Blunting of renal excretory responses to acute volume expansion by nicotine

Role of renal nerves

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12 Citations (Scopus)

Abstract

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
Volume274
Issue number3
StatePublished - Jan 1 1995

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Nicotine
Kidney
Natriuresis
Diuresis
Smoking
Sodium
Aptitude
Sympathetic Nervous System
Denervation
Cardiovascular System
Glomerular Filtration Rate
Reflex
Hemodynamics
Body Weight
Urine

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology

Cite this

@article{a58aa9c03ed4444f8ff76b4b52ee0dd9,
title = "Blunting of renal excretory responses to acute volume expansion by nicotine: Role of renal nerves",
abstract = "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.",
author = "Patel, {Kaushik P} and Zhang, {P. L.} and William Mayhan",
year = "1995",
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T1 - Blunting of renal excretory responses to acute volume expansion by nicotine

T2 - Role of renal nerves

AU - Patel, Kaushik P

AU - Zhang, P. L.

AU - Mayhan, William

PY - 1995/1/1

Y1 - 1995/1/1

N2 - 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.

AB - 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.

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