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161 records · Page 9Linked to original sources
PubMed1984

A functional role for the tubuloglomerular feedback mechanism.

Ever increasing evidence exists that the tubuloglomerular feedback system exerts a major influence on overall renal function. Several examples are potentially pertinent to clinical medicine in which there is reasonable evidence that activation or suppression of tubuloglomerular feedback mechanisms contribute significantly to alterations in normal renal physiology. However, in most examples reported, the feedback mechanism is one of several influences acting in concert to determine the final nephron filtration rate, its respective determinants, and the relationship of filtration to the rate of tubular reabsorption. A more complete understanding of all the factors which influence and modify the functional role of tubuloglomerular feedback mechanisms will aid our understanding significantly and the consequent therapy of a variety of altered physiologic conditions.

Acute Kidney Injury↗
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↗
PubMed1986

Active tetraethylammonium uptake across the basolateral membrane of rabbit proximal tubule.

Tetraethylammonium (TEA) uptake was measured in isolated, nonperfused rabbit S2 proximal tubule segments. The TEA cell-to-bath concentration ratio in bicarbonate-Ringer bathing medium was 10-fold higher than that predicted by passive equilibration according to the basolateral electrochemical potential, indicating that TEA uptake is an active process as reported by previous investigators. Removing bicarbonate and CO2 reduced TEA uptake to 22% of control. When bicarbonate-CO2 was replaced by HEPES-O2 or butyrate-O2, TEA uptake was unaltered, but uptake was inhibited when the major buffer anion was omitted. In the presence of 10(-4) M ouabain and bicarbonate-CO2, the TEA cell-to-bath concentration ratio was reduced to 20% of control. TEA uptake in the absence of bicarbonate and CO2 was unaltered by the addition of 10(-4) M ouabain. TEA uptake was inhibited when the bathing medium contained 0 mM K+ or 2 mM Ba2+. These data 1) demonstrate that active basolateral TEA uptake is dependent on medium buffer capacity and 2) support the concept that a portion of TEA uptake occurs via a passive equilibration pathway.

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↗
PubMed1998

Kinetics of CO2 excretion and intravascular pH disequilibria during carbonic anhydrase inhibition.

Inhibition of carbonic anhydrase (CA) activity (activity in red blood cells and activity available on capillary endothelium) results in decrements in CO2 excretion (VCO2) and plasma-erythrocyte CO2-HCO(-3)-H+ disequilibrium as blood travels around the circulation. To investigate the kinetics of changes in blood PCO2 and pH during progressive CA inhibition, we used our previously detailed mathematical model of capillary gas exchange to analyze experimental data of VCO2 and blood-gas/pH parameters obtained from anesthetized, paralyzed, and mechanically ventilated dogs after treatment with acetazolamide (Actz, 0-100 mg/kg i.v.). Arterial and mixed venous blood samples were collected via indwelling femoral and pulmonary arterial catheters, respectively. Cardiac output was measured by thermodilution. End-tidal PCO2, as a measure of alveolar PCO2, was obtained from continuous records of airway PCO2 above the carina. Experimental results were analyzed with the aid of a mathematical model of lung and tissue-gas exchange. Progressive CA inhibition was associated with stepwise increments in the equilibrated mixed venous-alveolar PCO2 gradient (9, 19, and 26 Torr at 5, 20, and 100 mg/kg Actz, respectively). The maximum decrements in VCO2 were 10, 24, and 26% with 5, 20, and 100 mg/kg Actz, respectively, without full recovery of VCO2 at 1 h postinfusion. Equilibrated arterial PCO2 overestimated alveolar PCO2, and tissue PCO2 was underestimated by the measured equilibrated mixed venous blood PCO2. Mathematical model computations predicted hysteresis loops of the instantaneous CO2-HCO(-3)-H+ relationship and in vivo blood PCO2-pH relationship due to the finite reaction times for CO2-HCO(-3)-H+ reactions. The shape of the hysteresis loops was affected by the extent of Actz inhibition of CA in red blood cells and plasma.

Acetazolamide↗
PubMed1992

Modulation of extracellular pH by glutamate and GABA in rat hippocampal slices.

1. Alkaline extracellular pH transients evoked by afferent stimulation, and local pressure ejection of glutamate and gamma-aminobutyric acid (GABA), were studied in the CA1 region of rat hippocampal slices. Amino acid-evoked responses were obtained by use of a dual micromanipulator, with the tip of a double-barreled pH-sensitive microelectrode positioned 50 microns from a pressure ejection pipette. 2. At 31 degrees C, in Ringer solutions buffered with 26 mM HCO3- and 5% CO2, mean extracellular pH in submerged 300-microns slices was 7.15 +/- 0.12 (n = 27 slices), at a tissue depth of approximately 150 microns. In Ringer buffered with 35 mM HCO3- and 5% CO2, extracellular pH was 7.29 +/- 0.10 (n = 19 slices). 3. Repetitive stimulation of the Schaffer collaterals caused an extracellular alkaline shift in stratum oriens, pyramidale, and radiatum, averaging 0.05 +/- 0.03 pH units among all regions (n = 138), with a maximum response of 0.16 pH units. Alkaline transients of similar appearance were obtained by local ejection of glutamate (0.01-0.12 pH units, n = 110) and GABA (0.01-0.18 pH units, n = 137). Control ejection of these amino acids into dilute agar caused only small acid shifts. 4. Superfusion of 100 microM picrotoxin abolished the GABA-evoked alkaline shift but failed to inhibit the Schaffer collateral- and glutamate-evoked alkalinizations. 5. Superfusion of 10(-5)-10(-3) M acetazolamide acidified the baseline by 0.05-0.10 pH units and amplified the Schaffer collateral- and glutamate-evoked alkaline shifts.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed1996

Role of voltage-gated calcium channels in the generation of activity-induced extracellular pH transients in the rat hippocampal slice.

1. The role of voltage-gated calcium channels in the generation of activity-induced alkaline shifts in extracellular pH (pHo) was studied in rat hippocampal slices (area CAI) by means of Ca(2+)-and H(+)-selective microlectrodes inserted into the stratum pyramidale and/or stratum radiatum. 2. After complete pharmacological blockade of ionotropic glutamate receptors and gamma-aminobutyric acid-A (GABAA) receptors, trains (5-10 Hz, 5-10s) of antidromic spikes in pyramidal neurons were associated with a fast alkaline transient of up to 0.17 pH units and a fall in the extracellular Ca2+ concentration ([Ca2+]o). The alkaline shift was strongly enhanced upon inhibition of extracellular carbonic anhydrase. 3. Application of 100 microM Ni2+ plus 100 microM Cd2+ inhibited both the fall in [Ca2+]o and the alkaline transient triggered by antidromic spikes. The alkaline shift was abolished in the absence of extracellular Ca2+. 4. In the absence of postsynaptic receptor antagonists, alkaline transients linked to a given level of synaptic excitation in s. radiatum were strongly suppressed after blockade of somatic (and, consequently, of dendritic "backpropagating") spikes by microdrop application of tetrodotoxin to the cell-body layer. 5. We have previously shown that activity-induced alkaline transients in the CAI region are due to an influx of Ca2+ into neurons, which triggers an influx of H+ ions probably caused by activation of a plasmalemmal Ca2+/H+ ATPase. The present results indicate that much (in s. pyramidale perhaps all) of the pH-changing influx of Ca2+ is mediated by voltage-gated Ca2+ channels.

Action Potentials↗
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↗
PubMed2000

Antifungal activity of Ag(I) and Zn(II) complexes of aminobenzolamide (5-sulfanilylamido-1,3,4-thiadiazole-2-sulfonamide) derivatives.

Aminobenzolamide (5-sulfanilylamido-1,3,4-thiadiazole-2-sulfonamide) is a potent inhibitor of the zinc enzyme carbonic anhydrase (CA, EC 4.2.1.1), being at the same time structurally similar to the antimicrobial sulfonamides. Here we report that the reaction of aminobenzolamide with arylsulfonyl isocyanates affords a series of new arylsulfonylureido derivatives which were subsequently used as ligands (in the form of conjugate bases, as sulfonamide anions) for the preparation of metal complexes containing Ag(I) and Zn(II). All the new compounds proved to be very potent inhibitors of CA (isozymes I, II and IV). The newly synthesized complexes, unlike the free ligands, also act as effective antifungal agents against several Aspergillus and Candida spp., some of them showing activities comparable to ketoconazole, with minimum inhibitory concentrations in the range of 1.8-5 microg/mL. The mechanism of antifungal action of these complexes seem to be unconnected with inhibition of lanosterol-14-alpha-demethylase, since the levels of sterols assessed in the fungi cultures were equal in the absence or in the presence of the tested compounds. Probably the new complexes act as inhibitors of phosphomannose isomerase, a key enzyme in the biosynthesis of yeast cell walls.

Aminobenzoates↗
PubMed1975

[Transmembrane exchange of C1- and HCO3- in erythrocytes: direct action of carbonic anhydrase inhibitors on the transport mechanism].

The only currently recognised role of unsubstituted sulphonamides is their specific inhibition of carbonic anhydrase. The results presented here show that they inhibit the HCO3/Cl- and Cl-/Cl- exchanges across the membrane of the ox erythrocyte. Carbonic anhydrase is not involved in this inhibition which is the result of a direct and specific action on the anion transfer mechanism at membrane level. This newly-recognised role of sulphonamides satisfactorily explains and integrates many experimental results concerning secretory tissues and the interpretation of the action of diuretics.

Animals↗