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Titolo:
THE EFFECTS OF RESPIRATORY ALKALOSIS AND ACIDOSIS ON NET BICARBONATE FLUX ALONG THE RAT LOOP OF HENLE IN-VIVO
Autore:
UNWIN R; STIDWELL R; TAYLOR S; CAPASSO G;
Indirizzi:
UNIV COLL LONDON,SCH MED,MIDDLESEX HOSP,CTR NEPHROL,INST UROL & NEPHROL,DEPT MED,MORTIMER ST LONDON W1N 8AA ENGLAND UNIV COLL LONDON,SCH MED,CTR NEPHROL,DEPT MED LONDON W1N 8AA ENGLAND UNIV COLL LONDON,SCH MED,CTR NEPHROL,DEPT PHYSIOL LONDON W1N 8AA ENGLAND UNIV NAPLES 2,FAC MED,DEPT NEPHROL I-803131 NAPLES ITALY
Titolo Testata:
American journal of physiology. Renal, fluid and electrolyte physiology
fascicolo: 5, volume: 42, anno: 1997,
pagine: 698 - 705
SICI:
0363-6127(1997)42:5<698:TEORAA>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
THICK ASCENDING LIMB; PROXIMAL CONVOLUTED TUBULE; ACUTE METABOLIC ALKALOSIS; INTRACELLULAR PH; H+-SECRETION; TRANSPORT; REABSORPTION; DEPENDENCE; ACIDIFICATION; ABSORPTION;
Keywords:
LOOP OF HENLE; BICARBONATE TRANSPORT; RESPIRATORY ACIDOSIS; RESPIRATORY ALKALOSIS; PERMEABILITY; BACKFLUX;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
46
Recensione:
Indirizzi per estratti:
Citazione:
R. Unwin et al., "THE EFFECTS OF RESPIRATORY ALKALOSIS AND ACIDOSIS ON NET BICARBONATE FLUX ALONG THE RAT LOOP OF HENLE IN-VIVO", American journal of physiology. Renal, fluid and electrolyte physiology, 42(5), 1997, pp. 698-705

Abstract

We have studied the effects of acute respiratory alkalosis (ARALK, hyperventilation) and acidosis (ARA, 8% CO2), chronic respiratory acidosis (CRA; 10% CO2 for 7-10 days), and subsequent recovery from CRA breathing air on loop of Henle (LOH) net bicarbonate Aux (J(HCO3)) by in vivo tubule microperfusion in anesthetized rats. In ARALK blood, pH increased to 7.6, and blood bicarbonate concentration ([HCO3-]) decreasedfrom 29 to 22 mM. Fractional urinary bicarbonate excretion (FEHCO3) )increased threefold, but LOH J(HCO3) was unchanged. In ARA, blood pH fell to 7.2, and blood [HCO3-] rose from 28 to 34 mM; FEHCO3 was reduced to <0.1%, but LOH J(HCO3) was unaltered. In CRA, blood pH fell to 7.2, and blood [HCO3-] increased to >50 mM, whereas FEHCO3 decreased to <0.1% J(HCO3) was reduced by similar to 30%. Bicarbonaturia occurred when CRA rats breathed air, yet LOH J(HCO3) increased (by 30%) to normal. These results suggest that LOH J(HCO3) is affected by the blood-to-tubule lumen [HCO3-] gradient and HCO3- backflux. When the usual perfusing solution at 20 nl/min was made HCO3- free, mean J(HCO3) was -34.5+/- 4.4 pmol/min compared with 210 +/- 28.1 pmol/min plus HCO3-. Whena low-NaCl perfusate (to minimize net fluid absorption) containing mannitol and acetazolamide 12 x 10(-4) M, to abolish H+-dependent J(HCO3)) was used, J(HCO3) was -112.8 +/- 5.6 pmol/min. Comparable values for J(HCO3) at 10 nl/min were -35.9 +/- 5.8 and -72.5 +/- 8.8 HCO, pmol/min, respectively. These data indicate significant back-flux of HCO3- along the LOH, which depends on the blood-to-lumen HCO3-] gradient; inaddition to any underlying changes in active acid-base transport mechanisms, HCO3- permeability and backflux are important determinants of LOH J(HCO3) in vivo.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 12:46:10