PMID: 8584500Aug 1, 1995Paper

Furosemide elicits immediate sympathoexcitation via a renal mechanism independent of angiotensin II

Pharmacology & Toxicology
J S Petersen, G F DiBona

Abstract

This investigation aimed at examing the hypothesis that furosemide elicits renal sympathoexcitation through stimulation of renal renin release, which in turn produces increased plasma angiotensin II levels, causing centrally mediated sympathoexcitation. In addition, direct central nervous actions of furosemide on central control of mean arterial pressure, heart rate, and efferent renal sympathetic nerve activity were examined. Furosemide (300 mg/kg intravenously) was administered to four groups of rats: (1) control; (2) nephrectomized; (3) with intravenous losartan blockade (10 mumol/kg); and (4) with intracerebroventricular losartan blockade (10 nmol). In a fifth group of rats, furosemide was administered intracerebroventricularly (0, 2.5, 25 or 250 micrograms). To eliminate reflex control of mean arterial pressure, heart rate and efferent renal sympathetic nerve activity, all experiments were performed in rats with sinoaortic denervation and bilateral vagotomy. Experiments were performed during Saffan anaesthesia (0.9% alphaxalone/0.3% alphadolone), and rats were paralyzed with pancuronium and artifically ventilated. Furosemide produced an immediate 40% increase in efferent renal sympathetic nerve activity while the furosemid...Continue Reading

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Citations

May 18, 1999·Pharmacology & Toxicology·J S Petersen
Jan 11, 2003·American Journal of Physiology. Heart and Circulatory Physiology·Maria Maliszewska-ScisloNoreen F Rossi
Feb 26, 2016·American Journal of Physiology. Renal Physiology·Xiaohua HuangBranko Braam
Apr 8, 1998·The American Journal of Physiology·M Sanchez-PalaciosG F DiBona
Apr 13, 2004·American Journal of Physiology. Renal Physiology·Hayo CastropJurgen Schnermann
Aug 13, 1999·The American Journal of Physiology·M D VoigtG F DiBona

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