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Biomedical subjects

O Hechter

Publications and source records attributed to O Hechter.

At least 55 records · Page 3Linked to original sources
PubMed1970

[8-Arginine]-vasopressinoic acid: an inhibitor of rabbit kidney adenyl cyclase.

Neurohypophyseal hormnones and several synthetic analogs stimulate adenyl cyclase prepared from rabbit kidney medullary tissue. [8-Arginine]-vasopressinoic acid inhibits the stimulation of medullary adenyl cyclase by neurohypophyseal peptides but does not influence the action of parathyroid hormone on adenyl cyclase from kidiney cortex.

Adenylyl Cyclase Inhibitors↗
PubMed1970

Glucocorticoid regulation of ACTH sensitivity of adenyl cyclase in rat fat cell membranes.

Plasma membrane sacs of isolated rat fat cells (ghots) possess an adenyl cyclase system, which is activated by lipolytic hormones of disparate molecular structure, including adrenocorticotropin (ACTH), glucagon, and epinephrine. Previous studies indicated that distinctive selectivity units for individual hormones are coupled to the same unit of adenyl cyclase in the fat cell membrane. The present study has shown that ghost cyclase from adrenalectomized and hypophysectomized rats exhibits a striking reduction in response to ACTH, the stimulatory effects of epinephrine, glucagon, or fluoride being unchanged. Pretreatment of adrenalectomized, hypophysectomized, sham operated, or intact rats with the synthetic glucocorticoid, dexamethasone, selectively increased the ACTH response in ghost cyclase preparations. Cortisol, like dexamethasone, increased the ACTH response in ghosts from adrenalectomized rats; 11-deoxycorticosterone was ineffective. The dexamethasone effect to enhance the ACTH response is blocked by actinomycin D or cycloheximide. The present results show that stimulation of rat fat cell adenyl cyclase by ACTH involves a distinctive molecular entity, which can be clearly differentiated from adenyl cyclase in the membrane as well as from the selectivity sites for epinephrine and glucagon. The data indicate that the biosynthesis of the component required for ACTH stimulation of ghost cyclase-either an ACTH selectivity unit or specific coupling factor-is induced by glucocorticoids at the level of gene regulation.

Adenine Nucleotides↗
PubMed1970

Neurohypophyseal hormone-sensitive adenyl cyclase of toad urinary bladder.

An adenyl cyclase preparation derived from epithelial cells of the urinary bladder of the toad, Bufo marinus, is described. This cyclase preparation is specifically stimulated by neurohypophyseal hormones and various synthetic analogs which evoke a hydroosmotic response in the intact bladder. The relative stimulatory effects of these compounds have been compared on the cyclase preparation and in the intact bladder. The peptide concentrations required for half-maximal stimulation (affinity) in the cell-free and intact systems were parallel; however the magnitude of stimulation produced by saturating concentrations of peptides did not correlate. Furthermore, it was found that peptide analogs which inhibit the hydroosmotic effect of [8-arginine]-vasopressin on the intact bladder also inhibit the stimulation of the toad bladder cyclase preparation by vasopressin. Prostaglandin E(1), mercaptans, and disulfides, which inhibit the hormone-induced hydroosmotic response of the intact bladder, did not antagonize the stimulation of the toad bladder cyclase preparation by vasopressin.

Adenylyl Cyclases↗
PubMed1969

Adenyl cyclase and hormone action. I. Effects of adrenocorticotropic hormone, glucagon, and epinephrine on the plasma membrane of rat fat cells.

A large number of hormones, of diverse molecular structure, evoke characteristic responses in target cells via the intermediary 3',5'-AMP, the specificity of hormone action upon cell type being achieved by selective stimulation of adenyl cyclase. In the fat cells of rat adipose tissue, adenyl cyclase is stimulated by a number of hormones of disparate molecular structure, posing the question whether this cell type posesses multiple cyclase systems with distinctive specificities for individual hormones, or a single cyclase with broad specificity to a variety of hormones. Studies of the stimulatory effects of adenocorticotropin, glucagon, and epinephrine upon the adenyl cyclase of the rat fat cell "ghosts" (plasma membrane sacs) have shown that distinctive selectivity sites for each of these hormones can be differentiated. The beta-adrenergic blocking agent Kö 592 abolished the stimulatory effect of epinephrine without influencing adenocorticotropin or glucagon; Ca was required for adenocorticotropin action, but not for glucagon or epinephrine. Dose-response curves show that the affinity of hormones to the cyclase system was in the order: glucagon > adenocorticotropin >> epinephrine; the magnitude of cyclase activation by maximal doses of hormones had a reversed order. Combinations of maximal doses of hormones failed to produce additive stimulation. The results show that in the membrane of the fat cell a single catalytic unit of adenyl cyclase is coupled to distinctive selectivity sites for three lipolytic hormones.

Adenylyl Cyclases↗