TY - JOUR
T1 - Effects of dopamine and nitric oxide on arterial pressure and renal function in volume expansion
AU - Costa, M. A.
AU - Loria, A.
AU - Marchetti, M.
AU - Balaszczuk, A. M.
AU - Arranz, C. T.
PY - 2002
Y1 - 2002
N2 - 1. The aim of the present study was to investigate the role of dopamine (DA) in the hypotensive and renal effects of L-arginine during extracellular fluid volume expansion (10% bodyweight). 2. Animals were randomized to non-expanded and expanded groups. Both groups received different treatments: L-arginine (250 mg/kg, i.v.), NG-nitro-L-arginine methyl ester (L-NAME; 1 mg/kg, i.v.), haloperidol (3 mg/kg, i.p.) and L-arginine + haloperidol (n = 8). Mean arterial pressure (MAP), diuresis, natriuresis, kaliuresis, glomerular filtration rate, renal plasma flow (RPF) and nitrite and nitrate (NOx) excretion were determined. 3. The increase in MAP induced by L-NAME was greater in expanded than in non-expanded rats (42 ± 3 vs 32 ± 3 mmHg, respectively; P < 0.01). Administration of haloperidol did not modify the L-arginine hypotensive effect. 4. Blockade of nitric oxide synthase diminished urine flow in non-expanded (4.15 ± 0.56 vs 0.55 ± 0.11 μL/min per 100 g; P < 0.01) and expanded animals (24.42 ± 3.67 vs 17.85 ± 2.16 μL/min per 100 g;P < 0.01). Diuresis induced by L-arginine was reduced by DA blockade in both non-expanded (17.15 ± 2.11 vs 6.82 ± 0.61 μL/min per 100 g; P < 0.01) and expanded animals (44.26 ± 8.45 vs 25.43 ± 5.12 μL/min per 100 g;P < 0.01). 5. Sodium excretion decreased with L-NAME treatment in non-expanded (0.22 ± 0.03 vs 0.06 ± 0.01 μEq/min per 100 g; P < 0.01) and expanded animals (3.72 ± 0.70 vs 1.89 ± 0.23 μEq/min per 100 g;P < 0.01). Natriuresis induced by L-arginine was diminished by haloperidol both in non-expanded (0.94 ± 0.13 vs 0.43 ± 0.04 μEq/min per 100 g; P < 0.01) and expanded rats (12.77 ± 0.05 vs 3.53 ± 0.75 μEq/min per 100 g; P < 0.01). Changes in kaliuresis changes seen following treatment with L-arginine, L-NAME and L-arginine + haloperidol followed a pattern similar to that observed for sodium excretion in both groups of rats. 6. L-Arginine enhanced RPF in non-expanded animals (11.96 ± 0.81 vs 14.52 ± 1.05 mL/min per 100 g; P < 0.01). Glomerular filtration rate was increased by extracellular volume expansion (3.08 ± 0.28 vs 5.42 ± 0.46 mL/min per 100 g;P < 0.01). 7. The increase in NOx induced by acute volume expansion (0.18 ± 0.03 vs 0.52 < 0.08 nmol/min per 100 g; P < 0.01) was diminished following the administration of haloperidol (0.52 ± 0.08 vs 0.26 ± 0.06 nmol/min per 100 g;P < 0.01). 8. Although DA does not participate in the actions of nitric oxide on vascular tone, both systems would play an important role in renal function adaptation during extracellular fluid volume expansion.
AB - 1. The aim of the present study was to investigate the role of dopamine (DA) in the hypotensive and renal effects of L-arginine during extracellular fluid volume expansion (10% bodyweight). 2. Animals were randomized to non-expanded and expanded groups. Both groups received different treatments: L-arginine (250 mg/kg, i.v.), NG-nitro-L-arginine methyl ester (L-NAME; 1 mg/kg, i.v.), haloperidol (3 mg/kg, i.p.) and L-arginine + haloperidol (n = 8). Mean arterial pressure (MAP), diuresis, natriuresis, kaliuresis, glomerular filtration rate, renal plasma flow (RPF) and nitrite and nitrate (NOx) excretion were determined. 3. The increase in MAP induced by L-NAME was greater in expanded than in non-expanded rats (42 ± 3 vs 32 ± 3 mmHg, respectively; P < 0.01). Administration of haloperidol did not modify the L-arginine hypotensive effect. 4. Blockade of nitric oxide synthase diminished urine flow in non-expanded (4.15 ± 0.56 vs 0.55 ± 0.11 μL/min per 100 g; P < 0.01) and expanded animals (24.42 ± 3.67 vs 17.85 ± 2.16 μL/min per 100 g;P < 0.01). Diuresis induced by L-arginine was reduced by DA blockade in both non-expanded (17.15 ± 2.11 vs 6.82 ± 0.61 μL/min per 100 g; P < 0.01) and expanded animals (44.26 ± 8.45 vs 25.43 ± 5.12 μL/min per 100 g;P < 0.01). 5. Sodium excretion decreased with L-NAME treatment in non-expanded (0.22 ± 0.03 vs 0.06 ± 0.01 μEq/min per 100 g; P < 0.01) and expanded animals (3.72 ± 0.70 vs 1.89 ± 0.23 μEq/min per 100 g;P < 0.01). Natriuresis induced by L-arginine was diminished by haloperidol both in non-expanded (0.94 ± 0.13 vs 0.43 ± 0.04 μEq/min per 100 g; P < 0.01) and expanded rats (12.77 ± 0.05 vs 3.53 ± 0.75 μEq/min per 100 g; P < 0.01). Changes in kaliuresis changes seen following treatment with L-arginine, L-NAME and L-arginine + haloperidol followed a pattern similar to that observed for sodium excretion in both groups of rats. 6. L-Arginine enhanced RPF in non-expanded animals (11.96 ± 0.81 vs 14.52 ± 1.05 mL/min per 100 g; P < 0.01). Glomerular filtration rate was increased by extracellular volume expansion (3.08 ± 0.28 vs 5.42 ± 0.46 mL/min per 100 g;P < 0.01). 7. The increase in NOx induced by acute volume expansion (0.18 ± 0.03 vs 0.52 < 0.08 nmol/min per 100 g; P < 0.01) was diminished following the administration of haloperidol (0.52 ± 0.08 vs 0.26 ± 0.06 nmol/min per 100 g;P < 0.01). 8. Although DA does not participate in the actions of nitric oxide on vascular tone, both systems would play an important role in renal function adaptation during extracellular fluid volume expansion.
KW - Arterial blood pressure
KW - Dopamine
KW - Extracellular volume expansion
KW - L-arginine
KW - Nitric oxide
KW - Rat
KW - Renal function
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U2 - 10.1046/j.1440-1681.2002.03729.x
DO - 10.1046/j.1440-1681.2002.03729.x
M3 - Article
C2 - 12165040
AN - SCOPUS:0036381050
SN - 0305-1870
VL - 29
SP - 772
EP - 776
JO - Clinical and Experimental Pharmacology and Physiology
JF - Clinical and Experimental Pharmacology and Physiology
IS - 9
ER -