TRPC3 participates in angiotensin II type 1 receptor-dependent stress-induced slow increase in intracellular Ca2+ concentration in mouse cardiomyocytes

Yohei Yamaguchi, Gentaro Iribe, Toshiyuki Kaneko, Ken Takahashi, Takuro Numaga-Tomita, Motohiro Nishida, Lutz Birnbaumer, Keiji Naruse

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

When a cardiac muscle is held in a stretched position, its [Ca2+] transient increases slowly over several minutes in a process known as stress-induced slow increase in intracellular Ca2+ concentration ([Ca2+]i) (SSC). Transient receptor potential canonical (TRPC) 3 forms a non-selective cation channel regulated by the angiotensin II type 1 receptor (AT1R). In this study, we investigated the role of TRPC3 in the SSC. Isolated mouse ventricular myocytes were electrically stimulated and subjected to sustained stretch. An AT1R blocker, a phospholipase C inhibitor, and a TRPC3 inhibitor suppressed the SSC. These inhibitors also abolished the observed SSC-like slow increase in [Ca2+]i induced by angiotensin II, instead of stretch. Furthermore, the SSC was not observed in TRPC3 knockout mice. Simulation and immunohistochemical studies suggest that sarcolemmal TRPC3 is responsible for the SSC. These results indicate that sarcolemmal TRPC3, regulated by AT1R, causes the SSC.

Original languageEnglish
Pages (from-to)153-164
Number of pages12
JournalJournal of Physiological Sciences
Volume68
Issue number2
DOIs
Publication statusPublished - Mar 1 2018

Fingerprint

Angiotensin Type 1 Receptor
Cardiac Myocytes
Angiotensin II Type 1 Receptor Blockers
Type C Phospholipases
Knockout Mice
Angiotensin II
Muscle Cells
Cations
Myocardium

All Science Journal Classification (ASJC) codes

  • Physiology

Cite this

TRPC3 participates in angiotensin II type 1 receptor-dependent stress-induced slow increase in intracellular Ca2+ concentration in mouse cardiomyocytes. / Yamaguchi, Yohei; Iribe, Gentaro; Kaneko, Toshiyuki; Takahashi, Ken; Numaga-Tomita, Takuro; Nishida, Motohiro; Birnbaumer, Lutz; Naruse, Keiji.

In: Journal of Physiological Sciences, Vol. 68, No. 2, 01.03.2018, p. 153-164.

Research output: Contribution to journalArticle

Yamaguchi, Yohei ; Iribe, Gentaro ; Kaneko, Toshiyuki ; Takahashi, Ken ; Numaga-Tomita, Takuro ; Nishida, Motohiro ; Birnbaumer, Lutz ; Naruse, Keiji. / TRPC3 participates in angiotensin II type 1 receptor-dependent stress-induced slow increase in intracellular Ca2+ concentration in mouse cardiomyocytes. In: Journal of Physiological Sciences. 2018 ; Vol. 68, No. 2. pp. 153-164.
@article{9881195227ef4f6797ef7d9b2fe99a31,
title = "TRPC3 participates in angiotensin II type 1 receptor-dependent stress-induced slow increase in intracellular Ca2+ concentration in mouse cardiomyocytes",
abstract = "When a cardiac muscle is held in a stretched position, its [Ca2+] transient increases slowly over several minutes in a process known as stress-induced slow increase in intracellular Ca2+ concentration ([Ca2+]i) (SSC). Transient receptor potential canonical (TRPC) 3 forms a non-selective cation channel regulated by the angiotensin II type 1 receptor (AT1R). In this study, we investigated the role of TRPC3 in the SSC. Isolated mouse ventricular myocytes were electrically stimulated and subjected to sustained stretch. An AT1R blocker, a phospholipase C inhibitor, and a TRPC3 inhibitor suppressed the SSC. These inhibitors also abolished the observed SSC-like slow increase in [Ca2+]i induced by angiotensin II, instead of stretch. Furthermore, the SSC was not observed in TRPC3 knockout mice. Simulation and immunohistochemical studies suggest that sarcolemmal TRPC3 is responsible for the SSC. These results indicate that sarcolemmal TRPC3, regulated by AT1R, causes the SSC.",
author = "Yohei Yamaguchi and Gentaro Iribe and Toshiyuki Kaneko and Ken Takahashi and Takuro Numaga-Tomita and Motohiro Nishida and Lutz Birnbaumer and Keiji Naruse",
year = "2018",
month = "3",
day = "1",
doi = "10.1007/s12576-016-0519-3",
language = "English",
volume = "68",
pages = "153--164",
journal = "Journal of Physiological Sciences",
issn = "1880-6546",
publisher = "Springer Japan",
number = "2",

}

TY - JOUR

T1 - TRPC3 participates in angiotensin II type 1 receptor-dependent stress-induced slow increase in intracellular Ca2+ concentration in mouse cardiomyocytes

AU - Yamaguchi, Yohei

AU - Iribe, Gentaro

AU - Kaneko, Toshiyuki

AU - Takahashi, Ken

AU - Numaga-Tomita, Takuro

AU - Nishida, Motohiro

AU - Birnbaumer, Lutz

AU - Naruse, Keiji

PY - 2018/3/1

Y1 - 2018/3/1

N2 - When a cardiac muscle is held in a stretched position, its [Ca2+] transient increases slowly over several minutes in a process known as stress-induced slow increase in intracellular Ca2+ concentration ([Ca2+]i) (SSC). Transient receptor potential canonical (TRPC) 3 forms a non-selective cation channel regulated by the angiotensin II type 1 receptor (AT1R). In this study, we investigated the role of TRPC3 in the SSC. Isolated mouse ventricular myocytes were electrically stimulated and subjected to sustained stretch. An AT1R blocker, a phospholipase C inhibitor, and a TRPC3 inhibitor suppressed the SSC. These inhibitors also abolished the observed SSC-like slow increase in [Ca2+]i induced by angiotensin II, instead of stretch. Furthermore, the SSC was not observed in TRPC3 knockout mice. Simulation and immunohistochemical studies suggest that sarcolemmal TRPC3 is responsible for the SSC. These results indicate that sarcolemmal TRPC3, regulated by AT1R, causes the SSC.

AB - When a cardiac muscle is held in a stretched position, its [Ca2+] transient increases slowly over several minutes in a process known as stress-induced slow increase in intracellular Ca2+ concentration ([Ca2+]i) (SSC). Transient receptor potential canonical (TRPC) 3 forms a non-selective cation channel regulated by the angiotensin II type 1 receptor (AT1R). In this study, we investigated the role of TRPC3 in the SSC. Isolated mouse ventricular myocytes were electrically stimulated and subjected to sustained stretch. An AT1R blocker, a phospholipase C inhibitor, and a TRPC3 inhibitor suppressed the SSC. These inhibitors also abolished the observed SSC-like slow increase in [Ca2+]i induced by angiotensin II, instead of stretch. Furthermore, the SSC was not observed in TRPC3 knockout mice. Simulation and immunohistochemical studies suggest that sarcolemmal TRPC3 is responsible for the SSC. These results indicate that sarcolemmal TRPC3, regulated by AT1R, causes the SSC.

UR - http://www.scopus.com/inward/record.url?scp=85009833951&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85009833951&partnerID=8YFLogxK

U2 - 10.1007/s12576-016-0519-3

DO - 10.1007/s12576-016-0519-3

M3 - Article

C2 - 28105583

AN - SCOPUS:85009833951

VL - 68

SP - 153

EP - 164

JO - Journal of Physiological Sciences

JF - Journal of Physiological Sciences

SN - 1880-6546

IS - 2

ER -