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T Yorio

Publications and source records attributed to T Yorio.

At least 73 records · Page 4Linked to original sources
PubMed1987

Aerobic and anaerobic metabolism of bovine ciliary process: effects of metabolic and transport inhibitors.

In the present study we have measured the oxygen consumption and lactic acid production, under aerobic and anaerobic conditions, in the bovine ciliary process epithelium (CPE) in the presence and absence of transport modifiers. Basal oxygen consumption was 8-15 microliters O2 consumed/mg protein/hr and decreased by 35% when sodium was removed or ouabain was added to the media. Anaerobic metabolism as measured by lactate production was also attenuated by sodium-free or ouabain treatment. When O2 consumption was severely limited by cyanide, lactic acid production increased significantly ("Pasteur effect"), whereas 2-deoxyglucose reduced lactate formation. Both chloride-free and acetazolamide treated CPE increased their dependency on aerobic glycolysis, and this response was also observed under anaerobic conditions, suggesting the presence of an anion transport mechanism. A net lactate production was also found to occur across the aqueous epithelium under aerobic and anaerobic conditions. These results are consistent with the presence of a bicarbonate-sensitive anion transport system located in the ciliary process epithelium.

Adenylyl Cyclases↗
PubMed1986

Inhibition of the antidiuretic hormone hydroosmotic response by phospholipids and phospholipid metabolites.

Phospholipid metabolities and phospholipids containing arachidonic acid (AA) inhibited the antidiuretic hormone (ADH)-induced increase in transepithelial water flow in the toad urinary bladder, but had no effect on basal water flow when added to the serosal bathing solution. Other fatty acid-substituted phospholipid metabolites had no effect on osmotic water movement in the presence or absence of ADH. Indomethacin attenuated the inhibitory effects of the AA containing phospholipid metabolities (PMAA), suggesting that the PMAA response required AA release and prostaglandin (PG) formation. PMAA increased PGE formation as measured by radioimmunoassay. PG have been reported to inhibit ADH-stimulated water flow by inhibiting adenylcyclase. PGE2 (10(-8) M) had no effect on cyclic AMP-stimulated water flow, whereas exogenous AA and PMAA attenuated the hydroosmotic response to added cyclic AMP. Indomethacin only partially reversed the inhibition by AA of the cyclic AMP-associated water movement, suggesting that the inhibition by AA and PMAA may involve other metabolites of AA than PG. PG and the AA cascade have been implicated as cellular modulators of the ADH hydroosmotic response. The present results offer additional support to the theory that this system may regulate the intracellular events that are transduced following receptor activation by ADH.

Animals↗
PubMed1985

Calcium/phospholipid-dependent protein kinase and its relationship to antidiuretic hormone in toad urinary bladder epithelium.

The hydro-osmotic response of the toad urinary bladder to antidiuretic hormone (ADH) and cyclic AMP was inhibited by phorbol myristate acetate (PMA) and 4 beta- phorbol dideconate (4 beta-PDD), activators of protein kinase C (PKC). The inactive epimer of 4 beta-PDD, had no effect on the ADH response. The osmotic transfer of water in the absence of ADH was unaffected by PMA. PKC activity, localized in the soluble fraction of isolated toad bladder cells, was activated by PMA. ADH initially inhibited and subsequently stimulated 32Pi incorporation into phosphatidic acid (PA) and phosphatidylinositol (PI). Carbachol, which inhibits ADH-induced water flow, also stimulated 32P incorporation into PA and PI. It is suggested that phosphoinositide breakdown to diacylglycerol may activate PKC which functions to attenuate the hormone-mediated permeability response.

Animals↗
PubMed1985

Inhibition of the hydro-osmotic response to vasopressin and hypertonicity by phenothiazines and W7, calmodulin antagonists.

Phenothiazines and W7, calmodulin antagonists, inhibit the water flow response produced by ADH, exogenous cyclic AMP, phosphodiesterase inhibition and serosal hypertonicity. Calmodulin antagonists had no effect on osmotic water movement in the absence of hormone. Calmodulin was isolated and localized by immunofluorescence in bladder epithelial cells. Phenothiazines inhibited toad bladder calmodulin activation of phosphodiesterase and prevented fluorescent antibody recognition. The results suggest that the calcium-calmodulin process plays a role in the hydro-osmotic response to ADH and that produced by serosal hypertonicity. The calmodulin common site occurs subsequent to cyclic AMP formation, perhaps on the microtubule-microfilament system.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1985

Alteration of membrane permeability by amphotericin B.

Amphotericin B (AmB) increased unidirectional Na transport and net transcellular sodium movements across the skin of the frog, Rana pipiens, when added to the solution bathing the corium side, but not from the outer epidermal surface. The AmB response was prevented with pretreatment with amiloride, ouabain and mucosal sodium substitution. Alteration in pH markedly reduced the permeability changes induced by AmB. AmB did not interfere with the increase in sodium transport induced by antidiuretic hormone. The present study demonstrates that AmB interacts with the skin of the frog, Rana pipiens, from the corium side specifically increasing transepithelial sodium transport. The increase in transport apparently occurs through the existing sodium pathway.

Amphotericin B↗
PubMed1985

Effects of antiglaucoma drugs on [32P]orthophosphate incorporation into phospholipids of cat iris and ciliary process.

The effects of antiglaucoma drugs on [32P]-orthophosphate incorporation into phospholipids of iris and ciliary process were investigated. Both iris and ciliary process rapidly incorporated 32Pi into the major phospholipids, with the acidic phosphoinositides demonstrating a greater labelling than phosphatidylcholine, indicating a greater turnover. The muscarinic agonists, carbachol and pilocarpine, stimulated 32Pi-labelling of phosphatidylinositol (PI) and phosphatidic acid (PA) in both iris and ciliary process. These effects were blocked by atropine, suggesting that the response was mediated through muscarinic receptors. The beta blocking ocular hypotensive drugs, propranolol, timolol and atenolol, produced varying effects on 32P incorporation into phospholipids of iris and ciliary process. Propranolol stimulated 32Pi-labelling into phosphatidylinositol 4', 5' bisphosphate (PIP2), phosphatidylinositol 4' phosphate (PIP), PI and PA. Timolol decreased 32Pi-incorporation into PIP2 and PI, whereas atenolol, a selective beta 1 antagonist, had no significant effect on 32Pi-labelling of phospholipids. The above findings on propranolol agree with previous observations which demonstrated that propranolol redirects glycerolipid metabolism through multiple effects on the enzymes in phospholipid biosynthesis, particularly in stimulating phosphatidylinositol kinases. The results with timolol suggest that this drug may decrease phosphoinositide hydrolysis. The effects of these ocular hypotensive, non-selective beta blocking drugs on phospholipid turnover may ultimately limit the accumulation of breakdown products which could serve as cellular messengers.

Animals↗
PubMed1985

Cellular mechanisms in the actions of antiglaucoma drugs.

There are several classes of drugs currently in use for the therapeutic management of the glaucomas. Although the ocular hypotensive effects of these agents have been well characterized and described, little is known of their site of action and cellular mechanism. This review attempts to describe those cellular mechanisms that may be linked to the actions of several classes of antiglaucoma drugs. Special emphasis was placed on drug actions and 1) the adenylate cyclase system; 2) receptor-coupled phosphoinositide turnover; 3) prostaglandins and 4) ion transport processes. Models are presented depicting proposed cellular sites of the interaction of the antiglaucoma drugs with these cellular processes.

Adenylyl Cyclases↗
PubMed1983

Fluoride-induced changes in renal papillary cyclic-AMP.

Studies were conducted which examined urinary excretion and papillary production of cyclic-AMP in the rat following vasopressin (ADH) stimulation in the presence or absence of inorganic fluoride ion (F). In one set of experiments, six anesthetized Fischer 344 rats were administered 5 munits arginine vasopressin during iv saline and sodium fluoride (NaF) infusions. Urinary cyclic-AMP concentration was unchanged by ADH but declined during NaF infusion, while urinary cyclic-AMP excretion rate was unchanged by ADH or ADH/NaF. In a second set of experiments, 30 rats were divided into six groups of 5 each, and renal papilla and cortex were analyzed for cyclic-AMP. Group I was decapitated and not otherwise surgically manipulated. A second group had iv saline for 90 min while a third group had iv saline and ADH. A fourth group had isotonic NaF iv for 90 min and a fifth group had NaF and ADH. The results indicate that papillary cyclic-AMP is significantly increased by both ADH and NaF doses which did not cause changes in urinary cyclic-AMP excretion rates. We conclude from these experiments that determination of urinary cyclic-AMP concentration is not the best measure of vasopressin action and that tubular sensitivity to the hormone in the presence of F was better demonstrated by changes in papillary cyclic-AMP concentration. Further, it appears that the site of the biochemical renal lesion caused by F is at a site beyond the generation of cyclic-AMP.

Animals↗
PubMed1983

Role of calcium and prostaglandins in the antidiuretic hormone response. Effect of ionophore A23187.

The calcium ionophore A23187 (IP) inhibited the antidiuretic hormone (ADH)-stimulated hydro-osmotic response in toad urinary bladder but had no effect on the osmotic transfer of water in the absence of hormone. Extracellular calcium was necessary for this effect at lower but not at higher IP concentrations. The hydro-osmotic response to exogenous cyclic AMP was unaltered by IP, but the same response produced by inhibition of phosphodiesterase was reduced significantly. Cyclic AMP concentrations in isolated toad bladder epithelial cells were reduced by 50% with IP or exogenous prostaglandin E2 (PGE2). Indomethacin, a prostaglandin synthesis inhibitor, prevented the inhibitory actions of the IP on the ADH-mediated response. Collectively, these observations suggest a key role for cellular calcium in modulating the actions of antidiuretic hormone and are consistent with the hypothesis that the ionophore, through increasing intracellular calcium, stimulates the synthesis of prostaglandins which have a negative feedback on adenylcyclase. This effect would terminate the action of the hormone.

Animals↗
PubMed1983

Alteration in membrane permeability by diacylglycerol and phosphatidylcholine containing arachidonic acid.

The phospholipid metabolites, stearoylarachidonylglycerol and diarachidonylglycerol, stimulate transepithelial sodium transport in frog skin epithelium. The increase in Na transport is due to an increase in the unidirectional influx of sodium, is amiloride sensitive and is prevented with pretreatment with indomethacin, mefanamic acid and phospholipase inhibitor, mepacrine. The data suggest a possible role of phospholipid metabolism and prostaglandin biosynthesis in the regulation of transepithelial ion transport.

Amiloride↗
PubMed1983

Alteration in surface substructure of frog urinary bladder by calcium ionophore, verapamil and antidiuretic hormone.

The calcium antagonist verapamil and the calcium ionophore A23187 have been shown to inhibit the hydro-osmotic actions of antidiuretic hormone (ADH) presumably by different mechanisms. Presently, urinary bladders of the frog (Rana pipiens) were examined under SEM following exposure to calcium ionophore A23187, verapamil and ADH in the presence and absence of an osmotic gradient. Cells exposed to ADH show marked changes in surface substructure which is accompanied by an expansion of microridges, cell borders and the appearance of microvilli in the granular cells. The microvilli are pronounced and appear at the junction of microridges. In the presence of an osmotic gradient, ADH induces granular cell swelling and some cells show a blistering effect. Calcium ionophore, in the absence of an osmotic gradient, induced pronounced morphological changes in the granular cells, where the microvilli become prominently visible as 'finger-like' projections. This effect may be due to the action of calcium in promoting elongation of microtubules. Cells exposed to ionophore plus ADH are indistinguishable from ionophore alone. The most apparent effect of verapamil on surface substructure was on the elevation of the mitochondrial-rich cells above the surrounding granular cells. These cells show some degree of separation from the granular cells and are accentuated in tissues exposed to verapamil plus ADH. The present observations suggest that these agents, verapamil and calcium ionophore, have marked effects on cellular morphology. These actions are mediated through alterations in calcium movements and reflect the relative importance of cellular calcium in transepithelial water flow and the actions of antidiuretic hormone.

Animals↗
PubMed1981

Fluoride inhibition of the hydro-osmotic response of the toad urinary bladder to antidiuretic hormone.

The hydro-osmotic response of the toad bladder to antidiuretic hormone and cyclic AMP was inhibited by the methoxyflurane metabolite, fluoride. The osmotic transfer of water in the absence of hormone was unaffected by fluoride as was the hydroosmotic response due to hypertonicity of the serosal bathing media. Osmotic water movements across N-ethylmaleimide-"fixed" vasopressin or cyclic AMP-stimulated bladders were likewise unchanged by fluoride, suggesting that fluoride is exerting an action subsequent to the endogenous formation of cyclic AMP but before the final effector mechanism. Fluoride increased intracellular cyclic AMP concentrations even in the presence of added hormone. Fluoride suppressed calmodulin activity and prevented its activation of phosphodiesterase. Fluoride had no effect on oxygen consumption of toad urinary bladder cells but reduced lactate formation and anerobic metabolism. This decrease in the glycolytic energy source did not contribute to the inhibition of the hormonal response since 2-deoxyglucose was without effect on hormonal mediated osmotic-water flow. It is postulated that the fluoride-induced polyuria after methoxyflurane anesthesia may be due in part to the ability of fluoride to interfere with calcium and calmodulin-initiated processes (other than phosphodiesterase activity) that may occur in the stimulus-reabsorption coupling response of antidiuretic hormone.

Aerobiosis↗
PubMed1979

Aerobic and anaerobic metabolism of the crystalline lens of a poikilotherm; the toad Bufo marinus.

1. The O2 consumption and lactic acid production of the lens of the toad Bufo marinus was measured under various conditions. The energy consumption was very low compared to other amphibian tissues and about 20% of that previously described in the rat lens. About 80% was derived from oxidative metabolism, which is the converse of that seen in mammals. 2. Cyanide abolished O2 consumption and increased lactate production 20-30 times ("Pasteur effect"). 3. Under aerobic conditions about 40% of the energy requirements of the lens are related to the presence of Na in the bathing-media but this was not seen in the presence of CN. 4. Oxidative metabolism was predominant in the outer cortical regions of the lens while glycolysis persisted even in the central nucleus. The energetic requirements of this region were, however, only about 10% of those in the intact lens. 5. Lactate readily leaves the lens and passes into its bathing fluids, and at high rates of glycolysis this occurs more readily across the posterior surface. 6. The results are discussed in relation to the unique physiological needs, structure and situation of the lens.

Aerobiosis↗
PubMed1978

The permeability of the skin of the aquatic anuran Xenopus laevis (Pipidae).

The undirectional transcutaneous fluxes of Na, Cl, water and urea were measured, in vitro, in the pipoid anuran Xenopus laevis. An active uptake (outside to inside) of Na was observed but Cl movements appeared to be passive. The effluxes of Na and Cl were low compared to those measured in other species of amphibians. The active Na transport was less than that of more terrestrial species and, although it could be stimulated by vasotocin, aldosterone was ineffective. The permeability of the skin to water was also low and although it was increased in the presence of vasotocin the magnitude of the response was much less than seen in more terrestrial anurans. The skin was permeable to urea but the movement of this solute was not remarkable when compared to that in other amphibians. These properties of the skin are discussed in relation to the animal's aquatic manner of life.

Animals↗
PubMed1978

Stimulation of the short-circuit current (sodium transport) across the skin of the frog (Rana pipiens) by corticosteroids: structure-activity relationships.

Aldosterone, at a concentration of 10(-8)mol/1, increases the short-circuit current (scc, a measure of active sodium transport) across the skin of the frog (Rana pipiens). The other natural amphibian corticosteroid hormone, corticosterone, is about 100 times less potent. The structure-activity relationships of a number of corticosteroids were studied with respect to this response. An 11 beta-hydroxyl group was essential, whereas unsaturation at the C-1 to C-2 positions abolished activity. A 17-hydroxyl group did not enhance the response. Fluorination at the 9 alpha-position increased the affinity of the steroid for the receptor. Synthetic corticosteroids which have a high ratio of glucocorticoid : mineralocorticoid action can increase the scc and one of these, dexamethasone, was even more potent than aldosterone. A methyl group at C-16 appeared to be an important constituent for this response but it had to be in the alpha-position. The effects of both aldosterone and dexamethasone were inhibited by spironolactone. The results are discussed in relation to the nature of the response and to corticosteroid receptors in the skin of amphibians.

Adrenal Cortex Hormones↗