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Endothelin‐1 increases the frequency of smooth muscle calcium waves in vena cava but not aorta
Author(s) -
Tykocki Nathan R.,
Jackson William F.,
Watts Stephanie W.
Publication year - 2011
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.25.1_supplement.1026.2
Subject(s) - contraction (grammar) , aorta , vascular smooth muscle , phenylephrine , medicine , extracellular , chemistry , endothelin 1 , intracellular , endothelin receptor , biophysics , endocrinology , receptor , smooth muscle , anatomy , biology , biochemistry , blood pressure
Vascular contraction is associated with a global increase in smooth muscle Ca 2+ . The frequency and amplitude of localized intracellular Ca 2+ release events, such as IP 3 receptor‐mediated Ca 2+ waves, can also regulate excitation‐contraction coupling in smooth muscle. While the vasoconstrictor ET‐1 does increase IP 3 formation, it is unclear if IP 3 receptor‐mediated Ca 2+ waves are a regulator of ET‐1‐induced contraction in arteries and veins. We hypothesized that ET‐1 increases the frequency and amplitude of Ca 2+ waves in rat aorta (RA) and vena cava (RVC). RA and RVC were mounted en face in an imaging superfusion chamber and incubated with the intensiometric fluorescent Ca 2+ indicator Fluo 4‐AM (10 μM). Using spinning‐disc confocal microscopy, image sequences were first recorded with buffer alone, and then maximal contractile concentrations of norepinephrine (NE, 10 μM) (RVC) or phenylephrine (PE, 10 μM) (RA), and finally ET‐1 (100 nM). ET‐1 (100 nM) increased Ca 2+ wave frequency significantly in RVC versus control (0.72±0.16 Hz vs . 0.45±0.13 Hz), but not in RA. Neither NE (10 μM) nor PE (10 μM) altered Ca 2+ wave frequency or amplitude in RA and RVC. These data indicate that intracellular Ca 2+ mobilization by ET‐1 is different in arteries and veins. These data also provide indirect evidence that ET receptors are coupled to IP 3 ‐mediated Ca 2+ release mechanisms in the vena cava but not aorta. Supported by NIH P01HL70687.