Immunoreactive Endothelin in Plasma of Nonmammalian Vertebrates

Uemura, Hirotsugu; Naruse, Masahiro; Naruse, Kiyoko; Hirohama, Tohru; Demura, Hiroshi; Kasuya, Y.

doi:10.1097/00005344-199100177-00117

Cited by 21 publications

(6 citation statements)

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“…ET-like immunoreactivity also has been found in gill, heart, or neural tissue in all major groups of fishes, including agnathans, elasmobranchs, and teleosts (e.g., 27,57), and a trout ET recently has been purified, sequenced, and synthesized (60). Infusion of either this peptide or human ET-1 produces a complex suite of cardiovascular responses in the trout, including a triphasic pressure change (pressor-depressor-pressor) in the dorsal aorta produced by changes in cardiac output, gill resistance, systemic resistance, and venous compliance (22).…”

mentioning

confidence: 99%

NaCl transport across the opercular epithelium ofFundulus heteroclitusis inhibited by an endothelin to NO, superoxide, and prostanoid signaling axis

Evans¹,

Rose²,

Roeser³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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Recent evidence suggests that paracrine signaling agents, such as endothelin (ET), nitric oxide (NO), superoxide (O2-), and prostanoids can modulate mammalian renal function by affecting both hemodynamic and epithelial ionic transport pathways. Since these signaling pathways have been described in fish blood vessels, we hypothesized that they may control salt transport across the gill epithelium--the primary site of ion excretion in marine teleost fishes. We found that ET, the NO donors sodium nitroprusside and spermine NONOate, and the prostanoid PGE2 each can produce a concentration-dependent reduction in the short circuit current (Isc) across the isolated opercular epithelium of the killifish (Fundulus heteroclitus), the generally accepted model for the marine teleost gill epithelium. Sarafotoxin S6c was equipotent to ET-1, suggesting that ETB receptors are involved. Incubation with NG-nitro-L-arginine methyl ester (L-NAME) or indomethacin reduced the effect of subsequent addition of SRXS6c by 17 and 89%, respectively, suggesting the presence of an ET to NO and PGE axis. The effects of l-NAME and indomethacin were not additive, but the superoxide dismutase mimetic 4-hydroxy-2,2,6,6-tetramethylpiperidine 1-oxyl (TEMPOL) reduced the effect of SRXS6c by 34% and preincubation with l-NAME, indomethacin, and TEMPOL reduced the SRXS6c response to zero. This suggests a direct role for O2- in this axis. COX-2 appears to be the major enzyme involved in this axis because the specific COX-2 inhibitor NS-398 was twice as effective as the COX-1 inhibitor SC560 in inhibiting the SRXS6c effect. The Isc was stimulated by the EP2 agonist butaprost and inhibited by the EP(1,3) agonist sulprostone, suggesting both stimulatory and inhibitory PGE receptors in this tissue. Carbaprostacyclin (PGI2 analog), thromboxane A2, PGF(2alpha), and PGD2 did not affect the Isc. Our data are the first to suggest the importance of an ET-stimulated and NO-, O2(-)-, and PGE2-mediated signaling axis that can modify active extrusion of NaCl across the killifish opercular epithelium and, by inference, the marine teleost gill epithelium.

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mentioning

confidence: 99%

NaCl transport across the opercular epithelium ofFundulus heteroclitusis inhibited by an endothelin to NO, superoxide, and prostanoid signaling axis

Evans¹,

Rose²,

Roeser³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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“…In conclusion, ETs have been demonstrated in invertebrates, protochordates, cyclostomes, holosteans and elasmobranchs (20, 21, 30). Not only the presence of ET B receptors [this work; (42)], but also an effective functional regulation of pigment cells by ET B /ETs, has been demonstrated in GEM‐81 cells.…”

Section: Discussionmentioning

confidence: 87%

“…Endothelins seem to have appeared early in evolution, as demonstrated by the presence of ET‐like factors in many invertebrates and vertebrates (20, 21). An endothelin (ET t ) from the trout, Oncorhynchus mykiss , has also been purified, with three and four amino acid substitutions, when compared with mammalian ET‐2 and ET‐1, respectively (22).…”

Section: Introductionmentioning

confidence: 99%

The Endothelin/Sarafotoxin‐Induced Increase of the Proliferation of Undifferentiated and DMSO‐Differentiated GEM‐81 Goldfish Erythrophoroma Cells is Mediated by ET_B Receptors

Filadelfi

Ramanzini

Visconti

et al. 2004

Pigment Cell Research

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Endothelins (ETs) and sarafotoxins (SRTXs) have been reported to exert ET(B)-mediated effects on vertebrate pigment cells. GEM-81 cell line, a red pigment cell-derived cutaneous tumor of the teleost Carassius auratus, expresses ET(B) receptors and can be differentiated with 1.5% DMSO treatment, thus constituting an useful model to investigate ET and SRTX effects on cultured fish pigment cells. Our aim was to characterize the pharmacology and biological effects mediated by ET receptors in DMSO-differentiated and undifferentiated cells. ET subtype receptors and their respective Ki values in both cell types were determined by competitive binding assays using (125)I ET-1 and BQ-485 (an ET(A) antagonist) or BQ-788 (an ET(B) antagonist). BQ-788, but not BQ-485, significantly reduced (125)I-ET-1 binding in both cell types, with similar low (Ki > nM) affinities. To determine the proliferation effects of ETs/SRTXs, cells were treated for 72 h with the hormones, and counted in a hemocytometer. The proliferation assays were repeated for SRTX S6c in the presence or absence of BQ-788. The results demonstrated that, with the exception of ET-1 (biphasic effect) and ET-3 (no significant effect) in undifferentiated GEM-81 cells, all the tested hormones induced increases in the proliferation of both types of cells. The hormones were equipotent in DMSO-differentiated cells, which exhibited increased sensitivity to ETs, but not to SRTXs, as compared with undifferentiated cells. The BQ-788 antagonistic effect was also exerted on the proliferation responses to SRTX S6c. These results corroborate the long and important evolutionary history of the ET/SRTX receptor system in vertebrate pigment cells.

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“…However, the fact that substantial amounts of Els are present in plasma of mammals (2,27) and non-mammalian vertebrates (28) indicates that these peptides may also exert hormonal activity on adrenocortical cells.…”

Section: Expression Of Ets In the Adrenal Glandmentioning

confidence: 99%

Mechanism of Action of Endothelins on Adrenocortical Cells

Rémy-Jouet¹,

Cartier²,

Lesouhaitier³

et al. 1998

Horm Metab Res

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Endothelins (ETs) play a pivotal role in the control of various endocrine and neuroendocrine tissues. In this review, we discuss the involvement of ETs as possible regulators of steroid secretion and we describe the mechanism of action of ETs on adrenocortical cells. The occurrence of ETs has been demonstrated in the human, porcine and rat adrenal gland. In humans, immunohistochemical and biochemical techniques have reported that ETs are localized exclusively in the cortex but the presence of ETs has also been detected in pheochromocytomas. In vitro studies have shown that ETs stimulate aldosterone secretion by adrenal tissues in various mammalian and amphibian animal models. The receptor subtype involved in the corticotropic action of ETs clearly differs among the various vertebrate species studied. In rat, the effect of ETs is mediated through an ET(B) receptor subtype while, in frog, an ET(A) receptor is implicated in the stimulatory action of ETs. In human adrenocortical cells, both ET(A) and ET(B) receptor subtypes are involved in the corticotropic effect of ETs. Activation of adrenal receptors causes an elevation of inositol trisphosphates associated with an increase in cytosolic calcium concentration. In addition, ETs induce an elevation of prostaglandin E2 (PGE2) and prostacyclin PGI2 production in the adrenal tissue, indicating that prostanoids may act as second messengers of ETs. It thus appears that ETs present in the adrenal gland may act as paracrine factors to stimulate the secretory activity of adrenocortical cells.

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Immunoreactive Endothelin in Plasma of Nonmammalian Vertebrates

Cited by 21 publications

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NaCl transport across the opercular epithelium ofFundulus heteroclitusis inhibited by an endothelin to NO, superoxide, and prostanoid signaling axis

NaCl transport across the opercular epithelium ofFundulus heteroclitusis inhibited by an endothelin to NO, superoxide, and prostanoid signaling axis

The Endothelin/Sarafotoxin‐Induced Increase of the Proliferation of Undifferentiated and DMSO‐Differentiated GEM‐81 Goldfish Erythrophoroma Cells is Mediated by ET_B Receptors

Mechanism of Action of Endothelins on Adrenocortical Cells

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Immunoreactive Endothelin in Plasma of Nonmammalian Vertebrates

Cited by 21 publications

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NaCl transport across the opercular epithelium ofFundulus heteroclitusis inhibited by an endothelin to NO, superoxide, and prostanoid signaling axis

NaCl transport across the opercular epithelium ofFundulus heteroclitusis inhibited by an endothelin to NO, superoxide, and prostanoid signaling axis

The Endothelin/Sarafotoxin‐Induced Increase of the Proliferation of Undifferentiated and DMSO‐Differentiated GEM‐81 Goldfish Erythrophoroma Cells is Mediated by ETB Receptors

Mechanism of Action of Endothelins on Adrenocortical Cells

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The Endothelin/Sarafotoxin‐Induced Increase of the Proliferation of Undifferentiated and DMSO‐Differentiated GEM‐81 Goldfish Erythrophoroma Cells is Mediated by ET_B Receptors