Binding of prostaglandin E2 to cultured bovine adrenal chromaffin cells and its effect on catecholamine secretion

Karaplis, Andrew C.; Funk, Colin D.; Powell, William S.

doi:10.1016/0167-4889(89)90064-5

Cited by 13 publications

(10 citation statements)

References 34 publications

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“…Moreover, systemic immune challenge or circulating cytokines rapidly recruit dendritic cells and macrophages to the adrenal gland and increase the expression of COX-2 and PGE synthase and presumably local PGE 2 production (Engström et al, 2008). Thus, the components are in place for local modulation of chromaffin cells by PGE 2 , but previous studies present confusing and contradictory findings: PGE 2 has been reported to increase (Marley et al, 1988;Yamada et al, 1988;Yokohama et al, 1988;Karaplis et al, 1989) or decrease (Karaplis et al, 1989) adrenal catecholamine release, elevate intracellular calcium levels (Mochizuki-Oda et al, 1991;Shibuya et al, 1999), or inhibit voltage-gated calcium channels (Currie et al, 2000). In sympathetic neurons, which are closely related to chromaffin cells, PGE 2 can modulate nicotinic ACh receptors (Tan et al, 1998;Du and Role, 2001) and voltage-gated calcium channels (Ikeda, 1992).…”

Section: Introductionmentioning

confidence: 74%

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Regulation of Calcium Channels and Exocytosis in Mouse Adrenal Chromaffin Cells by Prostaglandin EP3 Receptors

Jewell¹,

Breyer²,

Currie³

2011

Mol Pharmacol

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Prostaglandin (PG) E 2 controls numerous physiological functions through a family of cognate G protein-coupled receptors (EP1-EP4). Targeting specific EP receptors might be therapeutically useful and reduce side effects associated with nonsteroidal antiinflammatory drugs and selective cyclooxygenase-2 inhibitors that block prostanoid synthesis. Systemic immune challenge and inflammatory cytokines have been shown to increase expression of the synthetic enzymes for PGE 2 in the adrenal gland. Catecholamines and other hormones, released from adrenal chromaffin cells in response to Ca 2ϩ influx through voltage-gated Ca 2ϩ channels, play central roles in homeostatic function and the coordinated stress response. However, long-term elevation of circulating catecholamines contributes to the pathogenesis of hypertension and heart failure. Here, we investigated the EP receptor(s) and cellular mechanisms by which PGE 2 might modulate chromaffin cell function. PGE 2 did not alter resting intracellular [Ca 2ϩ ] or the peak amplitude of nicotinic acetylcholine receptor currents, but it did inhibit Ca V 2 voltage-gated Ca 2ϩ channel currents (I Ca ). This inhibition was voltage-dependent and mediated by pertussis toxin-sensitive G proteins, consistent with a direct G␤␥ subunit-mediated mechanism common to other G i/o -coupled receptors. mRNA for all four EP receptors was detected, but using selective pharmacological tools and EP receptor knockout mice, we demonstrated that EP3 receptors mediate the inhibition of I Ca . Finally, changes in membrane capacitance showed that Ca 2ϩ -dependent exocytosis was reduced in parallel with I Ca . To our knowledge, this is the first study of EP receptor signaling in mouse chromaffin cells and identifies a molecular mechanism for paracrine regulation of neuroendocrine function by PGE 2 .

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Section: Introductionmentioning

confidence: 74%

“…In some cases, PGE 2 inhibited release (Karaplis et al, 1989), whereas others report that PGE 2 potentiated release (Marley et al, 1988;Yamada et al, 1988;Yokohama et al, 1988). As discussed above, high concentrations of PGE 2 used in some of these studies raise the possibility of non-EP receptor involvement.…”

Section: Discussionmentioning

confidence: 99%

Regulation of Calcium Channels and Exocytosis in Mouse Adrenal Chromaffin Cells by Prostaglandin EP3 Receptors

Jewell¹,

Breyer²,

Currie³

2011

Mol Pharmacol

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“…PGE2 applied to the present preparation did not affect either bradykinin-evoked secre tion or its increase by indomethacin (Fig. 3b), although a very weak secretion was evoked by PGE2 alone as report ed in previous papers (17)(18)(19)(20).…”

Section: Potentiationmentioning

confidence: 59%

“…Effects of these agents on secretory responses in chromaffin cells have also been examined by various investigators. PGE2 induced CA secretion (17)(18)(19)(20) and potentiated secretions evoked by various secretagogues (17,18,21). PGE2 also induced an increase in [Ca 2+]; due to the promotion of Ca2+ entry (29).…”

Section: Potentiationmentioning

confidence: 99%

Potentiation by Indomethacin of Receptor-Mediated Catecholamine Secretion in Rat Adrenal Medulla

Warashina

1997

Japanese Journal of Pharmacology

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“…The differential effects of systemic and GI inflammation on SNS function may therefore be promoted by different concentrations of inflammatory mediators interacting with ACCs and postganglionic sympathetic neurons during each of these conditions. In support of this possibility, micromolar concentrations of PGE 2 have been shown to increase catecholamine secretion from bovine ACCs, whereas nanomolar concentrations of this inflammatory mediator inhibit catecholamine release [113]. Similar concentration-dependent effects may exist for other cytokines associated with sepsis and GI inflammation, and contribute to the dichotomous responses that are observed.…”

Section: Differential Effects Of Systemic and Gastrointestinal Inflammentioning

confidence: 96%

Divergent neuroendocrine responses to localized and systemic inflammation

Lukewich

Rogers

Lomax

2014

Seminars in Immunology

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The sympathetic nervous system (SNS) is part of an integrative network that functions to restore homeostasis following injury and infection. The SNS can provide negative feedback control over inflammation through the secretion of catecholamines from postganglionic sympathetic neurons and adrenal chromaffin cells (ACCs). Central autonomic structures receive information regarding the inflammatory status of the body and reflexively modulate SNS activity. However, inflammation and infection can also directly regulate SNS function by peripheral actions on postganglionic cells. The present review discusses how inflammation activates autonomic reflex pathways and compares the effect of localised and systemic inflammation on ACCs and postganglionic sympathetic neurons. Systemic inflammation significantly enhanced catecholamine secretion through an increase in Ca2+ release from the endoplasmic reticulum. In contrast, acute and chronic GI inflammation reduced voltage-gated Ca2+ current. Thus it appears that the mechanisms underlying the effects of peripheral and systemic inflammation neuroendocrine function converge on the modulation of intracellular Ca2+ signaling.

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Binding of prostaglandin E2 to cultured bovine adrenal chromaffin cells and its effect on catecholamine secretion

Cited by 13 publications

References 34 publications

Regulation of Calcium Channels and Exocytosis in Mouse Adrenal Chromaffin Cells by Prostaglandin EP3 Receptors

Regulation of Calcium Channels and Exocytosis in Mouse Adrenal Chromaffin Cells by Prostaglandin EP3 Receptors

Potentiation by Indomethacin of Receptor-Mediated Catecholamine Secretion in Rat Adrenal Medulla

Divergent neuroendocrine responses to localized and systemic inflammation

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