Premium
Calcium Homeostasis and Sensitization in Pulmonary Arterial Smooth Muscle
Author(s) -
Jernigan Nikki L.,
Resta Thomas C.
Publication year - 2014
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1111/micc.12096
Subject(s) - hypoxic pulmonary vasoconstriction , contractility , vasoconstriction , pulmonary hypertension , hypoxia (environmental) , paracrine signalling , homeostasis , medicine , endocrinology , microbiology and biotechnology , biology , chemistry , receptor , organic chemistry , oxygen
The pulmonary circulation is a low‐pressure, low‐resistance vascular bed with little to no resting tone under normal conditions. An increase in the [Ca 2+ ] i in PASMC s is an important determinant of contraction, migration, and proliferation. Both Ca 2+ influx through plasma membrane Ca 2+ channels and Ca 2+ release from the SR contribute to a rise in [Ca 2+ ] i . Additionally important in the pulmonary circulation are several kinase‐mediated signaling pathways that act to increase the sensitivity of the contractile apparatus to [Ca 2+ ] i . Similarly, cytoskeletal processes resulting in dynamic remodeling of the actin cytoskeleton can further contribute to contractility in the pulmonary circulation. In addition to endocrine, paracrine, and autocrine factors, alveolar hypoxia is an important stimulus for pulmonary vasoconstriction. However, prolonged hypoxia is a critical pathological stimulus associated with the development of pulmonary hypertension and cor pulmonale. In this review, we will discuss recent advances in our understanding of how Ca 2+ homeostasis and sensitization regulate PASMC contractility under both physiological and pathophysiological conditions.