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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Autor principal: Monzon, C.M
Otros Autores: Occhipinti, R., Pignataro, O.P, Garvin, J.L
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: American Physiological Society 2017
Acceso en línea:Registro en Scopus
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024 7 |2 cas  |a chloride, 16887-00-6; nitric oxide, 10102-43-9; sodium, 7440-23-5; arginine, 1119-34-2, 15595-35-4, 7004-12-8, 74-79-3; cyclic GMP, 7665-99-8; n(g) nitroarginine methyl ester, 50903-99-6; nitric oxide synthase, 125978-95-2; Arginine; Chlorides; Cyclic GMP; Enzyme Inhibitors; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitric Oxide Synthase; Sodium 
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100 1 |a Monzon, C.M. 
245 1 0 |a Nitric oxide reduces paracellular resistance in rat thick ascending limbs by increasing Na+ and Cl- permeabilities 
260 |b American Physiological Society  |c 2017 
270 1 0 |m Monzon, C.M.; Case Western Reserve University, Department of Physiology and Biophysics, Robbins E532, 10900 Euclid Ave., MS 4970, United States; email: casandra.monzon@case.edu 
506 |2 openaire  |e Política editorial 
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504 |a Monzon, C.M., Garvin, J.L., Nitric oxide decreases the permselectivity of the paracellular pathway in thick ascending limbs (2015) Hypertension, 65, pp. 1245-1250 
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520 3 |a 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.  |l eng 
536 |a Detalles de la financiación: National Institutes of Health, HL-070985, HL-028982, K01-DK-107787 
536 |a Detalles de la financiación: This work was in part supported by National Institutes of Health Grants HL-028982 and HL-070985 to J. L. Garvin and K01-DK-107787 to R. Occhipinti. 
593 |a Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, OH, United States 
593 |a Departamento de Química Biológica, Facultad de Ciencias Exactas Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina 
593 |a Laboratorio de Endocrinología Molecular y Transducción de Señales, Instituto de Biología y Medicina Experimental, Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina 
690 1 0 |a KIDNEY 
690 1 0 |a NITRIC OXIDE 
690 1 0 |a PARACELLULAR PERMEABILITY 
690 1 0 |a SODIUM TRANSPORT 
690 1 0 |a CHLORIDE 
690 1 0 |a NITRIC OXIDE 
690 1 0 |a SODIUM 
690 1 0 |a ARGININE 
690 1 0 |a CHLORIDE 
690 1 0 |a CYCLIC GMP 
690 1 0 |a ENZYME INHIBITOR 
690 1 0 |a N(G) NITROARGININE METHYL ESTER 
690 1 0 |a NITRIC OXIDE 
690 1 0 |a NITRIC OXIDE SYNTHASE 
690 1 0 |a SODIUM 
690 1 0 |a ANIMAL EXPERIMENT 
690 1 0 |a ARTICLE 
690 1 0 |a CELL MEMBRANE PERMEABILITY 
690 1 0 |a CONDUCTANCE 
690 1 0 |a CONTROLLED STUDY 
690 1 0 |a ELECTRIC POTENTIAL 
690 1 0 |a LIMB 
690 1 0 |a MALE 
690 1 0 |a MICHAELIS MENTEN KINETICS 
690 1 0 |a NONHUMAN 
690 1 0 |a OSMOLALITY 
690 1 0 |a PRIORITY JOURNAL 
690 1 0 |a RAT 
690 1 0 |a STEADY STATE 
690 1 0 |a TRANSCYTOSIS 
690 1 0 |a TRANSEPITHELIAL RESISTANCE 
690 1 0 |a VELOCITY 
690 1 0 |a ANIMAL 
690 1 0 |a ANTAGONISTS AND INHIBITORS 
690 1 0 |a BIOLOGICAL MODEL 
690 1 0 |a DRUG EFFECTS 
690 1 0 |a HENLE LOOP 
690 1 0 |a IMPEDANCE 
690 1 0 |a IN VITRO STUDY 
690 1 0 |a KIDNEY TUBULE ABSORPTION 
690 1 0 |a METABOLISM 
690 1 0 |a PERFUSION 
690 1 0 |a PERMEABILITY 
690 1 0 |a SPRAGUE DAWLEY RAT 
690 1 0 |a TRANSPORT AT THE CELLULAR LEVEL 
690 1 0 |a ANIMALS 
690 1 0 |a ARGININE 
690 1 0 |a BIOLOGICAL TRANSPORT 
690 1 0 |a CHLORIDES 
690 1 0 |a CYCLIC GMP 
690 1 0 |a ELECTRIC IMPEDANCE 
690 1 0 |a ENZYME INHIBITORS 
690 1 0 |a IN VITRO TECHNIQUES 
690 1 0 |a LOOP OF HENLE 
690 1 0 |a MALE 
690 1 0 |a MODELS, BIOLOGICAL 
690 1 0 |a NG-NITROARGININE METHYL ESTER 
690 1 0 |a NITRIC OXIDE 
690 1 0 |a NITRIC OXIDE SYNTHASE 
690 1 0 |a PERFUSION 
690 1 0 |a PERMEABILITY 
690 1 0 |a RATS, SPRAGUE-DAWLEY 
690 1 0 |a RENAL REABSORPTION 
690 1 0 |a SODIUM 
700 1 |a Occhipinti, R. 
700 1 |a Pignataro, O.P. 
700 1 |a Garvin, J.L. 
773 0 |d American Physiological Society, 2017  |g v. 312  |h pp. F1035-F1043  |k n. 6  |p Am. J. Physiol. Renal Physiol.  |x 03636127  |t American Journal of Physiology - Renal Physiology 
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