EXPERIMENTAL ACIDEMIA AND MUSCLE-CELL PH IN CHRONIC ACIDOSIS AND RENAL-FAILURE

被引:35
作者
BAILEY, JL
ENGLAND, BK
LONG, RC
WEISSMAN, J
MITCH, WE
机构
[1] EMORY UNIV, SCH MED, DEPT MED, ATLANTA, GA 30322 USA
[2] EMORY UNIV, SCH MED, DEPT NEUROL, ATLANTA, GA 30322 USA
[3] EMORY UNIV, SCH MED, FRITZ PHILIPS MAGNET RESONANCE LAB RADIOL, ATLANTA, GA 30322 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY | 1995年 / 269卷 / 03期
关键词
CHRONIC RENAL FAILURE; METABOLIC ACIDOSIS; NUCLEAR MAGNETIC RESONANCE; UREMIA;
D O I
10.1152/ajpcell.1995.269.3.C706
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
To test whether muscle intracellular pH (pH(i)) decreases when extracellular pH falls, P-31-nuclear magnetic resonance was utilized in rats made acidotic by infusion of HCl, gavage-feeding NH4Cl, or induction of chronic renal failure (CRF). A 2- or 4-h HCl infusion did not fewer muscle pH(i), even though serum bicarbonate fell to 5 mM. With chronic acidemia, blood pH was 7.15 +/- 0.01 vs. 7.38 +/- 0.02 in pair-fed controls, and muscle pH(i) was 7.09 +/- 0.01 and 7.14 +/- 0.02, respectively (P < 0.01). pH(i) in muscle of CRF rats (7.16 +/- 0.01) did not differ from sham-operated, pair-fed controls (7.19 +/- 0.01) despite a blood pH of 7.23 +/- 0.05 in CRF vs. 7.39 +/- 0.01 in controls. Because ion transport is abnormal in CRF, we examined whether recovery of pH(i) is impaired when muscles of six CRF and control rats were exercised to tetany by stimulation of the sciatic nerve. Neither pH(i) nor the recovery of pH(i) differed between CRF and control rats. We conclude that pH(i) is maintained in muscle in uremia and that signals other than changing pH(i) must be necessary to disrupt metabolism.
引用
收藏
页码:C706 / C712
页数:7
相关论文
共 29 条
[1]   NMR-VISIBLE INTRACELLULAR P-I AND PHOSPHOESTERS DURING REGULATION OF NA+-P-I COTRANSPORT IN OPOSSUM KIDNEY-CELLS [J].
BARACNIETO, M ;
SPITZER, A .
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 1994, 267 (04) :C915-C919
[2]   INTRACELLULAR HYDROGEN ION CHANGES AND POTASSIUM MOVEMENT [J].
BROWN, EB ;
GOOTT, B .
AMERICAN JOURNAL OF PHYSIOLOGY, 1963, 204 (05) :765-&
[3]   CORRECTION OF UREMIC CELLULAR INJURY WITH A PROTEIN-RESTRICTED AMINO ACID-SUPPLEMENTED DIET [J].
COTTON, JR ;
WOODARD, T ;
KNOCHEL, JP .
AMERICAN JOURNAL OF KIDNEY DISEASES, 1985, 5 (05) :233-236
[4]   EFFECTS OF ACUTE AND CHRONIC UREMIA ON ACTIVE CATION-TRANSPORT IN RAT MYOCARDIUM [J].
DRUML, W ;
KELLY, RA ;
ENGLAND, BK ;
OHARA, DS ;
MITCH, WE .
KIDNEY INTERNATIONAL, 1990, 38 (06) :1061-1067
[5]   ABNORMAL CATION-TRANSPORT IN UREMIA - MECHANISMS IN ADIPOCYTES AND SKELETAL-MUSCLE FROM UREMIC RATS [J].
DRUML, W ;
KELLY, RA ;
MAY, RC ;
MITCH, WE .
JOURNAL OF CLINICAL INVESTIGATION, 1988, 81 (04) :1197-1203
[6]   ABNORMALITIES IN PROTEIN-SYNTHESIS AND DEGRADATION INDUCED BY EXTRACELLULAR PH IN BC3H1 MYOCYTES [J].
ENGLAND, BK ;
CHASTAIN, JL ;
MITCH, WE .
AMERICAN JOURNAL OF PHYSIOLOGY, 1991, 260 (02) :C277-C282
[7]   NA PUMP DEFECTS IN CHRONIC UREMIA CANNOT BE ATTRIBUTED TO CHANGES IN NA-K-ATPASE MESSENGER-RNA OR PROTEIN [J].
GREIBER, S ;
ENGLAND, BK ;
PRICE, SR ;
MEDFORD, RM ;
EBB, RG ;
MITCH, WE .
AMERICAN JOURNAL OF PHYSIOLOGY, 1994, 266 (04) :F536-F542
[8]  
GREIBER S, 1995, J AM SOC NEPHROL, V5, P1689
[9]   ACIDOSIS, NOT AZOTEMIA, STIMULATES BRANCHED-CHAIN, AMINO-ACID CATABOLISM IN UREMIC RATS [J].
HARA, Y ;
MAY, RC ;
KELLY, RA ;
MITCH, WE .
KIDNEY INTERNATIONAL, 1987, 32 (06) :808-814
[10]   INFLUENCE OF AMMONIA AND PH ON PROTEIN AND AMINO-ACID-METABOLISM IN LLC-PK1 CELLS [J].
JURKOVITZ, CT ;
ENGLAND, BK ;
EBB, RG ;
MITCH, WE .
KIDNEY INTERNATIONAL, 1992, 42 (03) :595-601