scholarly journals Engaging Undergraduates in Mechanisms of Tubular Reabsorption and Secretion in the Mammalian Kidney.

CourseSource ◽  
2021 ◽  
Vol 8 ◽  
Author(s):  
Kristen A. Roosa
Keyword(s):  
Tubular Reabsorption ◽  
Mammalian Kidney

Renal effects of nitric oxide synthesis inhibition in cirrhotic rats

1994 ◽  
Vol 267 (6) ◽  
pp. R1454-R1460 ◽  
Author(s):  
N. M. Atucha ◽  
J. Garcia-Estan ◽  
A. Ramirez ◽  
M. C. Perez ◽  
T. Quesada ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Renal Excretion ◽  
Renal Plasma Flow ◽  
Tubular Reabsorption ◽  
Nitric Oxide Synthesis ◽  
Important Mediator ◽  
Experimental Liver Cirrhosis ◽  
Endogenous Nitric Oxide ◽  
And Control ◽  
Experimental Liver

In the present study, we have characterized the renal response to inhibition of endogenous nitric oxide (NO) synthesis [intravenous NG-nitro-L-arginine methyl ester (L-NAME) for 3 h] in anesthetized cirrhotic rats, with (ASC) and without (CIR) ascites, at doses that do not change blood pressure (BP). Administration of L-NAME induced opposite effects on water (UV) and sodium (UNaV) excretion in cirrhotic and control animals. Infusion of 1 microgram.kg-1.min-1 of L-NAME in CIR (n = 5) decreased renal plasma flow (RPF) at the end of the 3-h period, whereas UV, UNaV, and glomerular filtration rate (GFR) were unaltered. In contrast, infusion of L-NAME at 10 micrograms.kg-1.min-1 in six more CIR increased UV and UNaV significantly by the 1st h, without changes in BP or GFR, and these parameters remained elevated throughout the experiment. Infusion of 1 microgram.kg-1.min-1 in ASC (n = 6) did not change BP or GFR but significantly enhanced UV and UNaV after the 1st h. These effects were prevented by pretreatment with L-arginine (0.1 mg.kg-1.min-1) in another group of ASC infused with 1 microgram.kg-1.min-1 of L-NAME. These results indicate that, in ASC and CIR cirrhotic rats, inhibition of NO synthesis at nonpressor does improves renal excretion of sodium and water via a decrease in tubular reabsorption. NO is an important mediator of the renal excretory and hemodynamic alterations of experimental liver cirrhosis.

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