| Literature DB >> 3302211 |
Abstract
The role of prostaglandins in the mechanism of the tubuloglomerular feed-back was examined in the anaesthetized dog using the infusion of hypertonic saline to increase renal plasma sodium concentration by 30 mmol/l as the stimulus to activate the tubuloglomerular feed-back. Two sequential infusions of hypertonic saline into the renal artery for 10 min separated by 90 min resulted in equivalent reductions in renal blood flow (264 +/- 32 to 174 +/- 20 ml/min first time; 280 +/- 29 to 200 +/- 15 ml/min second time). Administration of indomethacin, 8 mg/kg, between the two infusions did not alter the renovascular response to hypertonic saline (319 +/- 26 to 226 +/- 35 ml/min vs. 288 +/- 32 to 202 +/- 24 ml/min). Infusion of either prostaglandin E2 (PGE2) or prostaglandin I2 (PGI2) during the second hypertonic saline infusion period also resulted in no change in the renovascular response (251 +/- 37 to 141 +/- 31 ml/min vs. 297 +/- 53 to 184 +/- 51 ml/min; and 223 +/- 31 to 162 +/- 35 ml/min vs. 254 +/- 33 to 186 +/- 39 ml/min, respectively). Intrarenal theophylline, to a concentration of 40 micrograms/ml, however, totally abolished the renovascular response to hypertonic saline (279 +/- 20 to 209 +/- 13 ml/min control vs. 390 +/- 26 to 402 +/- 17 ml/min during theophylline). The systemic hypertensive response during the infusion of hypertonic saline was unaltered by indomethacin or prostaglandins but was totally abolished by theophylline.(ABSTRACT TRUNCATED AT 250 WORDS)Entities:
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Year: 1986 PMID: 3302211 PMCID: PMC1182922 DOI: 10.1113/jphysiol.1986.sp016270
Source DB: PubMed Journal: J Physiol ISSN: 0022-3751 Impact factor: 5.182