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T Dixon

Publications and source records attributed to T Dixon.

11 recordsLinked to original sources
PubMed1989

Acetazolamide inhibits acidification by the turtle bladder independent of cell pH.

Acetazolamide (ACZL) inhibits luminal acidification by the turtle urinary bladder, a process thought to be mediated by the drug's ability to inhibit carbonic anhydrase (CA) and thus elevate cell pH. To test the hypothesis that these transport changes are actually mediated by changes of cell pH, we measured this parameter in single, identifiable mucosal cells using 4-methylumbelliferone and fluorescence microscopy. In control bladders 5 X 10(-4) M ACZL inhibited proton transport by 80 +/- 6%, and alkalinized cell pH, especially in a subpopulation of CA cells. A much larger cell alkalinization was induced by serosal HCO3- but proton transport fell only 30 +/- 7%. When cell pH was clamped at approximately 7.0 using 50 mM dimethyloxazolidinedione, or when cell pH was acidified using 7.5 mM propionate, transport rates still declined by 74 +/- 2, and 100 +/- 12%, respectively, in response to ACZL. In propionate-acidified bladders, 1 mM sodium azide blocked the inhibition of transport seen with 5 X 10(-4) M ACZL and reversed the inhibition with 10(-5) M ACZL. The apical endocytosis rate was increased by ACZL in normal and propionate-acidified bladders, but was not stimulated by alkalinizing the cell with NH4Cl. We conclude that ACZL can induce cellular alkalinization in this tissue, but that this pH change is not required for the inhibition of transport, or the ACZL-associated stimulation of endocytosis. The drug's ability to inhibit acidification appears to be the result of an azide-sensitive mechanism that has yet to be defined.

Acetazolamide↗
PubMed1989

Phorbol myristate acetate inhibits acidification by turtle urinary bladder.

The effects of phorbol myristate acetate (PMA) on acid secretion by the turtle urinary bladder were examined to evaluate the importance of protein phosphorylation in modulating the distal acidification system. In HCO3-free PO4 buffer 0.2 mM mucosal PMA inhibited reverse short-circuit current (RSCC) by 42%. The inhibition of RSCC was dose dependent, and RSCC approached zero at high concentrations of PMA. PMA also inhibited acid secretion measured titrimetrically but had no effect on RSCC from bladders in which proton secretion was selectively inhibited by an adverse pH gradient or serosal 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid. The inhibition by PMA was duplicated by 1-oleoyl-2-acetyl-rac-glycerol, but not by an inactive phorbol ester. The PMA inhibition was much more potent with mucosal compared with serosal application. The PMA inhibition caused a significant 0.15 pH unit reduction of carbonic anhydrase (CA) cell cytoplasmic pH and a change in the CA cell morphology. Unlike the inhibition of proton transport induced by acetazolamide, the PMA inhibition was neither reversed nor prevented by sodium azide. We conclude that PMA decreases basal acid secretion and blocks the stimulatory effects of CO2 by an azide-insensitive mechanism distinct from that of acetazolamide. In view of recent findings that PMA stimulates HCO3 secretion by the turtle bladder, these results suggest that kinase C-mediated protein phosphorylation may be a central event in the transition from the secretion of acid to the secretion of base.

1-Methyl-3-isobutylxanthine↗
PubMed1984

Alteration of type A behavior and reduction in cardiac recurrences in postmyocardial infarction patients.

Eight hundred sixty-two postmyocardial infarction patients volunteered to be randomly selected and enrolled into: (1) a control section of 270 patients, who received group cardiologic counseling; and (2) an experimental section of 592 patients, who received group type A behavior counseling in addition to group cardiologic counseling. Reduction in type A behavior at the end of 3 years was observed in 43.8% of the 592 participants, who initially were enrolled to receive group cardiologic and type A behavioral counseling. This degree of behavioral reduction was significantly greater than that observed in participants who initially were enrolled to receive only group cardiologic counseling. The 3-year cumulative cardiac recurrence rate was 7.2% in participants who initially were enrolled to receive group cardiologic and type A behavioral counseling. This was significantly less (p less than 0.005) than that (13%) observed in participants who initially were enrolled to receive only cardiologic counseling. This difference in recurrence rates was due to a lesser incidence of nonfatal infarctions in the patients who had been enrolled in the section receiving type A behavioral as well as cardiologic counseling. These data suggest that type A behavior can be altered in a sizable fraction of postinfarction patients and that such alteration is associated with a significantly reduced rate of nonfatal myocardial infarctions.

Behavior↗
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