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Are we missing a mineralocorticoid in teleost fish? Effects of cortisol, deoxycorticosterone and aldosterone on osmoregulation, gill Na+,K+ -ATPase activity and isoform mRNA levels in Atlantic salmon.
Gen Comp Endocrinol. 2008 May 15; 157(1):35-40.GC

Abstract

It has long been held that cortisol, acting through a single receptor, carries out both glucocorticoid and mineralocorticoid actions in teleost fish. The recent finding that fish express a gene with high sequence similarity to the mammalian mineralocorticoid receptor (MR) suggests the possibility that a hormone other than cortisol carries out some mineralocorticoid functions in fish. To test for this possibility, we examined the effect of in vivo cortisol, 11-deoxycorticosterone (DOC) and aldosterone on salinity tolerance, gill Na(+),K(+)-ATPase (NKA) activity and mRNA levels of NKA alpha 1a and alpha 1b in Atlantic salmon. Cortisol treatment for 6-14 days resulted in increased, physiological levels of cortisol, increased gill NKA activity and improved salinity tolerance (lower plasma chloride after a 24h seawater challenge), whereas DOC and aldosterone had no effect on either NKA activity or salinity tolerance. NKA alpha 1a and alpha 1b mRNA levels, which increase in response to fresh water and seawater acclimation, respectively, were both upregulated by cortisol, whereas DOC and aldosterone were without effect. Cortisol, DOC and aldosterone had no effect on gill glucocorticoid receptor GR1, GR2 and MR mRNA levels, although there was some indication of possible upregulation of GR1 by cortisol (p=0.07). The putative GR blocker RU486 inhibited cortisol-induced increases in salinity tolerance, NKA activity and NKA alpha 1a and alpha 1b transcription, whereas the putative MR blocker spironolactone had no effect. The results provide support that cortisol, and not DOC or aldosterone, is involved in regulating the mineralocorticoid functions of ion uptake and salt secretion in teleost fish.

Authors+Show Affiliations

USGS, Conte Anadromous Fish Research Center, One Migratory Way, PO Box 796, Turners Falls, MA 01376, USA. mccormick@umext.umass.eduNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

18462736

Citation

McCormick, Stephen D., et al. "Are We Missing a Mineralocorticoid in Teleost Fish? Effects of Cortisol, Deoxycorticosterone and Aldosterone On Osmoregulation, Gill Na+,K+ -ATPase Activity and Isoform mRNA Levels in Atlantic Salmon." General and Comparative Endocrinology, vol. 157, no. 1, 2008, pp. 35-40.
McCormick SD, Regish A, O'Dea MF, et al. Are we missing a mineralocorticoid in teleost fish? Effects of cortisol, deoxycorticosterone and aldosterone on osmoregulation, gill Na+,K+ -ATPase activity and isoform mRNA levels in Atlantic salmon. Gen Comp Endocrinol. 2008;157(1):35-40.
McCormick, S. D., Regish, A., O'Dea, M. F., & Shrimpton, J. M. (2008). Are we missing a mineralocorticoid in teleost fish? Effects of cortisol, deoxycorticosterone and aldosterone on osmoregulation, gill Na+,K+ -ATPase activity and isoform mRNA levels in Atlantic salmon. General and Comparative Endocrinology, 157(1), 35-40. https://doi.org/10.1016/j.ygcen.2008.03.024
McCormick SD, et al. Are We Missing a Mineralocorticoid in Teleost Fish? Effects of Cortisol, Deoxycorticosterone and Aldosterone On Osmoregulation, Gill Na+,K+ -ATPase Activity and Isoform mRNA Levels in Atlantic Salmon. Gen Comp Endocrinol. 2008 May 15;157(1):35-40. PubMed PMID: 18462736.
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TY - JOUR T1 - Are we missing a mineralocorticoid in teleost fish? Effects of cortisol, deoxycorticosterone and aldosterone on osmoregulation, gill Na+,K+ -ATPase activity and isoform mRNA levels in Atlantic salmon. AU - McCormick,Stephen D, AU - Regish,Amy, AU - O'Dea,Michael F, AU - Shrimpton,J Mark, Y1 - 2008/03/31/ PY - 2008/02/29/received PY - 2008/03/20/revised PY - 2008/03/26/accepted PY - 2008/5/9/pubmed PY - 2008/9/9/medline PY - 2008/5/9/entrez SP - 35 EP - 40 JF - General and comparative endocrinology JO - Gen Comp Endocrinol VL - 157 IS - 1 N2 - It has long been held that cortisol, acting through a single receptor, carries out both glucocorticoid and mineralocorticoid actions in teleost fish. The recent finding that fish express a gene with high sequence similarity to the mammalian mineralocorticoid receptor (MR) suggests the possibility that a hormone other than cortisol carries out some mineralocorticoid functions in fish. To test for this possibility, we examined the effect of in vivo cortisol, 11-deoxycorticosterone (DOC) and aldosterone on salinity tolerance, gill Na(+),K(+)-ATPase (NKA) activity and mRNA levels of NKA alpha 1a and alpha 1b in Atlantic salmon. Cortisol treatment for 6-14 days resulted in increased, physiological levels of cortisol, increased gill NKA activity and improved salinity tolerance (lower plasma chloride after a 24h seawater challenge), whereas DOC and aldosterone had no effect on either NKA activity or salinity tolerance. NKA alpha 1a and alpha 1b mRNA levels, which increase in response to fresh water and seawater acclimation, respectively, were both upregulated by cortisol, whereas DOC and aldosterone were without effect. Cortisol, DOC and aldosterone had no effect on gill glucocorticoid receptor GR1, GR2 and MR mRNA levels, although there was some indication of possible upregulation of GR1 by cortisol (p=0.07). The putative GR blocker RU486 inhibited cortisol-induced increases in salinity tolerance, NKA activity and NKA alpha 1a and alpha 1b transcription, whereas the putative MR blocker spironolactone had no effect. The results provide support that cortisol, and not DOC or aldosterone, is involved in regulating the mineralocorticoid functions of ion uptake and salt secretion in teleost fish. SN - 1095-6840 UR - https://www.unboundmedicine.com/medline/citation/18462736/Are_we_missing_a_mineralocorticoid_in_teleost_fish_Effects_of_cortisol_deoxycorticosterone_and_aldosterone_on_osmoregulation_gill_Na+K+__ATPase_activity_and_isoform_mRNA_levels_in_Atlantic_salmon_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0016-6480(08)00134-2 DB - PRIME DP - Unbound Medicine ER -