ArticleVascular pharmacology
Evidence both L-type and non-L-type voltage-dependent calcium channels contribute to cerebral artery vasospasm following loss of NO in the rat.
Article in Vascular pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- Long-term hypoxia modulates depolarization activation of BKFrontiers in physiology · 2024Article
- Vascular mechanotransduction.Physiological reviews · 2023Review
- Large-conductance calcium-activated KBritish journal of pharmacology · 2021Article
- Endothelial Nitric Oxide Suppresses Action-Potential-Like Transient Spikes and Vasospasm in Small Resistance Arteries.Hypertension (Dallas, Tex. : 1979) · 2020Article
- Elementary calcium signaling in arterial smooth muscle.Channels (Austin, Tex.) · 2019Review
- Stimulation of calcium-sensing receptors induces endothelium-dependent vasorelaxations via nitric oxide production and activation of IKCa channels.Vascular pharmacology · 2016Article
- Eugenol dilates mesenteric arteries and reduces systemic BP by activating endothelial cell TRPV4 channels.British journal of pharmacology · 2015Article
- Role of T-type channels in vasomotor function: team player or chameleon?Pflugers Archiv : European journal of physiology · 2014Review
- Contribution of transient and sustained calcium influx, and sensitization to depolarization-induced contractions of the intact mouse aorta.BMC physiology · 2012Article
- Article
- The promise of inhibition of smooth muscle tone as a treatment for erectile dysfunction: where are we now?International journal of impotence researchReview
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
We recently found block of NO synthase in rat middle cerebral artery caused spasm, associated with depolarizing oscillations in membrane potential (E(m)) similar in form but faster in frequency (circa 1 Hz) to vasomotion. T-type voltage-gated Ca(2+) channels contribute to cerebral myogenic tone and vasomotion, so we investigated the significance of T-type and other ion channels for membrane potential oscillations underlying arterial spasm. Smooth muscle cell membrane potential (E(m)) and tension were measured simultaneously in rat middle cerebral artery. NO synthase blockade caused temporally coupled depolarizing oscillations in cerebrovascular E(m) with associated vasoconstriction. Both events were accentuated by block of smooth muscle BK(Ca). Block of T-type channels or inhibition of Na(+)/K(+)-ATPase abolished the oscillations in E(m) and reduced vasoconstriction. Oscillations in E(m) were either attenuated or accentuated by reducing [Ca(2+)](o) or block of K(V), respectively. TRAM-34 attenuated oscillations in both E(m) and tone, apparently independent of effects against K(Ca)3.1. Thus, rapid depolarizing oscillations in E(m) and tone observed after endothelial function has been disrupted reflect input from T-type calcium channels in addition to L-type channels, while other depolarizing currents appear to be unimportant. These data suggest that combined block of T and L-type channels may represent an effective approach to reverse cerebral vasospasm.
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