T-type Ca2+ channels facilitate NO-formation, vasodilatation and NO-mediated modulation of blood pressure
| Autor: | Kenneth Andersen, Boye L. Jensen, Anne D Thuesen, Caryl E. Hill, Paul M. Vanhoutte, Pernille B. Lærkegaard Hansen, Hee-Sup Shin, Ole Skøtt, Per Svenningsen |
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| Rok vydání: | 2014 |
| Předmět: |
Male
medicine.medical_specialty Nitric Oxide Synthase Type III Endothelium Physiology Clinical Biochemistry Blood Pressure Vasodilation Nitric Oxide Nitric oxide Calcium Channels T-Type Mice chemistry.chemical_compound Enos Physiology (medical) Internal medicine Animals Medicine Mesenteric arteries biology Voltage-dependent calcium channel business.industry biology.organism_classification Mesenteric Arteries Mice Inbred C57BL Endocrinology medicine.anatomical_structure Blood pressure chemistry Anesthesia Female medicine.symptom business Vasoconstriction |
| Zdroj: | Svenningsen, P, Andersen, K, Thuesen, A D, Shin, H-S, Vanhoutte, P M, Skøtt, O, Jensen, B L, Hill, C & Hansen, P B L 2014, ' T-type Ca(2+) channels facilitate NO-formation, vasodilatation and NO-mediated modulation of blood pressure ', Pflügers Archiv-European Journal of Physiology, vol. 466, no. 12, pp. 2205-2214 . https://doi.org/10.1007/s00424-014-1492-4 |
| ISSN: | 1432-2013 0031-6768 |
| DOI: | 10.1007/s00424-014-1492-4 |
| Popis: | Voltage-gated calcium channels are involved in the vascular excitation-contraction mechanism and regulation of arterial blood pressure. It was hypothesized that T-type channels promote formation of nitric oxide from the endothelium. The present experiments determine the involvement of T-type channels in depolarization-dependent dilatation of mesenteric arteries and blood pressure regulation in Cav3.1 knock-out mice. Nitric oxide-dependent vasodilatation following depolarization-mediated vasoconstriction was reduced significantly in mesenteric arteries from Cav3.1(-/-) compared to wild type mice. Four days of systemic infusion of a nitric oxide (NO)-synthase-inhibitor to conscious wild type elicited a significant increase in mean arterial blood pressure that was absent in Cav3.1(-/-) mice. Immunoprecipitation and immunofluorescence labeling showed co-localization of Cav3.1 and endothelial nitric oxide synthase (eNOS) in arteries from wild type mice. Nitric oxide release measured as DAF fluorescence and cGMP levels were significantly lower in depolarized Cav3.1(-/-) compared to wild type arteries. In summary, the absence of T-type Cav3.1 channels attenuates NO-dependent dilatation in mesenteric arteries in vitro, as well as the hypertension after L-NAME infusion in vivo. Furthermore, Cav3.1 channels cluster with eNOS and promote formation of nitric oxide by the endothelium. The present findings suggest that this mechanism is important for the systemic impact of NO on peripheral resistance. |
| Databáze: | OpenAIRE |
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