Nitric oxide reduces paracellular resistance in rat thick ascending limbs by increasing Na+ and Cl- permeabilities

About 50% of the Na+ reabsorbed in thick ascending limbs traverses the paracellular pathway. Nitric oxide (NO) reduces the permselectivity of this pathway via cGMP, but its effects on absolute Na+ (PNa +) and Cl- (PCl -) permeabilities are unknown. To address this, we measured the effect of L-argini...

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Detalles Bibliográficos
Autores principales: Monzon, C.M., Occhipinti, R., Pignataro, O.P., Garvin, J.L.
Formato: JOUR
Materias:
Kidney
Nitric oxide
Paracellular permeability
Sodium transport
chloride
nitric oxide
sodium
arginine
cyclic GMP
enzyme inhibitor
n(g) nitroarginine methyl ester
nitric oxide synthase
animal experiment
Article
cell membrane permeability
conductance
controlled study
electric potential
limb
male
Michaelis Menten kinetics
nonhuman
osmolality
priority journal
rat
steady state
transcytosis
transepithelial resistance
velocity
animal
antagonists and inhibitors
biological model
drug effects
Henle loop
impedance
in vitro study
kidney tubule absorption
metabolism
perfusion
permeability
Sprague Dawley rat
transport at the cellular level
Animals
Arginine
Biological Transport
Chlorides
Cyclic GMP
Electric Impedance
Enzyme Inhibitors
In Vitro Techniques
Loop of Henle
Male
Models, Biological
NG-Nitroarginine Methyl Ester
Nitric Oxide
Nitric Oxide Synthase
Perfusion
Permeability
Rats, Sprague-Dawley
Renal Reabsorption
Sodium
Acceso en línea:http://hdl.handle.net/20.500.12110/paper_03636127_v312_n6_pF1035_Monzon
Aporte de:
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires
Descripción
Sumario:About 50% of the Na+ reabsorbed in thick ascending limbs traverses the paracellular pathway. Nitric oxide (NO) reduces the permselectivity of this pathway via cGMP, but its effects on absolute Na+ (PNa +) and Cl- (PCl -) permeabilities are unknown. To address this, we measured the effect of L-arginine (0.5 mmol/l; NO synthase substrate) and cGMP (0.5 mmol/l) on PNa + and PCl - calculated from the transepithelial resistance (Rt) and PNa +/PCl - in medullary thick ascending limbs. Rt was 7,722 ± 1,554 ohm·cm in the control period and 6,318 ± 1,757 ohm·cm after L-arginine treatment (P < 0.05). PNa +/PCl - was 2.0 ± 0.2 in the control period and 1.7 ± 0.1 after L-arginine (P < 0.04). Calculated PNa + and PCl - were 3.52 ± 0.2 and 1.81 ± 0.10 × 10-5 cm/s, respectively, in the control period. After L-arginine they were 6.65 ± 0.69 (P < 0.0001 vs. control) and 3.97 ± 0.44 (P < 0.0001) × 10-5 cm/s, respectively. NOS inhibition with Nω-nitro-L-arginine methyl ester (5 mmol/l) prevented L-arginine’s effect on Rt. Next we tested the effect of cGMP. Rt in the control period was 7,592 ± 1,470 and 4,796 ± 847 ohm·cm after dibutyryl-cGMP (0.5 mmol/l; db-cGMP) treatment (P < 0.04). PNa +/PCl - was 1.8 ± 0.1 in the control period and 1.6 ± 0.1 after db-cGMP (P < 0.03). PNa + and PCl - were 4.58 ± 0.80 and 2.66 ± 0.57 × 10-5 cm/s, respectively, for the control period and 9.48 ± 1.63 (P < 0.007) and 6.01 ± 1.05 (P < 0.005) × 10-5 cm/s, respectively, after db-cGMP. We modeled NO’s effect on luminal Na+ concentration along the thick ascending limb. We found that NO’s effect on the paracellular pathway reduces net Na+ reabsorption and that the magnitude of this effect is similar to that due to NO’s inhibition of transcellular transport. © 2017 the American Physiological Society.

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