T-type Ca2+ channels facilitate NO-formation, vasodilatation and NO-mediated modulation of blood pressure
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- 作者：Per Svenningsen (1)
Kenneth Andersen (1)
Anne D. Thuesen (1)
Hee-Sup Shin (2)
Paul M. Vanhoutte (3)
Ole Sk?tt (1)
Boye L. Jensen (1)
Caryl Hill (4)
Pernille B. L. Hansen (1) - 关键词：Resistance ; Hypertension ; Depolarization ; L ; type
- 刊名：Pfl篓鹿gers Archiv - European Journal of Physiology
- 出版年：2014
- 出版时间：December 2014
- 年：2014
- 卷：466
- 期：12
- 页码：2205-2214
- 全文大小：633 KB
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Kenneth Andersen (1)
Anne D. Thuesen (1)
Hee-Sup Shin (2)
Paul M. Vanhoutte (3)
Ole Sk?tt (1)
Boye L. Jensen (1)
Caryl Hill (4)
Pernille B. L. Hansen (1)
1. Department of Cardiovascular and Renal Research, University of Southern Denmark, Winsl?wparken 21, 3, Odense, DK-5000, Denmark
2. Center for Cognition and Sociality, Institute for Basic Science, Seoul, South Korea
3. Department of Pharmacology and Pharmacy and State Key Laboratory for Pharmaceutical Biotechnology, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, China
4. John Curtin School of Medical Research, Australian National University, Canberra, ACT, Australia - ISSN：1432-2013
文摘
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??/sup> 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??/sup> 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??/sup> 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.