Influence of heart failure and sodium content in the diet on the natriuretic response to furosemide in hamsters
Lambert, C.; Larose, P.; Ong, H.; Gutkowska, J.; du Souich, P.
Research Communications in Chemical Pathology and Pharmacology 50(2): 181-199
1985
ISSN/ISBN: 0034-5164 PMID: 3909271 Document Number: 267319
The aims of this study were to investigate the influence of heart failure and dietary sodium content on the natriuretic effect of furosemide. Ten healthy Golden Syrian hamsters (HH) and 10 hamsters with a cardiomyopathy (CMH) were maintained on a normal sodium diet (NSD) and an equal number of animals on sodium deficient diet (SDD) for a minimum of 40 days. Three experiments were conducted on days 1, 20 and 40. Each experiment started with a 24-hour urine collection (control), followed by the administration of 5 mg/kg of furosemide i.p. and a second 24-hour urine collection and finally, the administration of 2 mg/kg of indomethacin i.p. followed 30 minutes later by 5 mg/kg of furosemide and a 24-hour urine collection as well as blood sampling. Sodium, creatinine, furosemide and arginine vasopressin (AVP) were measured in the urine and sodium, creatinine and AVP in plasma. After 134 days on a SDD, four HH resumed a NSD and the response to furosemide was again assessed after 12 days. Our results indicate that the natriuretic response to furosemide is higher in CMH than in HH. The SDD tended to increase the response to furosemide in HH as well as in CMH. Indomethacin did not influence the response to furosemide under any experimental condition. In four HH the increment in the fractional excretion of sodium in response to furosemide was 0.88 +/- 0.21% after 134 days on SDD and decreased to 0.35 +/- 0.12 (p less than 0.05) after 12 days on NSD. In all cases urinary excretion of furosemide was similar. Plasma AVP was higher in CMH and was not influenced by the SDD. In conclusion, SDD as well as cardiomyopathy with congestive heart failure do not decrease the natriuretic effect of furosemide and may not be a cause in the variability of the natriuretic response to furosemide.