Hemodynamic and renal effects of acute and progressive nitric oxide synthesis inhibition in anesthetized dogs

Aleix Cases, John Haas, John C Jr. Burnett, Juan Carlos Romero

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12 Citations (Scopus)

Abstract

This study evaluated the effects of progressive nitric oxide (NO) inhibition in the regulation of systemic and regional hemodynamics and renal function in anesthetized dogs. The NG-nitro-L-arginine methyl ester group (n = 9) received progressive doses of 0.1, 1, 10, and 50 μg·kg-1·min-1. Renal (RBF), mesenteric (MBF), iliac (IBF) blood flows, mean arterial pressure (MAP), pulmonary pressures, cardiac output (CO), and systemic and pulmonary vascular resistances were measured. During NGnitro-L-arginine methyl ester infusion, MAP and systemic vascular resistances increased in a dose-dependent manner. Mean pulmonary pressure and pulmonary vascular resistances increased in both the NG-nitro-L-arginine methyl ester and the control group, but the increase was more marked in the NG-nitro-L-arginine methyl ester group during the last two infusion periods. CO decreased progressively, before any significant change in blood pressure was noticeable in the NG-nitro-L-arginine methyl ester group. IBF decreased nificantly from the first NG-nitro-L-arginine methyl ester dose, whereas RBF and MBF only decreased significantly during the highest NG-nitro-L-arginine methyl ester dose. Urinary volume and sodium excretion only increased significantly in the time control group during the two last time periods. The pulmonary vasculature was more sensitive than the systemic vasculature, whereas skeletal muscle and renal vasculatures showed a greater sensitivity to the inhibition of NO production than the mesenteric vasculature. NO synthesis inhibition induces a progressive antidiuretic and antinatriuretic effect, which is partially offset by the increase in blood pressure.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume280
Issue number1 49-1
StatePublished - Jan 2001

Fingerprint

NG-Nitroarginine Methyl Ester
Nitric Oxide
Hemodynamics
Dogs
Kidney
Vascular Resistance
Cardiac Output
Lung
Arterial Pressure
Antidiuretic Agents
Blood Pressure
Pressure
Control Groups
Skeletal Muscle
Sodium

Keywords

  • N-nitro-L-arginine methyl ester
  • Regional blood flows
  • Renal function
  • Systemic hemodynamics
  • Urinary sodium excretion

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

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abstract = "This study evaluated the effects of progressive nitric oxide (NO) inhibition in the regulation of systemic and regional hemodynamics and renal function in anesthetized dogs. The NG-nitro-L-arginine methyl ester group (n = 9) received progressive doses of 0.1, 1, 10, and 50 μg·kg-1·min-1. Renal (RBF), mesenteric (MBF), iliac (IBF) blood flows, mean arterial pressure (MAP), pulmonary pressures, cardiac output (CO), and systemic and pulmonary vascular resistances were measured. During NGnitro-L-arginine methyl ester infusion, MAP and systemic vascular resistances increased in a dose-dependent manner. Mean pulmonary pressure and pulmonary vascular resistances increased in both the NG-nitro-L-arginine methyl ester and the control group, but the increase was more marked in the NG-nitro-L-arginine methyl ester group during the last two infusion periods. CO decreased progressively, before any significant change in blood pressure was noticeable in the NG-nitro-L-arginine methyl ester group. IBF decreased nificantly from the first NG-nitro-L-arginine methyl ester dose, whereas RBF and MBF only decreased significantly during the highest NG-nitro-L-arginine methyl ester dose. Urinary volume and sodium excretion only increased significantly in the time control group during the two last time periods. The pulmonary vasculature was more sensitive than the systemic vasculature, whereas skeletal muscle and renal vasculatures showed a greater sensitivity to the inhibition of NO production than the mesenteric vasculature. NO synthesis inhibition induces a progressive antidiuretic and antinatriuretic effect, which is partially offset by the increase in blood pressure.",
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