Contractile force is enhanced in Aortas from pendrin null mice due to stimulation of angiotensin II-dependent signaling.

Pendrin is a Cl-/HCO3- exchanger expressed in the apical regions of renal intercalated cells. Following pendrin gene ablation, blood pressure falls, in part, from reduced renal NaCl absorption. We asked if pendrin is expressed in vascular tissue and if the lower blood pressure observed in pendrin nu...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Roy L Sutliff, Erik R Walp, Young Hee Kim, Lori A Walker, Alexander M El-Ali, Jing Ma, Robert Bonsall, Semra Ramosevac, Douglas C Eaton, Jill W Verlander, Laura Hansen, Rudolph L Gleason, Truyen D Pham, Seongun Hong, Vladimir Pech, Susan M Wall
Formato: article
Lenguaje:EN
Publicado: Public Library of Science (PLoS) 2014
Materias:
R
Q
Acceso en línea:https://doaj.org/article/bb1451a941eb423ba64bad8a0b856ab8
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:bb1451a941eb423ba64bad8a0b856ab8
record_format dspace
spelling oai:doaj.org-article:bb1451a941eb423ba64bad8a0b856ab82021-11-25T06:03:33ZContractile force is enhanced in Aortas from pendrin null mice due to stimulation of angiotensin II-dependent signaling.1932-620310.1371/journal.pone.0105101https://doaj.org/article/bb1451a941eb423ba64bad8a0b856ab82014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/25148130/?tool=EBIhttps://doaj.org/toc/1932-6203Pendrin is a Cl-/HCO3- exchanger expressed in the apical regions of renal intercalated cells. Following pendrin gene ablation, blood pressure falls, in part, from reduced renal NaCl absorption. We asked if pendrin is expressed in vascular tissue and if the lower blood pressure observed in pendrin null mice is accompanied by reduced vascular reactivity. Thus, the contractile responses to KCl and phenylephrine (PE) were examined in isometrically mounted thoracic aortas from wild-type and pendrin null mice. Although pendrin expression was not detected in the aorta, pendrin gene ablation changed contractile protein abundance and increased the maximal contractile response to PE when normalized to cross sectional area (CSA). However, the contractile sensitivity to this agent was unchanged. The increase in contractile force/cross sectional area observed in pendrin null mice was due to reduced cross sectional area of the aorta and not from increased contractile force per vessel. The pendrin-dependent increase in maximal contractile response was endothelium- and nitric oxide-independent and did not occur from changes in Ca2+ sensitivity or chronic changes in catecholamine production. However, application of 100 nM angiotensin II increased force/CSA more in aortas from pendrin null than from wild type mice. Moreover, angiotensin type 1 receptor inhibitor (candesartan) treatment in vivo eliminated the pendrin-dependent changes contractile protein abundance and changes in the contractile force/cross sectional area in response to PE. In conclusion, pendrin gene ablation increases aorta contractile force per cross sectional area in response to angiotensin II and PE due to stimulation of angiotensin type 1 receptor-dependent signaling. The angiotensin type 1 receptor-dependent increase in vascular reactivity may mitigate the fall in blood pressure observed with pendrin gene ablation.Roy L SutliffErik R WalpYoung Hee KimLori A WalkerAlexander M El-AliJing MaRobert BonsallSemra RamosevacDouglas C EatonJill W VerlanderLaura HansenRudolph L GleasonTruyen D PhamSeongun HongVladimir PechSusan M WallPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 8, p e105101 (2014)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Roy L Sutliff
Erik R Walp
Young Hee Kim
Lori A Walker
Alexander M El-Ali
Jing Ma
Robert Bonsall
Semra Ramosevac
Douglas C Eaton
Jill W Verlander
Laura Hansen
Rudolph L Gleason
Truyen D Pham
Seongun Hong
Vladimir Pech
Susan M Wall
Contractile force is enhanced in Aortas from pendrin null mice due to stimulation of angiotensin II-dependent signaling.
description Pendrin is a Cl-/HCO3- exchanger expressed in the apical regions of renal intercalated cells. Following pendrin gene ablation, blood pressure falls, in part, from reduced renal NaCl absorption. We asked if pendrin is expressed in vascular tissue and if the lower blood pressure observed in pendrin null mice is accompanied by reduced vascular reactivity. Thus, the contractile responses to KCl and phenylephrine (PE) were examined in isometrically mounted thoracic aortas from wild-type and pendrin null mice. Although pendrin expression was not detected in the aorta, pendrin gene ablation changed contractile protein abundance and increased the maximal contractile response to PE when normalized to cross sectional area (CSA). However, the contractile sensitivity to this agent was unchanged. The increase in contractile force/cross sectional area observed in pendrin null mice was due to reduced cross sectional area of the aorta and not from increased contractile force per vessel. The pendrin-dependent increase in maximal contractile response was endothelium- and nitric oxide-independent and did not occur from changes in Ca2+ sensitivity or chronic changes in catecholamine production. However, application of 100 nM angiotensin II increased force/CSA more in aortas from pendrin null than from wild type mice. Moreover, angiotensin type 1 receptor inhibitor (candesartan) treatment in vivo eliminated the pendrin-dependent changes contractile protein abundance and changes in the contractile force/cross sectional area in response to PE. In conclusion, pendrin gene ablation increases aorta contractile force per cross sectional area in response to angiotensin II and PE due to stimulation of angiotensin type 1 receptor-dependent signaling. The angiotensin type 1 receptor-dependent increase in vascular reactivity may mitigate the fall in blood pressure observed with pendrin gene ablation.
format article
author Roy L Sutliff
Erik R Walp
Young Hee Kim
Lori A Walker
Alexander M El-Ali
Jing Ma
Robert Bonsall
Semra Ramosevac
Douglas C Eaton
Jill W Verlander
Laura Hansen
Rudolph L Gleason
Truyen D Pham
Seongun Hong
Vladimir Pech
Susan M Wall
author_facet Roy L Sutliff
Erik R Walp
Young Hee Kim
Lori A Walker
Alexander M El-Ali
Jing Ma
Robert Bonsall
Semra Ramosevac
Douglas C Eaton
Jill W Verlander
Laura Hansen
Rudolph L Gleason
Truyen D Pham
Seongun Hong
Vladimir Pech
Susan M Wall
author_sort Roy L Sutliff
title Contractile force is enhanced in Aortas from pendrin null mice due to stimulation of angiotensin II-dependent signaling.
title_short Contractile force is enhanced in Aortas from pendrin null mice due to stimulation of angiotensin II-dependent signaling.
title_full Contractile force is enhanced in Aortas from pendrin null mice due to stimulation of angiotensin II-dependent signaling.
title_fullStr Contractile force is enhanced in Aortas from pendrin null mice due to stimulation of angiotensin II-dependent signaling.
title_full_unstemmed Contractile force is enhanced in Aortas from pendrin null mice due to stimulation of angiotensin II-dependent signaling.
title_sort contractile force is enhanced in aortas from pendrin null mice due to stimulation of angiotensin ii-dependent signaling.
publisher Public Library of Science (PLoS)
publishDate 2014
url https://doaj.org/article/bb1451a941eb423ba64bad8a0b856ab8
work_keys_str_mv AT roylsutliff contractileforceisenhancedinaortasfrompendrinnullmiceduetostimulationofangiotensiniidependentsignaling
AT erikrwalp contractileforceisenhancedinaortasfrompendrinnullmiceduetostimulationofangiotensiniidependentsignaling
AT youngheekim contractileforceisenhancedinaortasfrompendrinnullmiceduetostimulationofangiotensiniidependentsignaling
AT loriawalker contractileforceisenhancedinaortasfrompendrinnullmiceduetostimulationofangiotensiniidependentsignaling
AT alexandermelali contractileforceisenhancedinaortasfrompendrinnullmiceduetostimulationofangiotensiniidependentsignaling
AT jingma contractileforceisenhancedinaortasfrompendrinnullmiceduetostimulationofangiotensiniidependentsignaling
AT robertbonsall contractileforceisenhancedinaortasfrompendrinnullmiceduetostimulationofangiotensiniidependentsignaling
AT semraramosevac contractileforceisenhancedinaortasfrompendrinnullmiceduetostimulationofangiotensiniidependentsignaling
AT douglasceaton contractileforceisenhancedinaortasfrompendrinnullmiceduetostimulationofangiotensiniidependentsignaling
AT jillwverlander contractileforceisenhancedinaortasfrompendrinnullmiceduetostimulationofangiotensiniidependentsignaling
AT laurahansen contractileforceisenhancedinaortasfrompendrinnullmiceduetostimulationofangiotensiniidependentsignaling
AT rudolphlgleason contractileforceisenhancedinaortasfrompendrinnullmiceduetostimulationofangiotensiniidependentsignaling
AT truyendpham contractileforceisenhancedinaortasfrompendrinnullmiceduetostimulationofangiotensiniidependentsignaling
AT seongunhong contractileforceisenhancedinaortasfrompendrinnullmiceduetostimulationofangiotensiniidependentsignaling
AT vladimirpech contractileforceisenhancedinaortasfrompendrinnullmiceduetostimulationofangiotensiniidependentsignaling
AT susanmwall contractileforceisenhancedinaortasfrompendrinnullmiceduetostimulationofangiotensiniidependentsignaling
_version_ 1718414243298017280