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)

1. Acute experiments were carried out on anaesthetized dogs during metabolic alkalosis produced by I.V. administration of NaHCO(3). Partial constriction of one ureter led to a significant rise in the HCO(3) (-) threshold, beyond the simultaneous value for the other kidney. The magnitude of the increase was not correlated with the reduction of glomerular filtration.2. Stop-flow analysis, following complete unilateral obstruction of urine flow, demonstrated proximal as well as distal tubular reabsorption of bicarbonate. At any given plasma P(co2) the detailed configuration of the concentration changes which developed depended on (a) the presence and concentration of mannitol, (b) the duration of urinary stasis, and (c) the plasma concentration of HCO(3) (-).3. If a solution containing 15% (w/v) mannitol was infused I.V., the HCO(3) (-) concentration in free flow urine was lower than in plasma, and it fell further during arrest of flow in the entire column of trapped fluid. If less mannitol was infused, or none at all, interruption of urine flow led to a striking increase of HCO(3) (-) concentration in the distal portion of the occluded column, and to a fall in the fluid arrested in the proximal segments.4. It was demonstrated that the HCO(3) (-) concentration attained after 2(1/2), 6, or 15 min of urinary stasis at any point in the trapped fluid column was due to the combined effects of water reabsorption and HCO(3) (-) reabsorption which proceeded independently, and with a different time course.5. If mannitol was administered the lowest urinary HCO(3) (-) concentration in the series moved progressively to a more distal location with increasing duration of urinary stasis. When HCO(3) (-) concentration peaks were present in distal fluid they were conspicuous only after short interruptions of urine flow; during extended stop-flow periods they became attenuated, or disappeared. If no mannitol was administered this did not occur.6. Provided the plasma level of HCO(3) (-) was sufficiently elevated, mannitol (15%, w/v) was administered, and the time available for reabsorption was lengthened by ureter obstruction, much larger concentration differences between plasma and trapped fluid developed than the largest that are ever found between the plasma and freely draining urine. The magnitude of the largest plasma-urine (P-U) concentration difference for HCO(3) (-) increased with intratubular ;contact time', and no limiting value was found.7. Potassium concentration in distal occluded fluid fell with prolonged duration of stasis. This was related to the slow and progressive diminution of distal HCO(3) (-) concentration. But if instead of bicarbonate a nonreabsorbable anion, such as phosphate, was the dominant distal anion, K(+) concentration in distal fractions remained high and rose further with time.
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PMID:Factors modifying renal tubular bicarbonate reabsorption in the dog. 563 89

1. Mechanisms involved in the regulation of intracellular pH (pHi) in smooth muscle cells of guinea-pig ureter have been investigated using double-barrelled pH-sensitive microelectrodes in isolated strips of tissue. 2. Removal of CO2-HCO3- from the superfusing solution caused a fall in the steady-state pHi except in a few cells which had been excised from the animal for many hours (usually > 24 h). The pHi value was 7.22 +/- 0.09 (n = 89; mean +/- S.D. of an observation) in solution buffered with 5% CO2-21 mM HCO3-, compared with 6.92 +/- 0.24 (n = 67) in the nominal absence of CO2-HCO3-. Recovery from experimentally induced acidosis was faster in the presence, rather than nominal absence, of CO2-HCO3- (mean half-times of 2.7 +/- 0.7 min, n = 41, and 4.6 +/- 1.3 min, n = 12, respectively). These results suggest the presence of both HCO(3-)-dependent and -independent mechanisms for the effective extrusion of acid equivalents. 3. Recovery from acidosis was dependent on external Na+ (Na+o) in both the presence and nominal absence of CO2-HCO3-, with an apparent half-maximal activation at approximately 4 and 20 mM Na+o, respectively. Removal of Na+o in the steady state caused a fall in pHi which proceeded at a faster rate in the presence rather than in the nominal absence of CO2-HCO3-. 4. Amiloride (100 microM-1 mM) reversibly inhibited the recovery from acidosis and caused a fall in the steady-state pHi when applied in the nominal absence of CO2-HCO3-, but had no measurable effect on either the recovery from acidosis or steady-state pHi in the presence of CO2-HCO3-. These results suggest that Na(+)-H+ exchange was responsible for extrusion of acid equivalents in the nominal absence of CO2 and HCO3-, but that it played little part under more physiological conditions. 5. Although Na(+)-H+ exchange appeared to be activated below a pHi of about 7.2, it was incapable of maintaining a 'normal' pHi in the nominal absence of CO2-HCO3- in freshly excised cells, where values between 6.06 and 6.89 were recorded. Only in aged preparations, in which the intrinsic intracellular acid loading was substantially reduced (as judged from the rate of acidification on application of amiloride in the nominal absence of CO2-HCO3-) did the steady-state value approximate to that observed in the presence of CO2-HCO3-, at about 7.2.
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PMID:Regulation of intracellular pH in the smooth muscle of guinea-pig ureter: Na+ dependence. 779 29