Literature DB >> 12640252

High-salt-induced increase in blood pressure: role of capsaicin-sensitive sensory nerves.

Jianping Li1, Donna H Wang.   

Abstract

OBJECTIVE: To test the hypothesis that sensory afferents are significant functional components in preventing salt-induced increases in blood pressure. DESIGN AND METHODS: Neonatal Wistar rats were subcutaneously injected with 50 mg/kg capsaicin or vehicle on the first and second days of life. After weaning, male rats were divided into three groups and treated for 4 weeks with: control plus normal (0.5%, CON-NS) or high (4%, CON-HS) sodium diet, and capsaicin pretreatment plus HS diet (CAP-HS). Mean arterial pressure (MAP) and its response to bolus injection of calcitonin gene-related peptide (CGRP) and its antagonist, CGRP(8-37), were measured by carotid arterial catheterization. Radioimmunoassay was used to measure CGRP levels in plasma and dorsal root ganglia (DRG). Expression of components of the CGRP receptor, calcitonin receptor-like receptor (CRLR) and receptor activity modifying protein 1 (RAMP1), was determined by the use of Western blot analysis.
RESULTS: Baseline MAP was increased in CAP-HS compared with CON-HS and CON-NS rats, and it was higher in CON-HS than in CON-NS rats. MAP response to exogenous CGRP was enhanced in CAP-HS and CON-HS than in CON-NS rats, but MAP response to CGRP(8-37) was increased only in CON-HS rats. Plasma CGRP levels were not different among three groups, but CGRP content in DRG was decreased in CAP-HS compared with CON-HS and CON-NS rats. CRLR expression in mesenteric resistance arteries was upregulated in CAP-HS and CON-HS compared with CON-NS rats, but RAMP1 content was not different among these groups.
CONCLUSION: Chronic high-salt intake upregulates expression of mesenteric CGRP receptors without altering CGRP levels in plasma and DRG. Increased expression of mesenteric CGRP receptors may play a counter regulatory role in attenuating salt-induced increases in blood pressure.

Entities:  

Mesh:

Substances:

Year:  2003        PMID: 12640252     DOI: 10.1097/00004872-200303000-00024

Source DB:  PubMed          Journal:  J Hypertens        ISSN: 0263-6352            Impact factor:   4.844


  6 in total

1.  TRPV1 attenuates intracranial arteriole remodeling through inhibiting VSMC phenotypic modulation in hypertension.

Authors:  Ming-Jie Zhang; Yun Liu; Zi-Cheng Hu; Yi Zhou; Yan Pi; Lu Guo; Xu Wang; Xue Chen; Jing-Cheng Li; Li-Li Zhang
Journal:  Histochem Cell Biol       Date:  2016-10-24       Impact factor: 4.304

2.  Activation of TRPV1 by dietary capsaicin improves endothelium-dependent vasorelaxation and prevents hypertension.

Authors:  Dachun Yang; Zhidan Luo; Shuangtao Ma; Wing Tak Wong; Liqun Ma; Jian Zhong; Hongbo He; Zhigang Zhao; Tingbing Cao; Zhencheng Yan; Daoyan Liu; William J Arendshorst; Yu Huang; Martin Tepel; Zhiming Zhu
Journal:  Cell Metab       Date:  2010-08-04       Impact factor: 27.287

3.  Enhanced salt sensitivity following shRNA silencing of neuronal TRPV1 in rat spinal cord.

Authors:  Shuang-quan Yu; Donna H Wang
Journal:  Acta Pharmacol Sin       Date:  2011-06       Impact factor: 6.150

Review 4.  TRP channels and their implications in metabolic diseases.

Authors:  Zhiming Zhu; Zhidan Luo; Shuangtao Ma; Daoyan Liu
Journal:  Pflugers Arch       Date:  2010-11-26       Impact factor: 3.657

5.  Perirenal adipose afferent nerves sustain pathological high blood pressure in rats.

Authors:  Peng Li; Boxun Liu; Xiaoguang Wu; Yan Lu; Ming Qiu; Yihui Shen; Yunfan Tian; Chi Liu; Xiru Chen; Chuanxi Yang; Mengqing Deng; Yaqing Wang; Jia Gu; Zhongping Su; Xuguan Chen; Kun Zhao; Yanhui Sheng; Shijiang Zhang; Wei Sun; Xiangqing Kong
Journal:  Nat Commun       Date:  2022-06-06       Impact factor: 17.694

Review 6.  Transient receptor potential vanilloid channels in hypertension, inflammation, and end organ damage: an imminent target of therapy for cardiovascular disease?

Authors:  Donna H Wang
Journal:  Curr Opin Cardiol       Date:  2008-07       Impact factor: 2.161

  6 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.