Interactions between calcium and reactive oxygen species in pulmonary arterial smooth muscle responses to hypoxia

Larissa Shimoda, Clark Undem

Research output: Contribution to journalArticle

Abstract

In contrast to the systemic vasculature, where hypoxia causes vasodilation, pulmonary arteries constrict in response to hypoxia. The mechanisms underlying this unique response have been the subject of investigation for over 50 years, and still remain a topic of great debate. Over the last 20 years, there has emerged a general consensus that both increases in intracellular calcium concentration and changes in reactive oxygen species (ROS) generation play key roles in the pulmonary vascular response to hypoxia. Controversy exists, however, regarding whether ROS increase or decrease during hypoxia, the source of ROS, and the mechanisms by which changes in ROS might impact intracellular calcium, and vice versa. This review will discuss the mechanisms regulating [Ca2+]i and ROS in PASMCs, and the interaction between ROS and Ca2+ signaling during exposure to acute hypoxia.

Original languageEnglish (US)
Pages (from-to)221-229
Number of pages9
JournalRespiratory Physiology and Neurobiology
Volume174
Issue number3
DOIs
StatePublished - Dec 31 2010

Fingerprint

Smooth Muscle
Reactive Oxygen Species
Calcium
Lung
Vasodilation
Pulmonary Artery
Blood Vessels
Hypoxia

Keywords

  • Mitochondria
  • PASMCs
  • Ventilation

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Neuroscience(all)

Cite this

Interactions between calcium and reactive oxygen species in pulmonary arterial smooth muscle responses to hypoxia. / Shimoda, Larissa; Undem, Clark.

In: Respiratory Physiology and Neurobiology, Vol. 174, No. 3, 31.12.2010, p. 221-229.

Research output: Contribution to journalArticle

@article{347415ef04e648089f03fb0cffcbfdcf,
title = "Interactions between calcium and reactive oxygen species in pulmonary arterial smooth muscle responses to hypoxia",
abstract = "In contrast to the systemic vasculature, where hypoxia causes vasodilation, pulmonary arteries constrict in response to hypoxia. The mechanisms underlying this unique response have been the subject of investigation for over 50 years, and still remain a topic of great debate. Over the last 20 years, there has emerged a general consensus that both increases in intracellular calcium concentration and changes in reactive oxygen species (ROS) generation play key roles in the pulmonary vascular response to hypoxia. Controversy exists, however, regarding whether ROS increase or decrease during hypoxia, the source of ROS, and the mechanisms by which changes in ROS might impact intracellular calcium, and vice versa. This review will discuss the mechanisms regulating [Ca2+]i and ROS in PASMCs, and the interaction between ROS and Ca2+ signaling during exposure to acute hypoxia.",
keywords = "Mitochondria, PASMCs, Ventilation",
author = "Larissa Shimoda and Clark Undem",
year = "2010",
month = "12",
day = "31",
doi = "10.1016/j.resp.2010.08.014",
language = "English (US)",
volume = "174",
pages = "221--229",
journal = "Respiratory Physiology and Neurobiology",
issn = "1569-9048",
publisher = "Elsevier",
number = "3",

}

TY - JOUR

T1 - Interactions between calcium and reactive oxygen species in pulmonary arterial smooth muscle responses to hypoxia

AU - Shimoda, Larissa

AU - Undem, Clark

PY - 2010/12/31

Y1 - 2010/12/31

N2 - In contrast to the systemic vasculature, where hypoxia causes vasodilation, pulmonary arteries constrict in response to hypoxia. The mechanisms underlying this unique response have been the subject of investigation for over 50 years, and still remain a topic of great debate. Over the last 20 years, there has emerged a general consensus that both increases in intracellular calcium concentration and changes in reactive oxygen species (ROS) generation play key roles in the pulmonary vascular response to hypoxia. Controversy exists, however, regarding whether ROS increase or decrease during hypoxia, the source of ROS, and the mechanisms by which changes in ROS might impact intracellular calcium, and vice versa. This review will discuss the mechanisms regulating [Ca2+]i and ROS in PASMCs, and the interaction between ROS and Ca2+ signaling during exposure to acute hypoxia.

AB - In contrast to the systemic vasculature, where hypoxia causes vasodilation, pulmonary arteries constrict in response to hypoxia. The mechanisms underlying this unique response have been the subject of investigation for over 50 years, and still remain a topic of great debate. Over the last 20 years, there has emerged a general consensus that both increases in intracellular calcium concentration and changes in reactive oxygen species (ROS) generation play key roles in the pulmonary vascular response to hypoxia. Controversy exists, however, regarding whether ROS increase or decrease during hypoxia, the source of ROS, and the mechanisms by which changes in ROS might impact intracellular calcium, and vice versa. This review will discuss the mechanisms regulating [Ca2+]i and ROS in PASMCs, and the interaction between ROS and Ca2+ signaling during exposure to acute hypoxia.

KW - Mitochondria

KW - PASMCs

KW - Ventilation

UR - http://www.scopus.com/inward/record.url?scp=78449268302&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=78449268302&partnerID=8YFLogxK

U2 - 10.1016/j.resp.2010.08.014

DO - 10.1016/j.resp.2010.08.014

M3 - Article

VL - 174

SP - 221

EP - 229

JO - Respiratory Physiology and Neurobiology

JF - Respiratory Physiology and Neurobiology

SN - 1569-9048

IS - 3

ER -