T-type Ca2+ channels facilitate NO-formation, vasodilatation and NO-mediated modulation of blood pressure

Cited 15 time in webofscience Cited 0 time in scopus
1,427 Viewed 89 Downloaded
Title
T-type Ca2+ channels facilitate NO-formation, vasodilatation and NO-mediated modulation of blood pressure
Author(s)
Per Svenningsen; Kenneth Andersen; Anne D. Thuesen; Hee Sup Shin; Paul M. Vanhoutte; Ole Skøtt; Boye L. Jensen; Caryl Hill; Pernille B. L. Hansen
Publication Date
2014-12
Journal
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, v.466, no.12, pp.2205 - 2214
Publisher
SPRINGER
Abstract
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 towild 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.
URI
https://pr.ibs.re.kr/handle/8788114/749
ISSN
0031-6768
Appears in Collections:
Center for Cognition and Sociality(인지 및 사회성 연구단) > Journal Papers (저널논문)
Files in This Item:
164_Pflugers Arch_T-type Ca2+ channels facilitate NO.pdfDownload

qrcode

  • facebook

    twitter

  • Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.
해당 아이템을 이메일로 공유하기 원하시면 인증을 거치시기 바랍니다.

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse