Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 1034
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3152
Function: GetPubMedArticleOutput_2016
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
Hypertension (HTN) is a chronic disease that affects more than 972 million people throughout the world, which is usually associated with endothelial dysfunction. Scientists are closely investigating endothelial dysfunction and have recently discovered the endothelium-derived relaxing factor (EDRF) known as NO (nitric oxide), which is derived from a semi-essential amino acid, L-arginine, by the action of endothelial nitric oxide synthase (eNOS). Production of adequate amounts of NO by vascular endothelial cells is essential to maintain normal blood pressure and prevent the development of HTN. Asymmetrical dimethylarginine (ADMA) is an endogenous NOS inhibitor that is increased in those with HTN especially in patients with renal dysfunction. In the present review, the role of L-arginine, arginine transporters, and ADMA in the pathobiology of HTN and their potential clinical significance are discussed.
Download full-text PDF |
Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8761475 | PMC |
http://dx.doi.org/10.7759/cureus.20485 | DOI Listing |
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