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A C Elliott

Publications and source records attributed to A C Elliott.

44 records · Page 3Linked to original sources
PubMed1989

Indirect evidence for the presence of non-specific anion channels in rabbit mandibular salivary gland acinar cells.

1. Intracellular pH (pHi) was measured using the fluorescent pH-sensitive dye 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein in acini isolated from the rabbit mandibular salivary gland. 2. Stimulation of the acinar cells with acetylcholine (ACh) evoked an intracellular acidosis, the size of which was dependent on the HCO3-concentration in the bathing medium. A half-maximal acidosis was observed at approximately 10 mM-HCO3-. ACh also evoked an acidosis in HCO3(-)-free solutions containing acetate; a half-maximal acidosis was observed at about 10 mM-acetate. 3. Propionate, lactate and butyrate were also able to support the ACh-evoked acidosis to varying extents. In contrast, formate, pyruvate and salicylate did not support the ACh-induced acidosis to any great extent. 4. Acetazolamide greatly reduced the size of the acidosis in HCO3(-)-buffered medium, but had no effect in acetate-buffered medium, suggesting that the inhibitory effect of acetazolamide was due to a specific inhibition of carbonic anhydrase activity. 5. The Cl- channel blockers diphenylamine-2-carboxylic acid (DPC, 1 mM) and 5-nitro-2-(3-phenylpropylamino)-benzoic acid (0.5 mM) abolished the ACh-evoked acidosis in both HCO3(-) -and acetate-buffered media. 6. The data are consistent with the presence in the acinar cell of relatively non-specific anion channels sensitive to DPC and its derivatives. Such channels, activated on stimulation with ACh, would allow HCO3- and other weak acid ions to leave the cell, leading to the observed acidosis. The existence of such channels, located in the apical membrane, could explain why HCO3- or acetate can sustain fluid secretion in the intact perfused rabbit mandibular gland in the absence of Cl-.

Acetates↗
PubMed1989

Acetylcholine-induced intracellular acidosis in rabbit salivary gland acinar cells.

Intracellular pH (pHi) was measured in acini isolated from rabbit mandibular salivary glands using the fluorescent pH-sensitive probe 2,7-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF). Resting pHi was estimated to be 7.13 +/- 0.01 (mean +/- SE of 29 experiments). Stimulation with acetylcholine (ACh) caused an intracellular acidosis followed by a return of pHi toward the control value with a half time of approximately 3 min. The intracellular acidosis was dose dependent and could be abolished by pretreatment of the acini with atropine (10 microM), suggesting that it was due to a receptor-mediated event. Incubation of the acini in HCO3- -free solutions or treatment of the acini with the carbonic anhydrase inhibitor acetazolamide (1 mM) abolished the acidosis, suggesting that the acidosis might be caused by loss of HCO3- from the cell. The acidosis was not affected by either 1) pretreatment of the acini with the anion exchange inhibitor 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), or 2) equilibration of the acini in Cl- -free solution (Cl- substituted with glucuronate). These results suggest that the postulated HCO3- efflux does not occur by Cl- -HCO3- exchange. However, Cl- -HCO3- exchange did appear to be present because replacement of Cl- caused a large DIDS-sensitive alkalinization of pHi, presumably caused by HCO3- uptake in exchange for Cl-. The recovery of pHi after the initial acidosis on stimulation with ACh could be blocked by 1 mM amiloride, suggesting that the recovery phase was mediated by Na+-H+ exchange.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1989

Simultaneous measurements of action potential duration and intracellular ATP in isolated ferret hearts exposed to cyanide.

Shortening of the cardiac action potential during ischemia and anoxia is likely to contribute to the decline in contractility that occurs under such conditions. It has been hypothesized that a decrease in the intracellular ATP concentration ([ATP]i) underlies the changes in the action potential. The recently discovered potassium channel activated at low ATP concentrations might provide the link between action potential shortening and low [ATP]i. However, it has yet to be shown that [ATP]i falls to the range required for channel activation at the time when action potential shortening occurs. We have measured action potentials and [ATP]i simultaneously in isolated ferret hearts during inhibition of both oxidative phosphorylation and anaerobic glycolysis (metabolic blockade). Metabolic blockade caused a rapid decline in cardiac contractility, accompanied by a rapid fall in action potential duration. [ATP]i fell only slightly and remained well above the range where activation of the ATP-sensitive K+ channel would be expected to occur. Moreover, reintroduction of glucose to the perfusate led to a substantial recovery in both contraction and in action potential duration, again in the absence of any great change in [ATP]i. These results suggest that the action potential shortening observed in metabolic blockade cannot be explained by the simple hypothesis of K+ channel opening as a consequence of a decrease in bulk [ATP]i unless the Km for suppression of channel activity by ATP is very much higher in intact cells than in any of the patch configurations studied. An alternative explanation is that the channel may be regulated under these conditions by mechanisms other than a change in [ATP]i.

Action Potentials↗
PubMed1987

The contribution of intracellular acidosis to the decline of developed pressure in ferret hearts exposed to cyanide.

1. The concentrations of phosphorus-containing metabolites were measured using 31P nuclear magnetic resonance (n.m.r.) in Langendorff-perfused ferret hearts. The hearts were stimulated at a constant rate and developed pressure was measured. 2. The inhibition of oxidative phosphorylation with cyanide (2 mM) decreased developed pressure. This was accompanied by an intracellular acidosis, a fall in the concentration of phosphocreatine ([PCr]) and a rise in that of inorganic phosphate ([Pi]). 3. The effects of cyanide on developed pressure were compared with those of simply decreasing the intracellular pH (pHi) (by elevating CO2) to match the change produced by cyanide. The change of pHi alone resulted in about 33% of the decrease of force produced by cyanide. 4. The relationship between developed pressure and pHi was investigated by altering CO2. It could be described by an equation of the form:log developed pressure = a + b pHi where a and b were independent of pHi. The addition of cyanide decreased a but had no significant effect on b. In other words a given change of pHi had the same fractional effect on pressure in the absence as in the presence of cyanide. 5. In another series of experiments, after cyanide had been added, pHi was returned to control levels by decreasing CO2. This increased developed pressure. Nevertheless the pressure was still considerably less than in control. Furthermore, if the acidosis was abolished by decreasing CO2 at the same time as cyanide was added developed pressure still decreased. 6. We conclude that most of the decrease of developed pressure produced by cyanide is not produced by intracellular acidosis and may result from increased [Pi].

Animals↗
PubMed1986

Tripartite injury of the clavicle. A case report.

A rare injury of the clavicle and its articulations is reported. A possible mechanism of injury is suggested, and the management and outcome are discussed. The importance of being on the look-out for the potentially lethal posterior dislocation of the sternoclavicular joint is stressed.

Acromioclavicular Joint↗