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At least 289 records · Page 16Linked to original sources
PubMed1991

Volume-activated taurine efflux from skate erythrocytes: possible band 3 involvement.

In a previous study (L. Goldstein, S.R. Brill, and E.V. Freund, J. Exp. Zool. 254: 114-118, 1990) it was suggested that volume-activated (VA) taurine efflux from skate (Raja erinacea) erythrocytes might involve the anion exchanger band 3. The aim of the present study was to obtain further evidence for (or against) this possibility. We found that in addition to stilbene disulfonates, two other band 3 inhibitors, N-(azido-2-nitrophenyl)-2-amino sulfonic acid (NAP)-taurine and niflumic acid, also inhibit VA taurine efflux. In addition, there is a close relationship between the dose-response curves for 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid inhibition of VA taurine efflux and sulfate efflux. Furthermore, taurine influx, as well as efflux, is activated by volume expansion, as would be expected with transport facilitated by band 3. However, sulfate (a known band 3 substrate) efflux is not activated by volume expansion, and sulfate influx is only activated minimally, but sulfate does inhibit VA taurine uptake. Thus there is considerable evidence in favor of the involvement of band 3 in VA taurine efflux, but the issue of the sulfate fluxes remains to be resolved.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1984

Effects of acidosis and carbonic anhydrase inhibition in the elasmobranch rectal gland.

We studied the effects of acidosis and carbonic anhydrase inhibition on rectal gland fluid secretion. In the anesthetized dogfish shark, Squalus acanthias, volume expanded by a constant infusion of Ringer solution, fluid formation was halved by severe systemic metabolic and respiratory acidosis (pH approximately 7.10) and carbonic anhydrase inhibition. Mild respiratory acidosis (pH approximately 7.6) equivalent to the measured systemic pH during carbonic anhydrase inhibition was without effect. Inhibition of rectal gland enzyme produced severe glandular acidosis, which is indicated by an increase in gland fluid PCO2 (from 7 to 26 mmHg) and HCO3- (from 1.2 to 2.4 mM) and a decrease in pH (from 6.7 to 6.4). Gland tissue total CO2 dropped from 18 to 11 mmol/kg. These changes occurred despite nearly 50% reduction in fluid formation, O2 consumption, and CO2 output. We propose that carbonic anhydrase facilitates CO2 transfer from sites of metabolism to capillary blood by its conversion to HCO3-. This maintains a tolerable intracellular acid-base milieu during stimulated fluid secretion.

Acidosis↗
PubMed1987

Regulation of brain water and electrolytes during acute hyperosmolality in rats.

Regulation of brain water and electrolytes during acute hyperosmolal states has been studied in anesthetized rats. Rats were injected intravenously or intraperitoneally with hypertonic NaCl, mannitol, or sucrose (hyperosmolal series) or with isotonic NaCl (isosmolal controls). Terminal plasma osmolality varied from 290 to 385 mosmol/kg and the experimental duration from 15 to 120 min. Osmotically induced water loss from brain tissue for the different protocols was only 26-78% of that predicted for ideal osmotic behavior, revealing a degree of tissue volume regulation, and the brain gained Na, Cl, and K. This gain was sufficient to account quantitatively for tissue volume regulation at 120 min of hypernatremia but not at shorter times or during mannitol- or sucrose-induced hyperosmolality. Water loss and electrolyte uptake occur simultaneously, over 30 min, which limits the degree of brain shrinkage. Results of this analysis of the time course and magnitude of tissue electrolyte gain during acute hyperosmolality form the basis for the following two studies of the volume regulatory influx of electrolyte from plasma and CSF, respectively.

Animals↗
PubMed1987

Volume regulatory influx of electrolytes from plasma to brain during acute hyperosmolality.

Brain volume is regulated during acute hyperosmolal states based, in part, on the tissue gain of Na, Cl, and K [H. F. Cserr, M. DePasquale, and C.S. Patlak, Am. J. Physiol. 253 (Renal Fluid Electrolyte Physiol. 22): F522-F529, 1987]. This study evaluates the contribution of influx from plasma to the volume regulatory gain of electrolyte. Blood-to-brain transfer constants, K1, were measured as a function of plasma osmolality, over the range 300-385 mosmol/kg, for sodium (22Na) and potassium (42K or 86Rb) and as a marker for nonselective changes in permeability for [14C]mannitol. Osmolality was elevated by intraperitoneal injection of hypertonic NaCl, mannitol, or sucrose. K1 for Na, K, and mannitol each increased linearly with plasma osmolality. Increases in K1 for Na and mannitol were small and were proportional to their respective diffusion coefficients, consistent with the development of a small leak pathway. Increases in K1 for K were much larger, consistent with osmotic stimulation of a selective permeability pathway. Quantitative analysis of the results suggests that uptake from plasma accounts for most of the K gained by brain tissue in response to acute hyperosmolality but for only a small fraction of the Na. This provides indirect evidence for an additional source of Na, presumably from cerebrospinal fluid.

Animals↗
PubMed1992

Renal acid-base physiology in marine teleost, the long-horned sculpin (Myoxocephalus octodecimspinosus).

We have sought to define urinary acid-base excretion in the marine teleost using the long-horned sculpin, Myoxocephalus octodecimspinosus. Urine flow (1.7 ml.h-1.kg-1) is relatively high, and glomerular filtration rate is very low (2.9 ml.h-1.kg-1). The urine-to-plasma ratio of inulin is 2. Renal clearance of p-aminohippurate is very high (108 ml.h-1.kg-1); phosphate and divalent cations are also secreted. In this framework we found urinary pH to average 6.6, but infusion of acid or alkali elicited a pH range of 6.1-7.8. Untreated fish may also have alkaline urine; so it is not surprising that precipitates of calcium or magnesium phosphate are sometimes found in bladder. These are of fine sandy quality and never cause blockage. Infusion of buffer (imidazole) increased the concentration of titratable acid 11-fold and output 2.5-fold. Carbonic anhydrase inhibitors had no effect on any urinary component, and histochemical studies revealed that cytoplasm and membranes did not yield the specific cobalt stain for the enzyme. An alkaline load (NaHCO3) is rapidly dissipated by gill excretion, mediated in part by carbonic anhydrase. An acid load (HCl) is rapidly dissipated by gill excretion, not dependent on carbonic anhydrase, and some renal excretion. Comparison and contrast of the low rates of HCO3- reabsorption in the marine teleost (and elasmobranch) with those of mammals suggest strongly that renal carbonic anhydrase evolved in connection with these high reabsorptive rates beginning in freshwater fish and continuing through amphibia and birds.

Acid-Base Equilibrium↗
PubMed1979

Effect of varying CO2 equilibria on rates of HCO3- formation in cerebrospinal fluid.

The effects of elevated plasma CO2 partial pressure (PCO2) and [HCO3-] on cerebrospinal fluid (CSF) HCO3- accession have been reviewed in the context of the basal route of CSF HCO3- formation. The basal rate of 53 mM/h appears to be a consequence entirely of formation, via the reaction CO2 + OH- leads to HCO3-. Two-thirds of this rate is catalyzed by carbonic anhydrase, and the remainder uncatalyzed. The HCO3- accession matches 37% that of sodium, so that the HCO3- rate is involved with CSF turnover. When PCO2 is elevated twofold, the rate of HCO3- formation increase 10%, and results in elevation of CSF [HCO3-] by 5 mM in 1 h. Also, when plasma [HCO3-] is elevated 15 mM, CSF [HCO3-] rises about 5 mM/h; this is transfer of HCO3- "as such" by diffusion from plasma. The effects of hypercapnia and metabolic alkalosis on CSF HCO3- accumulation are additive, but they occur by separate processes. The effect of hypercapnia is an exaltation of the normal process due to increased substrate (CO2), but that of increased plasma HCO3- is due to imposition of an abnormal diffusion gradient for this ion between plasma and CSF. The effect of hypercapnia in elevating brain HCO3- operates to maintain brain pH and is also based on the formation of HCO3- from CO2. Brain HCO3- may also be a source of CSF HCO3-. Relations have been sought between the chemically calculated rates of HCO3- formation in CSF and those observed. The chemically calculated catalytic rate is 1,600 times greater than that observed, agreeing with the fact that more than 99.9% of choroid plexus carbonic anhydrase must be inhibited to yield a decrease in fluid formation or ion transport from plasma to CSF. The calculated uncatalyzed rate agrees closely with what is observed after complete inhibition of the enzyme. These considerations support the idea that all the HCO3- reaching the CSF is formed from CO2, rather than by transfer of the ion from plasma to CSF.

Acetazolamide↗
PubMed2005

Proton-mediated feedback inhibition of presynaptic calcium channels at the cone photoreceptor synapse.

Generation of center-surround antagonistic receptive fields in the outer retina occurs via inhibitory feedback modulation of presynaptic voltage-gated calcium channels in cone photoreceptor synaptic terminals. Both conventional and unconventional neurotransmitters, as well as an ephaptic effect, have been proposed, but the intercellular messaging that mediates the inhibitory feedback signal from postsynaptic horizontal cells (HCs) to cones remains unknown. We examined the possibility that proton concentration in the synaptic cleft is regulated by HCs and that it carries the feedback signal to cones. In isolated, dark-adapted goldfish retina, we assessed feedback in the responses of HCs to light and found that strengthened pH buffering reduced both rollback and the depolarization to red light. In zebrafish retinal slices loaded with Fluo-4, depolarization with elevated K(+) increased Ca signals in the synaptic terminals of cone photoreceptors. Kainic acid, which depolarizes HCs but has no direct effect on cones, depressed the K(+)-induced Ca signal, whereas CNQX, which hyperpolarizes HCs, increased the Ca signals, suggesting that polarization of HCs alters inhibitory feedback to cones. We found that these feedback signals were blocked by elevated extracellular pH buffering, as well as amiloride and divalent cations. Voltage clamp of isolated HCs revealed an amiloride-sensitive conductance that could mediate modulation of cleft pH dependent on the membrane potential of these postsynaptic cells.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1985

Ocular pharmacology of sulfonamides: the cornea as barrier and depot.

In the past five years we have studied the penetration of locally applied sulfonamides into the eye, with a view toward developing new topical carbonic anhydrase inhibitors for the treatment of glaucoma. The drugs varied by 400 fold in their permeability to the anterior chamber and 20,000 fold in permeability to the posterior chamber. We report now on two particular findings related to drug structure: 1) Transcorneal permeability of the ionic or dissociated form of the drug is relatively high -- some 1/4 that of the undissociated form. 2) Depending on the structure, certain compounds are sequestered in the cornea (presumably the stroma) and form a release system into the anterior aqueous.

Animals↗
PubMed1988

The effect of altitude on tests of reaction time and alertness.

Psychomotor performance was assessed in 20 subjects on each of 2 mountaineering expeditions. During the first, which reached 5,008 m, simple reaction time and alertness were measured, on the second to 4,790 m these were replaced by a three-choice reaction time test. In both, mean reaction times increased significantly at altitude in subjects with marked symptoms of Acute Mountain Sickness (AMS), whereas the alertness tests showed no effects. Reaction times were not affected by other environmental factors but adverse conditions increased the number of errors. The increase in reaction time may be ascribed either to the lethargy associated with AMS or alternatively may have been a direct effect of hypoxia. The latter explanation is favoured because of reports by other workers of an increase in reaction time with altitude in the absence of AMS.

Acetazolamide↗
PubMed1970

[Diuretics. 47].

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Acetazolamide↗