Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Factors affecting intracellular pH (pHi) in the smooth muscle of guinea pig ureter have been investigated using pH-sensitive microelectrodes. Associated acids and bases appear to have free passage across the cell membrane but results suggest very low permeability to charged acid equivalents, thus implicating carrier-mediated movements in many of the observed pHi transients. Recovery from acidosis in the nominal absence of CO2 was inhibited by removal of Na+ and by the presence of amiloride, indicating that Na+/H+ exchange was responsible. The presence of CO2 resulted in a faster recovery from acidosis but, since intracellular buffering power was not increased, not a substantially faster effective extrusion of protons. Surprisingly, amiloride no longer caused discernable inhibition. Recovery from moderate acidosis remained Na+ dependent but was not inhibited by DIDS or acetazolamide or by the absence of Cl-, suggesting a dominant Na+-, and HCO3(-)-dependent mechanism unlike any hitherto described. Recovery from alkalosis was inhibited by DIDS and Cl(-)-free conditions, indicating that Cl-/HCO3- exchange was involved. Results suggest reversal of this mechanism on extreme acidosis. Experiments in vascular smooth muscle with fluorescent indicators confirm the presence of Na+/H+ exchange but provide conflicting evidence about the presence and properties of the HCO3(-)-dependent mechanism.
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PMID:Movement of acid equivalents across the mammalian smooth muscle cell membrane. 284 29

The intracellular Cl activity (aiCl) of smooth muscle cells in the guinea-pig ureter was measured using double-barrelled Cl-sensitive microelectrodes. The mean aiCl in normal Krebs solution was 51.1 mM, equivalent to an ECl of -18.6 mV, with a mean Em of -48.7 mV. Thus aiCl was three times higher than predicted from a passive distribution, aiCl exceeded the extracellular activity by nearly 10 mM in 10%-Cl solution. Complete removal of extracellular Cl (Cl0) caused a decline in aiCl to an apparent level of 3.3 mM with a mean time constant of 6.7 min. Cl ions were reaccumulated against their electrochemical gradient on readmission of Cl0 with a mean time constant of 6.6 min. Both the reaccumulation and loss of Cl ions on changing Cl0 were slowed about three-fold by the presence of the anion exchange inhibitor DIDS. It is therefore concluded that most of the transmembrane Cl movements are mediated by a reversible anion exchange carrier and that PCl is very low. These results are similar to those obtained in vas deferens and may be a general feature of smooth muscle cells.
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PMID:Microelectrode measurement of intracellular chloride activity in smooth muscle cells of guinea-pig ureter. 640 1

1. HCO3(-)-dependent mechanisms involved in the regulation of intracellular pH (pHi) were characterized using double-barrelled pH-sensitive microelectrodes in smooth muscle cells of the isolated guinea-pig ureter. 2. Removal of external Cl- in the presence of CO2-HCO3- caused a transient alkalosis, consistent with the presence of Cl(-)-HCO3- exchange, before pHi slowly recovered. Recovery from acidosis in the presence of CO2-HCO3- was not affected, at a time when intracellular Cl- would have been maximally depleted, indicating that a counter transport of Cl- and HCO3- was not involved. The recovery was also not affected by amiloride, indicating that Na(+)-H+ exchange was not involved. 3. A transient hyperpolarization was associated with the recovery from acidosis in the presence of CO2-HCO3-, consistent with rheogenic coupling of Na(+)-HCO3- cotransport. However, depolarization caused by elevation of the extracellular potassium (K+o) concentration, which should favour inward transport by the rheogenic mechanism, caused a fall in pHi and decreased the rate of recovery from acidosis. Furthermore, ouabain abolished the transient hyperpolarization without affecting the recovery of pHi. It is concluded that Na(+)-HCO3- cotransport in the ureter is electroneutral. 4. Recovery from acidosis in the presence of CO2-HCO3- was insensitive to DIDS even after prolonged pre-equilibriation and extreme acidosis. The results suggest that Na(+)-HCO3- cotransport in the ureter is insensitive to DIDS and that Cl(-)-HCO3- exchange does not reverse to contribute to the extrusion of acid equivalents. A HCO3- conductance may account for the Na(+)-independent, HCO3(-)-dependent recovery from extreme acidosis. 5. Recovery from experimentally induced alkalosis was inhibited by Cl(-)-free conditions and by DIDS, indicating that Cl(-)-HCO3- exchange was involved. 6. It is concluded that pHi in the smooth muscle of guinea-pig ureter is controlled by three transport mechanisms. By far the most important is an electroneutral Na(+)-HCO3- cotransporter. Na(+)-H+ exchange appears to play little role in the presence of the physiological buffer. Both of these mechanisms extrude acid equivalents and so protect the cell against its fairly substantial intrinsic intracellular acid loading. Cl(-)-HCO3- exchange, on the other hand, is stimulated by intracellular alkalosis to transport acid equivalents into the cell and so restore a more normal pHi.
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PMID:Regulation of intracellular pH in the smooth muscle of guinea-pig ureter: HCO3- dependence. 752 76

1. Intracellular pH (pHi) of smooth muscle cells in isolated strips of guinea-pig femoral artery was measured using double-barrelled pH-sensitive microelectrodes. 2. In modified Krebs solution equilibrated with 5% CO2, pHi was 7.26 +/- 0.14 (n = 36; mean +/- S.D. of an observation) and the membrane potential (Em) was -60.5 +/- 5.5 mV. Removal of CO2 from the superfusing solution caused an immediate transient alkalosis before pHi stabilized at much the same value (7.28 +/- 0.14; n = 16) as in the presence of CO2. 3. The rate of recovery of pHi from experimentally induced acidosis was not measurably affected by the presence or nominal absence of CO2-HCO3-. 4. Application of amiloride (100 microM) blocked recovery from acidosis in the nominal absence of CO2-HCO3- and caused a progressive fall in pHi. In the presence of CO2-HCO3-, application of amiloride allowed a slow recovery to pHi 6.7-7.0, but completely prevented full recovery to the normal pHi. 5. Removal of extracellular Na+ (Na+o) caused a dramatic, progressive fall in pHi in both the presence and nominal absence of CO2-HCO3-. 6. The amiloride-insensitive extrusion of acid equivalents observed in the presence of CO2-HCO3- to pHi 6.7-7.0 was inhibited by removal of Na+o but was not affected by preequilibration with DIDS (see Methods). 7. It is concluded that Na(+)-H+ exchange is largely responsible for the effective extrusion of acid equivalents in these arterial cells, at least from relatively small perturbations. A DIDS-insensitive, Na(+)- and HCO3(-)-dependent mechanism provides some recovery from acidosis to a relatively low pHi. 8. Comparison with data obtained in exactly the same manner in smooth muscle cells of the guinea-pig ureter indicates that there are significant differences in the regulation of pHi in different smooth muscles.
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PMID:Regulation of intracellular pH in smooth muscle cells of the guinea-pig femoral artery. 779 30