Sevoflurane and bradykinin-induced calcium mobilization in pulmonary arterial valvular endothelial cells in situ: Sevoflurane stimulates plasmalemmal calcium influx into endothelial cells

Tomoo Kanna, Takashi Akata, Kaoru Izumi, Mikio Nakashima, Yoshikazu Yonemitsu, Makoto Hashizume, Shosuke Takahashi

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Kinins locally synthesized in the cardiovascular tissue are believed to contribute to the regulation of cardiovascular homeostasis by stimulating the endothelial cells to release nitric oxide, prostacyclin, or a hyperpolarizing factor via autocrine-paracrine mechanisms. This study was designed to investigate the action of sevoflurane on bradykinin-induced Ca2+ mobilization in endothelial cells in situ. Utilizing fura-2-loaded rat pulmonary arterial valve leaflets, the effects of sevoflurane were examined on bradykinin-induced increases in intracellular Ca2+ concentration ([Ca2+]i) in endothelial cells in situ. In the presence of extracellular Ca2+ (1.5 mM), bradykinin (3-30 μM) produced an initial phasic and a subsequent tonic increase in [Ca2+]i in a concentration-dependent manner. However, it produced only the phasic increase in [Ca2+]i in the absence of extracellular Ca2+. Sevoflurane (5%, 0.67 mM) inhibited both the phasic and tonic responses to bradykinin. In these experiments, sevoflurane (3-5%) generated sustained increases (approximately 20-40% of the bradykinin-induced maximal increase in [Ca2+]i) in the resting [Ca2+]i level. Sevoflurane still increased [Ca2+]i after depletion of the intracellular Ca2+ stores with ionomycin (0.1 μM). However, the sevoflurane-induced increase in [Ca2+]i was eliminated by removal of the extracellular Ca2+ and attenuated by NiCl2 (1-3 mM). In conclusion, in the pulmonary arterial valvular endothelial cells, sevoflurane inhibits both bradykinin-induced Ca2+ release from the intracellular stores and bradykinin-induced plasmalemmal Ca2+ influx. In addition, sevoflurane appears to stimulate the plasmalemmal Ca+2 influx and thereby increase the endothelial [Ca2+]i level. Sevoflurane might influence the pulmonary vascular tone through its direct action on the pulmonary arterial valvular endothelial cells.

Original languageEnglish
Pages (from-to)714-724
Number of pages11
JournalJournal of Cardiovascular Pharmacology
Volume40
Issue number5
DOIs
Publication statusPublished - Nov 1 2002

Fingerprint

Bradykinin
Endothelial Cells
Calcium
Lung
sevoflurane
Pulmonary Valve
Kinins
Ionomycin
Fura-2
Epoprostenol
Blood Vessels
Nitric Oxide
Homeostasis

All Science Journal Classification (ASJC) codes

  • Pharmacology
  • Cardiology and Cardiovascular Medicine

Cite this

Sevoflurane and bradykinin-induced calcium mobilization in pulmonary arterial valvular endothelial cells in situ : Sevoflurane stimulates plasmalemmal calcium influx into endothelial cells. / Kanna, Tomoo; Akata, Takashi; Izumi, Kaoru; Nakashima, Mikio; Yonemitsu, Yoshikazu; Hashizume, Makoto; Takahashi, Shosuke.

In: Journal of Cardiovascular Pharmacology, Vol. 40, No. 5, 01.11.2002, p. 714-724.

Research output: Contribution to journalArticle

@article{44fc451392c84d0c84eea0b2f05102ee,
title = "Sevoflurane and bradykinin-induced calcium mobilization in pulmonary arterial valvular endothelial cells in situ: Sevoflurane stimulates plasmalemmal calcium influx into endothelial cells",
abstract = "Kinins locally synthesized in the cardiovascular tissue are believed to contribute to the regulation of cardiovascular homeostasis by stimulating the endothelial cells to release nitric oxide, prostacyclin, or a hyperpolarizing factor via autocrine-paracrine mechanisms. This study was designed to investigate the action of sevoflurane on bradykinin-induced Ca2+ mobilization in endothelial cells in situ. Utilizing fura-2-loaded rat pulmonary arterial valve leaflets, the effects of sevoflurane were examined on bradykinin-induced increases in intracellular Ca2+ concentration ([Ca2+]i) in endothelial cells in situ. In the presence of extracellular Ca2+ (1.5 mM), bradykinin (3-30 μM) produced an initial phasic and a subsequent tonic increase in [Ca2+]i in a concentration-dependent manner. However, it produced only the phasic increase in [Ca2+]i in the absence of extracellular Ca2+. Sevoflurane (5{\%}, 0.67 mM) inhibited both the phasic and tonic responses to bradykinin. In these experiments, sevoflurane (3-5{\%}) generated sustained increases (approximately 20-40{\%} of the bradykinin-induced maximal increase in [Ca2+]i) in the resting [Ca2+]i level. Sevoflurane still increased [Ca2+]i after depletion of the intracellular Ca2+ stores with ionomycin (0.1 μM). However, the sevoflurane-induced increase in [Ca2+]i was eliminated by removal of the extracellular Ca2+ and attenuated by NiCl2 (1-3 mM). In conclusion, in the pulmonary arterial valvular endothelial cells, sevoflurane inhibits both bradykinin-induced Ca2+ release from the intracellular stores and bradykinin-induced plasmalemmal Ca2+ influx. In addition, sevoflurane appears to stimulate the plasmalemmal Ca+2 influx and thereby increase the endothelial [Ca2+]i level. Sevoflurane might influence the pulmonary vascular tone through its direct action on the pulmonary arterial valvular endothelial cells.",
author = "Tomoo Kanna and Takashi Akata and Kaoru Izumi and Mikio Nakashima and Yoshikazu Yonemitsu and Makoto Hashizume and Shosuke Takahashi",
year = "2002",
month = "11",
day = "1",
doi = "10.1097/00005344-200211000-00009",
language = "English",
volume = "40",
pages = "714--724",
journal = "Journal of Cardiovascular Pharmacology",
issn = "0160-2446",
publisher = "Lippincott Williams and Wilkins",
number = "5",

}

TY - JOUR

T1 - Sevoflurane and bradykinin-induced calcium mobilization in pulmonary arterial valvular endothelial cells in situ

T2 - Sevoflurane stimulates plasmalemmal calcium influx into endothelial cells

AU - Kanna, Tomoo

AU - Akata, Takashi

AU - Izumi, Kaoru

AU - Nakashima, Mikio

AU - Yonemitsu, Yoshikazu

AU - Hashizume, Makoto

AU - Takahashi, Shosuke

PY - 2002/11/1

Y1 - 2002/11/1

N2 - Kinins locally synthesized in the cardiovascular tissue are believed to contribute to the regulation of cardiovascular homeostasis by stimulating the endothelial cells to release nitric oxide, prostacyclin, or a hyperpolarizing factor via autocrine-paracrine mechanisms. This study was designed to investigate the action of sevoflurane on bradykinin-induced Ca2+ mobilization in endothelial cells in situ. Utilizing fura-2-loaded rat pulmonary arterial valve leaflets, the effects of sevoflurane were examined on bradykinin-induced increases in intracellular Ca2+ concentration ([Ca2+]i) in endothelial cells in situ. In the presence of extracellular Ca2+ (1.5 mM), bradykinin (3-30 μM) produced an initial phasic and a subsequent tonic increase in [Ca2+]i in a concentration-dependent manner. However, it produced only the phasic increase in [Ca2+]i in the absence of extracellular Ca2+. Sevoflurane (5%, 0.67 mM) inhibited both the phasic and tonic responses to bradykinin. In these experiments, sevoflurane (3-5%) generated sustained increases (approximately 20-40% of the bradykinin-induced maximal increase in [Ca2+]i) in the resting [Ca2+]i level. Sevoflurane still increased [Ca2+]i after depletion of the intracellular Ca2+ stores with ionomycin (0.1 μM). However, the sevoflurane-induced increase in [Ca2+]i was eliminated by removal of the extracellular Ca2+ and attenuated by NiCl2 (1-3 mM). In conclusion, in the pulmonary arterial valvular endothelial cells, sevoflurane inhibits both bradykinin-induced Ca2+ release from the intracellular stores and bradykinin-induced plasmalemmal Ca2+ influx. In addition, sevoflurane appears to stimulate the plasmalemmal Ca+2 influx and thereby increase the endothelial [Ca2+]i level. Sevoflurane might influence the pulmonary vascular tone through its direct action on the pulmonary arterial valvular endothelial cells.

AB - Kinins locally synthesized in the cardiovascular tissue are believed to contribute to the regulation of cardiovascular homeostasis by stimulating the endothelial cells to release nitric oxide, prostacyclin, or a hyperpolarizing factor via autocrine-paracrine mechanisms. This study was designed to investigate the action of sevoflurane on bradykinin-induced Ca2+ mobilization in endothelial cells in situ. Utilizing fura-2-loaded rat pulmonary arterial valve leaflets, the effects of sevoflurane were examined on bradykinin-induced increases in intracellular Ca2+ concentration ([Ca2+]i) in endothelial cells in situ. In the presence of extracellular Ca2+ (1.5 mM), bradykinin (3-30 μM) produced an initial phasic and a subsequent tonic increase in [Ca2+]i in a concentration-dependent manner. However, it produced only the phasic increase in [Ca2+]i in the absence of extracellular Ca2+. Sevoflurane (5%, 0.67 mM) inhibited both the phasic and tonic responses to bradykinin. In these experiments, sevoflurane (3-5%) generated sustained increases (approximately 20-40% of the bradykinin-induced maximal increase in [Ca2+]i) in the resting [Ca2+]i level. Sevoflurane still increased [Ca2+]i after depletion of the intracellular Ca2+ stores with ionomycin (0.1 μM). However, the sevoflurane-induced increase in [Ca2+]i was eliminated by removal of the extracellular Ca2+ and attenuated by NiCl2 (1-3 mM). In conclusion, in the pulmonary arterial valvular endothelial cells, sevoflurane inhibits both bradykinin-induced Ca2+ release from the intracellular stores and bradykinin-induced plasmalemmal Ca2+ influx. In addition, sevoflurane appears to stimulate the plasmalemmal Ca+2 influx and thereby increase the endothelial [Ca2+]i level. Sevoflurane might influence the pulmonary vascular tone through its direct action on the pulmonary arterial valvular endothelial cells.

UR - http://www.scopus.com/inward/record.url?scp=0036873593&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036873593&partnerID=8YFLogxK

U2 - 10.1097/00005344-200211000-00009

DO - 10.1097/00005344-200211000-00009

M3 - Article

C2 - 12409980

AN - SCOPUS:0036873593

VL - 40

SP - 714

EP - 724

JO - Journal of Cardiovascular Pharmacology

JF - Journal of Cardiovascular Pharmacology

SN - 0160-2446

IS - 5

ER -