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The effect of lidocain on the renal function.

G Kövér1, R Herceg, H Tost

  • 1Department of Physiology, Semmelweis University, Medical School, Budapest, Hungary.

Acta Physiologica Hungarica
|January 1, 1990
PubMed
Summary

Direct neurogenic control of kidney function was studied. Lidocaine infusion into one renal artery reduced blood flow and excretion, suggesting intrarenal hemodynamic changes, not direct nerve control, are key.

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Area of Science:

  • Nephrology
  • Physiology
  • Neuroscience

Background:

  • The role of direct neurogenic control in regulating renal function is debated.
  • Sympathetic nervous system activity influences kidney function, but the precise mechanisms are not fully understood.

Purpose of the Study:

  • To investigate the evidence for direct neurogenic control of renal function.
  • To determine the effects of unilateral renal denervation on kidney function in anesthetized dogs.

Main Methods:

  • Twenty anesthetized dogs underwent unilateral renal denervation using lidocaine infusion into the left renal artery.
  • Kidney function parameters, including renal blood flow (RBF), glomerular filtration rate (GFR), urine, and sodium excretion, were compared between the infused (left) and non-infused (right) kidneys.
  • Arterial blood pressure was monitored throughout the experiment.

Main Results:

  • Lidocaine infusion significantly reduced RBF, GFR, urine, and sodium excretion in the left kidney compared to the right.
  • A small decrease in arterial blood pressure was observed but could not account for the observed renal function changes.
  • Comparison of measured RBF and calculated RBF (using CPAH) indicated greater decreases in calculated RBF, suggesting intrarenal hemodynamic alterations.

Conclusions:

  • Pharmacological denervation effects are best explained by intrarenal hemodynamically mediated changes.
  • Sympathectomy causes renal cortical vasoconstriction, decreasing RBF, GFR, and excretion.
  • Lidocaine's blockade of sympathetic nerves to medullary vessels increases medullary blood flow, challenging the notion that renal nerves are solely responsible for salt-loading natriuresis.

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