ArticleThe Journal of clinical investigation1997
Voltage-gated calcium channel currents in human coronary myocytes. Regulation by cyclic GMP and nitric oxide.
Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 80 citations in OpenAlex.
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
- Calcium Homeostasis, Transporters, and Blockers in Health and Diseases of the Cardiovascular System.International journal of molecular sciences · 2023Review
- Oxidative Regulation of Vascular CaAntioxidants (Basel, Switzerland) · 2022Review
- Oscillating calcium signals in smooth muscle cells underlie the persistent basal tone of internal anal sphincter.Journal of cellular physiology · 2021Article
- Biased activity of soluble guanylyl cyclase: the Janus face of thymoquinone.Acta pharmaceutica Sinica. B · 2017Review
- Regulation of Coronary Blood Flow.Comprehensive Physiology · 2017Review
- Antagonism of Nav channels and α1-adrenergic receptors contributes to vascular smooth muscle effects of ranolazine.Scientific reports · 2015Article
- Role of T-type channels in vasomotor function: team player or chameleon?Pflugers Archiv : European journal of physiology · 2014Review
- Article
- Hyperpolarization-activated ion channels as targets for nitric oxide signalling in deep cerebellar nuclei.The European journal of neuroscience · 2010Article
- Nongenomic inhibition of coronary constriction by 17ß-estradiol, 2-hydroxyestradiol, and 2-methoxyestradiol.Canadian journal of physiology and pharmacology · 2010Article
- Nitric oxide suppresses cerebral vasomotion by sGC-independent effects on ryanodine receptors and voltage-gated calcium channels.Journal of vascular research · 2010Article
- Relaxation patterns of human gastric corporal smooth muscle by cyclic nucleotides producing agents.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2009Article
- Deletion of inducible nitric oxide synthase provides cardioprotection in mice with 2-kidney, 1-clip hypertension.Hypertension (Dallas, Tex. : 1979) · 2009Article
- Effects of flavoxate hydrochloride on voltage-dependent Ba2+ currents in human detrusor myocytes at different experimental temperatures.Naunyn-Schmiedeberg's archives of pharmacology · 2007Article
- Atherosclerosis-related molecular alteration of the human CaV1.2 calcium channel alpha1C subunit.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Lack of inducible NO synthase reduces oxidative stress and enhances cardiac response to isoproterenol in mice with deoxycorticosterone acetate-salt hypertension.Hypertension (Dallas, Tex. : 1979) · 2005Article
- Modulation of voltage-dependent Ba2+ currents in the guinea-pig gastric antrum by cyclic nucleotide-dependent pathways.British journal of pharmacology · 2005Article
- Effect of serum withdrawal on the contribution of L-type calcium channels (CaV1.2) to intracellular Ca2+ responses and chemotaxis in cultured human vascular smooth muscle cells.British journal of pharmacology · 2005Article
- Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage-gated Ca2+ channels contribute to the maintenance of contractile tone in vascular myocytes and are potential targets for vasodilating agents. There is no information available about their nature and regulation in human coronary arteries. We used the whole-cell voltage-clamp technique to characterize Ca2+-channel currents immediately after enzymatic dissociation and after primary culture of coronary myocytes taken from heart transplant patients. We recorded a dihydropyridine-sensitive L-type current in both freshly isolated and primary cultured cells. A T-type current was recorded only in culture. The L- (but not the T-) type current was inhibited by permeable analogues of cGMP in a dose-dependent manner. This effect was mimicked by the nitric oxide-generating agents S-nitroso-N-acetylpenicillamine (SNAP) and 3-morpholinosydnonimine which increased intracellular cGMP. Methylene blue, known to inhibit guanylate cyclase, antagonized the effect of SNAP. Inhibitions by SNAP and cGMP were not additive and seemed to occur through a common pathway. We conclude that (a) L-type Ca2+ channels are the major pathway for voltage-gated Ca2+ entry in human coronary myocytes; (b) their inhibition by agents stimulating nitric oxide and/or intracellular cGMP production is expected to contribute to vasorelaxation and may be involved in the therapeutic effect of nitrovasodilators; and (c) the expression of T-type Ca2+ channels in culture may be triggered by cell proliferation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.