Biomedical subjects

S D Levine

Publications and source records attributed to S D Levine.

At least 55 records · Page 3Linked to original sources

PubMed1977

Synthesis of steroidal [16alpha,17-b][1,4]dioxanes.

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Dioxanes↗

PubMed1977

Urea transport in the dogfish kidney.

There is increasing evidence that urea movement across many epithelia involves more than passive diffusion. Of particular interest is the observation that urea transport across the erythrocyte membrane and across the vasopressin-stimulated urinary bladder of the toad occurs by facilitated diffusion, and can be selectively inhibited by phloretin and chromate. These inhibitory agents have been employed in studies of renal urea reabsorption by the spiny dogfish Squalus acanthias. Both agents inhibit urea reabsorption; the effect of chromate is of particular interest, since it blocks urea reabsorption to a proportionately greater extent than sodium reabsorption, and does so irreversibly.

Animals↗

PubMed1977

Relationship of aggregated intramembranous particles to water permeability in vasopressin-treated toad urinary bladder.

It has been previously demonstrated with freeze-fracture electron microscopy that vasopressin induces specific structural alterations of the luminal membrane of granular cells from toad urinary bladder in a dose-dependent fashion. These alterations consist of aggregated intramembranous particles and are observed both in the presence and absence of an osmotic gradient. We examined the effect of methohexital, a selective inhibitor of vasopressin-stimulated water flow, and the effect of phloretin, a selective inhibitor of urea permeability, on the structure of the granular cell luminal membrane. Methohexital treatment of the vasopressin-stimulated toad bladder reduced both the osmotic water flow and vasopressin-induced alterations of membrane structure to the same extent. Phloretin reduced urea permeability but not water flow or particle aggregation. Since neither agent affects vasopressin-stimulated sodium movement, these findings indicate that the phenomenon of particle aggregation is specifically related to vasopressin-induced water permeability and not to changes in urea or sodium permeability.

Animals↗

PubMed1976

Amide transport channels across toad urinary bladder.

Urea and other small amides cross the toad urinary bladder by a vasopressinsensitive pathway which is independent of osmotic water flow. Amide transport has characteristics of facilitated transport: saturation, mutual inhibition between amides, and selective depression by agents such as phloretin. The present studies were designed to distinguish among several types of transport including (1) movement through a fixed selective membrane channel and (2) movement via a mobile carrier. The former would be characterized by co-transport (acceleration of labeled amide flow in the direction of net flow of unlabeled amide), the latter by counter-transport (acceleration of labeled amide flow in the opposite direction). Mucosal to serosal (M leads to S) and serosal to mucosal (S leads to M) permeabilities of labeled amides were determined in paired bladders. Unlabeled methylurea, a particularly potent inhibitor of amide movement, was added to either the M or S bath, while osmotic water flow was eliminated by addition of ethylene glycol and ethanol could not be demonstrated. Methylurea did not alter water permeability or transmembrane electrical resistance. The demonstration of co-transport is consistent with the presence of ADH-sensitive amide-selective channels rather than a mobile carrier.

Acetamides↗

PubMed1976

Vasopressin-stimulated movement of drugs and uric acid across the toad urinary bladder.

Vasopressin is known to increase the permeability of the toad bladder, an analogue of the mammalian collecting duct, to water and hydrophilic solutes such as urea. In the present study, the effect of vasopressin on the permeability of a series of lipophilic compounds, including many commonly used drugs, has been determined. In all cases, permeability increased from 50 to 100%. The response to vasopressin was mediated by cyclic adenosine monophosphate (cAMP), and was generally not altered by phloretin, an agent that inhibits amide movement through the amide transport pathway. Evidence that these compounds move directly through the lipid phase of the membrane was provided in studies of phenobarbital permeability at low and high luminal pH. We would conclude from these studies that the effect of vasopressin on the luminal cell membrane is a widespread one, modifying both lipid components and components involved in amide, sodium and water transport. This may be of importance in the renal tubular reabsorption of many drugs, including barbiturates, glutethimide and antibiotics.

Adenine↗

PubMed1976

Selective inhibition of osmotic water flow by general anesthetics to toad urinary bladder.

Vasopressin increases the permeability of the total urinary bladder, an analogue of the mammalian renal collecting duct, to water and small solutes, especially the amide urea. We have observed that three general anesthetic agents of clinical importance, the gases methoxyflurane and halothane and the ultrashortacting barbiturate methohexital, reversibly inhibit vasopressin-stimulated water flow, but do not depress permeability to urea, or the the lipophilic solute diphenylhydantoin. In contrast to their effects in vasopressin-treated bladders, the anesthetics do not inhibit cyclic AMP-stimulated water flow, consistent with an effect on vasopressin-responsive adenylate cyclase. The selectivity of the anesthetic-induced depression of water flow suggests that separate adenylate cyclases and cyclic AMP pools may exist for control of water and urea permeabilities in to toad bladder. Furthermore, theophylline's usual stimulatory effect on water flow, but not its effect on urea permeability, was entirely abolished in methoxyflurane-treated bladders, suggesting that separate phosphodiesterases that control water and urea permeabilities are present as well. We conclude that the majority of water and urea transport takes place via separate pathways across the rate-limiting luminal membrane of the bladder cell, and that separate vasopressin-responsive cellular pools of cyclic AMP appear to control permeability to water and to urea.

Anesthetics↗

PubMed1975