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Blocking fast calcium‐dependent isometric force development unmasks a slow calcium‐independent contraction when porcine pulmonary artery (PPA) is depolarized
Author(s) -
Patel Hiten M,
McIntyre Nathan,
Allawzi Ayed M,
Kwon David M,
Pelaez Nancy J
Publication year - 2009
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.23.1_supplement.769.2
Subject(s) - chemistry , calcium , verapamil , egta , contraction (grammar) , nifedipine , cyclopiazonic acid , voltage dependent calcium channel , ionomycin , muscle contraction , biophysics , medicine , biology , organic chemistry
The absence of calcium in the extracellular solution ([Ca 2+ ] o ) abolishes contraction of vascular smooth muscle (VSM) in most arteries. In contrast, we find that VSM from fourth generation PPA contracts in response to high potassium depolarization in both the presence and absence of [Ca 2+ ] o . PPA contractile response is known to involve both [Ca 2+ ] o and intracellular sources. To test if the contraction in Krebs is due to influx of calcium, verapamil (50uM) or nifedipine (5uM) were used to inhibit voltage operated calcium channels (VOCC). Isometric force was measured in isolated PPA and the resulting rate constants were modeled using JSIM software. VOCC inhibitors reduced the contraction rate. No difference in rates was detected between contractions in calcium‐free saline containing 0.1 mM EGTA versus contraction in Krebs with VOCC inhibitors. Surprisingly, PPA contracted in response to high potassium depolarization in the presence of nifedipine to prevent calcium entry through VOCC and the SERCA inhibitor cyclopiazonic acid (10 uM CPA) to deplete calcium stores. Even a calcium ionophore, ionomycin (0.04 mM), did not affect the contraction in calcium‐free saline with EGTA. Perhaps these methods unmask a slow calcium‐independent contraction when PPA is depolarized.