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: 3122
Function: getPubMedXML
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
We examined the effects of acute indomethacin administration on the disposition of a potassium load in anesthetized rats. In response to the potassium load, indomethacin-treated animals had greater plasma potassium concentrations and smaller increases in fractional excretion of potassium than did vehicle-treated rats, but there was no change in urine flow rate. Findings were consistent with indomethacin-induced impairment of renal potassium excretion. The effects of indomethacin in adrenalectomized animals were comparable to those that were observed in intact rats, which indicates that inhibition of aldosterone release was not responsible for the acute effects of indomethacin. No differences in plasma potassium were noted after indomethacin or vehicle infusion in the animals that underwent bilateral ureteral ligation, which suggests that indomethacin did not impair extrarenal potassium disposition. These results indicate that acute administration of indomethacin impairs the response to a potassium load, not as a result of inhibition of aldosterone secretion or extrarenal potassium distribution but by means of inhibition of renal potassium excretion.
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