4.5 Article

Capacitative Ca2+ entry in agonist-induced pulmonary vasoconstriction

出版社

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.2001.280.5.L870

关键词

transient receptor potential gene; pulmonary hypertension; pulmonary artery smooth muscle cells

资金

  1. NHLBI NIH HHS [HL-54043, HL-64945] Funding Source: Medline

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Agonist-induced increases in cytosolic Ca2+ concentration ([Ca2+](cyt)) in pulmonary artery (PA) smooth muscle cells (SMCs) consist of a transient Ca2+ release from intracellular stores followed by a sustained Ca2+ influx. Depletion of intracellular Ca2+ stores triggers capacitative Ca2+ entry (CCE), which contributes to the sustained increase in [Ca2+](cyt) and the refilling of Ca2+ into the stores. In isolated PAs superfused with Ca2+-free solution, phenylephrine induced a transient contraction, apparently by a rise in [Ca2+](cyt) due to Ca2+ release from the intracellular stores. The transient contraction lasted for 3-4 min until the Ca2+ store was depleted. Restoration of extracellular Ca2+ in the presence of phentolamine produced a contraction potentially due to a rise in [Ca2+](cyt) via CCE. The store-operated Ca2+ channel blocker Ni2+ reduced the store depletion-activated Ca2+ currents, decreased CCE, and inhibited the CCE-mediated contraction. In single PASMCs, we identified, using RT-PCR, five transient receptor potential gene transcripts. These results suggest that CCE, potentially through transient receptor potential-encoded Ca2+ channels, plays an important role in agonist-mediated PA contraction.

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