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
The present study aimed to compare the basal brain polyamine levels and stress-induced brain polyamine level changes in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. For immobilization stress, both strains underwent acute (3 h per day immobilization for 2 days), chronic (3 h per day immobilization for 15 consecutive days), or no immobilization stress (control group). Basal putrescine (PU) levels in frontal cortex and hippocampus of SHR (11.03 +/- 0.81 and 11.36 +/- 0.33 nmol/g tissue, respectively) were significantly higher than WKY rats (6.90 +/- 1.44 and 7.82 +/- 0.71 nmol/g tissue, respectively). However, there were no strain differences in basal spermidine and spermine levels between the two. After acute stress, the PU levels in frontal cortex and hippocampus (15.99 +/- 0.45 and 14.10 +/- 0.95 nmol/g tissue, respectively) were significantly increased in SHR as compared to the non-stressed SHR (11.03 +/- 0.81 and 11.36 +/- 0.33 nmol/g tissue, respectively). In WKY rats, the PU level was significantly increased by acute stress in frontal cortex (11.68 +/- 1.12 nmol/g tissue) as compared to the non-stressed WKY (6.90 +/- 1.44 nmol/g tissue). After chronic stress, the PU levels in frontal cortex and hippocampus of SHR (12.44 +/- 0.54 and 11.34 +/- 0.66 nmol/g tissue, respectively) significantly decreased as compared to acute-stressed groups (15.99 +/- 0.45 and 14.01 +/- 0.95 nmol/g tissue, respectively). In WKY rats, after chronic stress, the PU level was significantly decreased in frontal cortex (5.73 +/- 0.36 nmol/g tissue) as compared to acute-stressed groups (11.68 +/- 1.12 nmol/g tissue). The PU levels in frontal cortex and hippocampus of acute-stressed (15.99 +/- 0.45 nmol/g tissue and 14.10 +/- 0.95 nmol/g tissue, respectively) and chronic-stressed (12.44 +/- 0.54 and 11.34 +/- 0.66 nmol/g tissue, respectively) SHR were significantly higher than acute-stressed (11.68 +/- 1.12 and 9.76 +/- 0.45 nmol/g tissue, respectively) and chronic-stressed (5.73 +/- 0.36 and 8.44 +/- 0.71 nmol/g tissue, respectively) WKY rats. The present study provides the higher basal PU level and stress-induced PU response in SHR as compared to WKY rats may be related to enhanced response of hypothalamic-pituitary-adrenocortical axis and sympathetic influence that may significantly contribute to the development of hypertension in SHR.
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http://dx.doi.org/10.1016/s0361-9230(01)00746-8 | DOI Listing |
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