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Lack of tight and local coupling between L‐type Cav 1.2 Ca2+ channels and RyRs in single calcium release units of arterial vascular smooth muscle cells
Author(s) -
Essin Kirill,
Moosmang Sven,
Welling Andrea,
Hofmann Franz,
Luft Friedrich C.,
Gollasch Maik
Publication year - 2007
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.21.6.lb92-a
Subject(s) - depolarization , vascular smooth muscle , chemistry , biophysics , membrane potential , voltage dependent calcium channel , calcium , anatomy , neuroscience , endocrinology , smooth muscle , biology , biochemistry , organic chemistry
We tested the hypothesis that local and tight coupling between the Cav1.2 channels and RyRs is not required to initiate Ca2+ sparks in arterial vascular smooth muscle cells (VSMC). Cross‐signaling between Cav1.2 channels and RyR was studied using an approach based on Poisson statistical analysis of elementary calcium release events (ECRE). ECRE were recorded as Ca2+ sparks or STOCs in tibial VSMCs of smooth muscle‐specific L‐type Cav 1.2 channel knockout (SMAKO) mice. Cav1.2 channel gene inactivation reduced Ca2+ spark frequency and amplitude by ~50% and ~80%, respectively. The first‐latency histograms of sparks only slightly depended on the depolarization level and peaked at a relatively positive potential in wild‐type VSMCs, i.e., ~+20 mV. Furthermore, average latencies between −30 mV and +50 mV occurred at > 100 ms. Average latency of the first identified STOCs was similar and >100 ms in wild‐type, nimodipine‐treated and SMAKO VSMC and only slightly depended on the depolarization level. All‐latency histograms in all three VSMC cell groups did not show a tendency to decline upon depolarization time. The observation that the first‐latency and all‐latency histograms have different waveforms implies that the release waveform is not determined by the time course of first event activation, with relatively fewer reopenings, as is the case in skeletal and cardiac muscle. Thus, Cav1.2 channels are important for frequency and amplitude modulation of VSMC Ca2+ sparks. However, local and tight coupling between the Cav1.2 channels and RyRs is not required to initiate Ca2+ sparks from single calcium release units in arterial VSMC.