PubMed Health⌕ Search

Biomedical subjects

D Atlas

Publications and source records attributed to D Atlas.

At least 91 records · Page 5Linked to original sources
PubMed1978

Localization of beta receptors in the anterior segment of the rat eye by a fluorescent analogue of propranolol.

A fluorescent analogue of propranolol, 9-AAP, was injected intravenously in order to detect beta-adrenergic receptors in the anterior segment of the albino rat eye. Specific 9-AAP fluorescence was noted along cell membranes of the ciliary epithelium and to lesser extent in the walls of blood vessels in the ciliary processes and episclera at the limbus. The iris showed maximum 9-AAP binding in the region of the sphincter muscle. These data suggest that 9-AAP may label beta receptors in the anterior segment of the rat eye.

Adrenergic beta-Antagonists↗
PubMed1978

Heavy water effects on leaky heart muscle cells and actomyosin.

Heavy water inhibition of skeletal muscle contraction in barnacle and frog is thought to occur through inhibition of Ca release by SR. If this were so, D2O might be useful for studies on control of the inotropic state in mammalian myocardium. We therefore compared selected properties of mechanically disaggregated leaky myocardial fragments, and actomyosin, in D2O and H2O. At equal values of electrode-determined acidity the contraction frequency, initial velocity of 45Ca uptake, and equilibrium (Ca)i/(Ca)o of the myocardial fragments were all less when heavy water was used. For each of these parameters, and for actomyosin superprecipitation, the H2O and D2O acidity-response curves were similar but the D2O curve was shifted to the right. The actomyosin sedimentation rate was less in D2O than in H2O at near neutral acidity but not different under more acidic or basic conditions. Actomyosin ATPase showed an acidity-dependent increased activity in D2O. These results verify that heavy water inhibits contraction in mammalian myocardium, as is the case with invertebrate and frog skeletal muscle. The effect, however, cannot be attributed to inhibition of Ca release from SR.

Actomyosin↗
PubMed1977

Probing of beta-adrenergic receptors by novel fluorescent beta-adrenergic blockers.

The synthesis of two high-affinity fluorescent beta-adrenergic blockers is described: dl-N(1)-[2-hydroxy-3-(1-naphthyloxy)propyl]-N(2)-(9-acridyl)-1,2-propanediamine (9-aminoacridylpropanolol, 9-AAP) and dl-N-[2-hydroxy-3-(1-naphthyloxy)propyl]-N'-dansylethylenediamine (dansyl analogue of propranolol, DAPN). Both 9-AAP and DAPN inhibit competitively the l-epinephrine-dependent adenylate cyclase activity [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1] in turkey erythrocyte membranes without affecting the fluoride-stimulated adenylate cyclase activity. Similarly, 9-AAP and DAPN inhibit in a competitive manner the binding of [(125)I]-iodohydroxybenzylpindolol to these beta-adrenergic receptors. The two fluorescent beta-adrenergic blockers 9-AAP and DAPN probe specifically beta-adrenergic receptors in the central nervous system as well as in other organs when injected into rats. The fluorescence pattern can be monitored by fluorescence microscopy performed on cryostat slices of these organs. The appearance of the characteristic fluorescence pattern can be blocked in a stereospecific fashion by a prior injection of l-propranolol and not by a prior injection of d-propranolol. These compounds therefore offer a powerful means to map beta-adrenergic receptors in vivo. The stereospecific displacement of 9-AAP from the beta-adrenergic receptors of turkey erythrocyte membranes by l-propranolol and by l-epinephrine can be detected in vitro using front-face fluorescence. The potential use of these compounds to probe beta-receptors in vitro and in vivo is discussed.

Adenylyl Cyclase Inhibitors↗
PubMed1977

beta-Adrenergic receptors in rat kidney: direct localization by a fluorescent beta-blocker.

A new fluorescent beta-adrenergic blocker, 9-amino-acridin propranolol (9-AAP), was administered intravenously to albino rats. Fluorescent aggregates of 9-AAP binding sites were concentrated in the vascular poles of the glomeruli in association with the preglomerular afferent arterioles. 9-AAP fluorescence was reduced following pretreatment with (+/-)- and (-)-propranolol and was less affected in rats pretreated by the (+)-racemic isomer. 9-AAP binding sites were also observed on the lining epithelium of the renal collecting system. Our data suggest that 9-AAP may label beta-adrenergic receptors in rat kidney.

Adrenergic beta-Antagonists↗
PubMed1976

Beta-adrenergic receptors in rat myocardium: direct detection by a new fluorescent beta-blocker.

A new fluorescent beta-blocker, 9-amino-acridin propranolol (9-AAP), was administered i.v. to rats. Multiple fluorescent 9-AAP binding sites were observed on cardiac muscle cells in frozen sections. Intensity and density of cardiac 9-AAP fluorescence were markedly reduced following pretreatment with (+/-)- and (-)-propranolol but not with (+)-propranolol. Our findings suggest that 9-AAP may label beta-adrenergic receptor sites in rat myocardium.

Acridines↗
PubMed1976

Affinity label for beta-adrenergic receptor in turkey erythrocytes.

The compound N-[2-hydroxy-3-(1-naphthoxy)-propyl]-N'-bromoacetylethylenediamine (NHNP-NBE) was found to label covalently the beta-adrenergic receptor in turkey erythrocytes. The compound inhibits irreversibly 1-epinephrine-dependent adenylate cyclase activity [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1] in the whole turkey erythrocyte as well as in the erythrocyte membranes possessing the beta-receptor. The affinity label blocks, also irreversibly, the specific [3H] propranolol binding, whereas other bromoacetyl compounds tested have no effect on binding, even at high concentrations, which cause enzyme inactivation. 1-Epinephrine and propranolol offer protection against the affinity label in whole turkey erythrocytes as well as in membranes prepared from these cells. The potential usefulness of an irreversible beta-antagonist is discussed.

Adenylyl Cyclase Inhibitors↗