vol % (mean +/- SD; P < 0.05). Minimal alveolar concentration awake and the duration of sleep were not affected by clevidipine in dogs. Clevidipine mildly reduces minimal alveolar concentration of isoflurane but does not prolong the duration of sleep and does not affect minimal alveolar concentration awake after a 2-h steady-state isoflurane anaesthesia.

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The calcium antagonist nimodipine increases β-endorphin release from rat hypophysis through an action on adrenal glands. An “in vivo” and “in vitro” study

Cited by 8 publications

References 15 publications

60 YEARS OF POMC: Biosynthesis, trafficking, and secretion of pro-opiomelanocortin-derived peptides

60 YEARS OF POMC: Biosynthesis, trafficking, and secretion of pro-opiomelanocortin-derived peptides

Effect of clevidipine, an ultra-short acting 1,4-dihydropyridine calcium channel blocking drug, on the potency of isoflurane in rats and dogs

Effect of clevidipine, an ultra-short acting 1,4-dihydropyridine calcium channel blocking drug, on the potency of isoflurane in rats and dogs

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