Blunting of renal excretory responses to acute volume expansion by nicotine: Role of renal nerves

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During smoking, an activated sympathetic nervous system can produce a variety of adverse effects on the cardiovascular system. There is evidence of increased renal nerve activation during smoking; however, whether the increased renal nerve activation in smokers translates into sodium retention by the kidney remains to be determined. In the present study, we examined the effect of nicotine on the renal nerve-mediated handling of sodium by the kidney during an acute volume expansion (VE) with isotonic saline (0.25% of body weight per minute for 30 or 40 min). Urine flow and sodium excretion from intact and denervated kidneys were measured before and during an acute graded VE in anesthetized control and nicotine-treated rats (2 μg/kg/min for 10 min before and 20 min during VE, respectively). In rats treated with nicotine, VE produced a significantly blunted diuresis (33% of control by 7.5% VE) and natriuresis (36% of control by 7.5% VE) from the intact kidneys compared with control rats. Glomerular filtration rate was not significantly different between the two groups, indicating that hemodynamic changes per se were not responsible for the altered volume reflex in rats infused with nicotine. However, renal denervation abolished the difference between the control and nicotine-treated rats in diuresis and natriuresis in response to VE. In addition, the decrease in renal nerve activity (renal sympathoinhibition) in response to acute VE was significantly blunted (53% of control by 5% VE) in rats treated with nicotine compared with the control rats. Because smoking leads to chronic elevation of nicotine, we simulated a chronic elevation of nicotine by administering nicotine (2 mg/kg/day) for 1 week. Acute graded VE also produced a significantly blunted renal sympathoinhibition (30% of control by 10% VE), diuresis (48% of control by 7.5% VE) and natriuresis (54% of control by 7.5% VE) in rats chronically treated with nicotine compared with control rats. These results suggest that the impaired ability to excrete an acute isotonic saline load in the presence of nicotine is in part dependent on basal efferent renal sympathetic nerve activity that fails to suppress normally in response to the isotonic saline load.

Original languageEnglish (US)
Pages (from-to)1174-1181
Number of pages8
JournalJournal of Pharmacology and Experimental Therapeutics
Issue number3
Publication statusPublished - Jan 1 1995


ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology

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