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Nitric oxide synthase blockade and body fluid volumes
A M Balaszczuk1, A Tomat, S Bellucci
1Departamento de Fisiología, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina. abalasz@huemul.ffyb.uba.ar
Summary
Chronic inhibition of nitric oxide synthase with N G-nitro-L-arginine methyl ester (L-NAME) in rats significantly altered body fluid distribution. L-NAME treatment led to increased extracellular and interstitial spaces, but decreased plasma and blood volumes, alongside increased renal mass.
Area of Science:
- Physiology
- Pharmacology
- Nephrology
Background:
- Nitric oxide synthase (NOS) inhibition is a model for studying hypertension.
- Understanding body fluid shifts is crucial in hypertensive states.
Purpose of the Study:
- To investigate the effects of chronic N G-nitro-L-arginine methyl ester (L-NAME) administration on body fluid distribution in rats.
- To assess changes in extracellular, interstitial, intracellular, plasma, and blood volumes under L-NAME-induced hypertension.
Main Methods:
- Male Wistar rats were treated with L-NAME (approx. 70 mg/kg/24h in drinking water) for three weeks.
- Measurements included extracellular, interstitial, intracellular spaces, plasma volume, and blood volume.
- Kidney and heart weights relative to body weight were analyzed.
Main Results:
- L-NAME treatment significantly increased extracellular space (16.1 vs 13.7 ml/100g) and interstitial space (14.0 vs 9.7 ml/100g).
- Plasma volume (2.8 vs 3.6 ml/100g) and blood volume (5.2 vs 7.2 ml/100g) were significantly reduced in L-NAME-treated rats.
- An increased kidney weight to body weight ratio was observed, suggesting increased renal mass without changes in cardiac mass.
Conclusions:
- Chronic L-NAME-induced hypertension causes significant alterations in body fluid distribution.
- The study indicates an increase in renal mass associated with this model of experimental hypertension.
- Cardiac mass remained unchanged despite elevated blood pressure, suggesting specific adaptations or lack of long-term cardiac remodeling in this timeframe.