Muscle 2012
DOI: 10.1016/b978-0-12-381510-1.00089-2
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Microcirculation

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Cited by 10 publications
(18 citation statements)
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“…The authors did find that the VGCC blockers abolished vasomotion, establishing the efficacy of the drugs in this system. Similar results have been obtained for arterioles in hamster cremaster muscles (670), where nifedipine did not produce steady-state dilation of arterioles with substantial myogenic tone, but abolished vasomotion of these vessels. A lack of effect of nifedipine on resting diameter of cheek pouch arterioles, in vivo , was reported by Boric and colleagues (159).…”
Section: Voltage-gated Ca2+ Channelssupporting
confidence: 86%
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“…The authors did find that the VGCC blockers abolished vasomotion, establishing the efficacy of the drugs in this system. Similar results have been obtained for arterioles in hamster cremaster muscles (670), where nifedipine did not produce steady-state dilation of arterioles with substantial myogenic tone, but abolished vasomotion of these vessels. A lack of effect of nifedipine on resting diameter of cheek pouch arterioles, in vivo , was reported by Boric and colleagues (159).…”
Section: Voltage-gated Ca2+ Channelssupporting
confidence: 86%
“…That nifedipine (785, 1171) and diltiazem (185), which are both selective for L-type VGCCs, substantially inhibit myogenic tone in cremaster arterioles, in vitro , suggests that L-type channels provide a major contribution (70%–90%) in vessels studied in vitro , but the potential for significant regional-, strain-, and species-dependent differences in the contribution of different classes of VGCCs are acknowledged. In mouse cremaster muscle, in vivo , in contrast to studies of rat (599) and hamster (670), 60% of resting tone is due to L-type VGCCs, with <20% from T-type VGCCs (628). Inhibition of NO synthesis increased the contribution of T-type VGCCs to ~38% in this model.…”
Section: Voltage-gated Ca2+ Channelsmentioning
confidence: 84%
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