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Department of Physiology, Mayo Foundation, Rochester, Minnesota 55905
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
NG-nitro-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 significantly 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.
NG-nitro-L-arginine methyl ester; regional blood flows; systemic hemodynamics; renal function; urinary sodium excretion
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