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Regulation of vascular smooth muscle contraction by Ca 2+ signaling and Ca 2+ sensitivity in intrapulmonary arteries
Author(s) -
PerezZoghbi Jose F,
Mukherjee Seema,
Sanderson Michael J.
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.1023.17
Subject(s) - contraction (grammar) , medicine , endocrinology , phorbol , protein kinase c , vascular smooth muscle , chemistry , endothelin 1 , nitric oxide , pulmonary artery , muscle contraction , endothelin receptor , ryanodine receptor , calcium , signal transduction , receptor , smooth muscle , biochemistry
The contraction of vascular smooth muscle cells (SMCs) of small pulmonary arteries is critical for the regulation of pulmonary vascular resistance and plays an important role in the development of pulmonary hypertension. We have studied the regulation of SMC contraction by Ca 2+ and Ca 2+ sensitivity in intrapulmonary arteries by measuring artery contraction and Ca 2+ signaling in mouse lung slices with phase‐contrast and confocal microscopy. The agonists serotonin (5‐HT) and endothelin (ET) induced artery contraction and stimulated Ca 2+ oscillations in their SMCs. Conversely, nitric oxide (NO) caused relaxation and decreased the frequency of Ca 2+ oscillations in arteries pre‐stimulated with agonists. Ca 2+ permeabilization with caffeine and ryanodine caused artery contraction but agonists stimulate further contraction. Activation of PKC with phorbol 12‐myristate 13‐acetate (PMA, 1–10 μM) induced strong and sustained artery contraction whereas the PKC inhibitor GF‐109203X (1 μM) inhibited the agonists‐induced contraction. In conclusion, our results suggest that the contraction of intrapulmonary arteries is regulated by the frequency of Ca 2+ oscillations and a PKC‐dependent increase in Ca 2+ sensitivity.