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 language | English (US) |
|---|---|
| Journal | American Journal of Physiology - Regulatory Integrative and Comparative Physiology |
| Volume | 280 |
| Issue number | 1 49-1 |
| State | Published - Jan 2001 |
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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
Hemodynamic and renal effects of acute and progressive nitric oxide synthesis inhibition in anesthetized dogs. / Cases, Aleix; Haas, John; Burnett, John C Jr.; Romero, Juan Carlos.
In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 280, No. 1 49-1, 01.2001.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Hemodynamic and renal effects of acute and progressive nitric oxide synthesis inhibition in anesthetized dogs
AU - Cases, Aleix
AU - Haas, John
AU - Burnett, John C Jr.
AU - Romero, Juan Carlos
PY - 2001/1
Y1 - 2001/1
N2 - 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.
AB - 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.
KW - N-nitro-L-arginine methyl ester
KW - Regional blood flows
KW - Renal function
KW - Systemic hemodynamics
KW - Urinary sodium excretion
UR - http://www.scopus.com/inward/record.url?scp=0035013901&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0035013901&partnerID=8YFLogxK
M3 - Article
C2 - 11124145
AN - SCOPUS:0035013901
VL - 280
JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology
JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology
SN - 1931-857X
IS - 1 49-1
ER -