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S P Banerjee

Publications and source records attributed to S P Banerjee.

At least 37 records · Page 2Linked to original sources
PubMed1981

Adrenergic and cholinergic receptors of cerebral microvessels.

The presence of alpha- and beta-adrenergic and muscarinic cholinergic receptors in cerebral microvessels of the rat and pig was assessed by ligand binding techniques. The results demonstrate the presence of specific binding to alpha 2- and beta-adrenergic receptors but no appreciable specific binding to alpha 1-adrenergic or muscarinic cholinergic receptors. beta-Adrenergic receptors of pig cerebral microvessels are similar to those of the brain and other organs in their binding characteristics to the tritiated ligand and in their stereospecificity of binding to the biologically active isomers of beta-adrenergic agonists. Further evidence derived from the differential potency of binding displacement by the various beta-adrenergic agonists and selective beta 1- and beta 2-adrenergic antagonists indicates that beta-adrenergic receptors of pig cerebral microvessels are mostly of the beta 2-subtype.

Animals↗
PubMed1981

Cerebral compensation for chronic noradrenergic denervation induced by locus ceruleus lesion: recovery of receptor binding, isoproterenol-induced adenylate cyclase activity, and oxidative metabolism.

The long term effects of specific noradrenergic denervation of rat cerebral cortex were considered in parallel studies of in vitro noradrenergic receptor binding and isoproterenol-induced adenosine 3':5'-monophosphate (cycle AMP) generation and of in vivo oxidative metabolism. Noradrenergic denervation was achieved by the local, unilateral injection of 6-hydroxydopamine into the locus ceruleus. Cerebral noradrenaline remained depleted throughout the 8-week duration of the study. Ligand-binding assays showed increased beta-adrenergic receptors 2 weeks after locus ceruleus lesion with recovery occurring by 4 weeks. There were no changes in alpha 1-adrenergic receptors. Isoproterenol-induced cyclic AMP generation increased at 2 weeks after lesion but recovered at 8 weeks. Dual wavelength reflection spectrophotometric measurements of cytochrome oxidase reduction/oxidation and local blood volume shifts, provoked in situ by direct cortical stimulation, also demonstrated abnormalities at 2 weeks with recovery by 4 weeks after lesion. Thus, in vivo and in vitro changes after locus ceruleus lesion are reversible and the time course of these changes is related temporally. These data suggest that cerebral cortex has adaptive capabilities which are activated to compensate for prolonged noradrenaline depletion. We also speculate that there may be a causal relationship between the in vitro and in vivo parameters studied.

Adenylyl Cyclases↗
PubMed1980

Ouabain stimulation of noradrenaline transport in guinea pig heart.

Cardiac glycosides such as ouabain inhibit Na+-dependent high-affinity noradrenaline uptake in sympathetic nerve terminals by interacting with (Na+ + K+)ATPase located in the neuronal membrane. It has been suggested that the augmentation of noradrenaline concentration at the neuromuscular junctions following the inhibition of its uptake may contribute to the ouabain-induced cardiac arrhythmia seen with toxic doses of the drug. Although it is generally accepted that the biochemical basis for the pharmacological response of cardiac glycosides must involve specific interaction of this class of drugs with the cardiac cell membrane Na+, K+-exchange pump, the precise molecular mechanism for the improvement of muscle performance by ouabain is controversial. Many investigators claim that cardiac glycosides increase myocardial force of contraction by inhibiting (Na+ + K+)ATPase. According to this hypothesis, such an inhibition might increase the intracellular concentration of Na+, which may augment the activity of the transmembrane Na+, Ca2+-exchange pump described by several workers. We have found that ouabain stimulates Na+-dependent transport of noradrenaline by guinea pig heart sympathetic nerve terminals.

Animals↗
PubMed1979

Cocaine and D-amphetamine induce changes in central beta-adrenoceptor sensitivity: effects of acute and chronic drug treatment.

The effects of acute and chronic treatment with psychomotor stimulants on specific binding of [3H]dihydroalprenolol to beta-adrenoceptors in rat brain were examined. At a dose of 10 mg/kg both acute and chronic treatment with cocaine and chronic treatment with D-amphetamine (10 mg/kg) caused increased binding of [3H]dihydroalprenolol. The molecular mechanism for this enhanced binding appears to be augmentation of the density of beta-adrenoceptors in rat brain. At a lower dose (5 mg/kg), however, chronic administration of D-amphetamine caused a decrease in the density of beta-adrenoceptors in rat brain. Chronic treatment with either D-amphetamine (10 mg/kg) or cocaine induced a marked increase in the magnitude of cyclic AMP accumulation in rat brain slices elicited by norepinephrine. Acute as well as chronic administration of D-amphetamine in vivo inhibited the temperature-dependent uptake of [3H]norepinephrine in rat brain synaptosomal homogenates, but no such inhibition was observed after chronic or acute treatment with cocaine. The results suggest that psychomotor stimulants induce beta-adrenoceptor supersensitivity which may be involved in the phenomenon of reverse tolerance and possibly psychosis in humans. The development of beta-adrenoceptor supersensitivity does not appear to be mediated through alterations in norepinephrine transport at the presynaptic sites.

Animals↗
PubMed1979

Effect of chronic ethanol treatment on specific [3H]ouabain binding to (Na+ + K+)-ATPase in different areas of cat brain.

Chronic ethanol administration to cats increased specific [3H]ouabain binding by 63% in cerebral cortex, 47% in cerebellum, 84% in amygdala, and 100% in hippocampus when the binding assays were performed in the presence of 160 nM [3H]ouabain. There was no significant change in specific [3H]ouabain binding in hypothalamus, thalamus, corpus striatum, and brain stem following chronic ethanol ingestion. Scatchard analysis revealed that enhancement of specific [3H]ouabain binding following chronic ethanol treatment in some areas of cat brain is primarily due to changes in densities of ouabain binding sites. Since ouabain is a specific inhibitor of (Na+ + K+)-ATPase the present observations suggest that the molecular mechanism for the enhancement of (Na+ + K+)-ATPase activity after chronic ethanol ingestion may be due to increased net rate of synthesis of (Na+ + K+)-ATPase molecules or exposure of non-functional enzyme system following conformational change of plasma membrane.

Alcoholism↗
PubMed1979

Alpha- and beta-adrenergic receptors of the rat salivary gland. Elevation after chemical sympathectomy.

Binding of [3H]dihydroergokryptine and [3H]dihydroalprenolol to membrane preparations from rat submaxillary gland was measured to characterize the alpha- and beta-adrenergic receptors, respectively. Kinetic analysis of the data revealed a high affinity binding site for each radioligand. Inhibition of binding at each site was stereospecific for the active isomer of the catecholamine used. The greater ability of a beta1 than beta2 specific beta-adrenergic antagonist to displace [3H]dihydroalprenolol binding indicated that this binding site was of the beta1 type. Chemical sympathectomy with reserpine or 6-hydroxydopamine resulted in a significant increase in both [3H]dihydroalprenolol and [3H]dihydroergokryptine binding in the rat submaxillary gland. 3scatchard analysis of the data indicated that these increases in binding were due to a change in total number of binding sites for [3H]dihydroergokryptine and [3H]dihydroalprenolol with little change in apparent affinities. This suggests that changes in alpha- and beta-adrenergic receptor density may be important in the development of supersensitivity in salivary glands after reserpine and 6-hydroxydopamine treatment.

Animals↗
PubMed1979

Stimulation of specific [3H]-ouabain binding to microsomal preparations from rat heart and skeletal muscle by thyroid hormones: effects of 6-hydroxydopamine.

1. Surgical thyroidectomy decreased specific [3H]-ouabain binding to heart ventricular microsomes by 43% and gastrocnemius muscle microsomes by 34%. Administration of triiodothyronine to euthyroid rats enhanced specific [3H]-ouabain binding to heart and skeletal muscle membrane by 60% and 33% respectively. 2. Treatment of thyroidectomized rats with triiodothyronine increased specific [3H]-ouabain binding by 44% in skeletal muscle membrane preparation and 428% in cardiac microsomes. 3. Specific [3H]-ouabain binding decreased by 55% in heart and 53% in gastrocnemius muscle preparations following chemical sympathectomy with 6-hydroxydopamine. 4. Treatment with triiodothyronine of euthyroid rats which had been sympathectomized did not significantly alter specific [3H]-ouabain binding to heart or skeletal muscle membrane preparations. 5. Administration of triiodothyronine to thyroidectomized and sympathectomized rats increased specific [3H]-ouabain binding by 80% in heart and 83% in skeletal muscle membrane preparations. 6. These results suggest that triiodothyronine may influence specific [3H]-ouabain binding to thyroid hormone nonresponsive tissue such as sympathetic nerve endings. Therefore, the present observations are incompatible with the hypothesis that induction of (Na+ +K+)-adenosine triphosphatase of skeletal muscle membrane is the molecular mechanism for the calorigenic actions of thyroid hormones.

Animals↗
PubMed1978

alpha-adrenergic receptor in rat heart. Effects of thyroidectomy.

The effects of thyroid status on alpha-adrenergic receptors in the rat myocardium were investigated. The potent antagonist [3H]dihydroergokryptine was used to identify alpha-adrenergic receptors in rat heart particulate and sarcolemmal fractions. Administration of triiodothyronine to thyroidectomized rats decreased specific binding to alpha-adrenergic receptors in heart particulate and sarcolemmal fractions by 41% and 45%, respectively. Scatchard analysis revealed that the cardiac sarcolemmal fraction from thyroidectomized rats contained 29.3 fmol/mg of protein, as compared with 17.0 fmol/mg of protein found in the heart preparation of thyroidectomized rats treated with triiodothyronine. The equilibrium dissociation constants for the interaction of receptors with dihydroergokryptine were similar (about 1.5 nM) in the heart sarcolemmal fractions derived from these two groups of rats. The results of this study demonstrate that thyroid hormone can regulate the number of cardiac alpha-adrenergic receptors. In addition, there appears to be a reciprocal relationship between alpha-adrenergic and beta-adrenergic receptors in the rat myocardium.

Animals↗
PubMed1978

beta-Adrenergic receptors in rat skeletal muscle. Effects of thyroidectomy.

Thyroid hormones may participate in the regulation of beta-adrenergic receptors in skeletal muscle sarcolemmal membrane. Since skeletal muscles are not innervated by sympathetic nerve endings, the biochemical mechanism involved in the control of beta-adrenergic receptors by thyroid hormones appears to be mediated by thyroid-induced regulation of serum levels of catecholamines.

Alprenolol↗
PubMed1978

[3H]-Ouabain binding to peripheral organs of cats: effect of ethanol.

1 The specific [3H]-ouabain binding to microsomal fractions derived from cat heart, liver, spleen, and kidney increased significantly following chronic administration of ethanol. 2 Since ouabain binds exclusively to cell membrane (Na+ + K+)-adenosine triphosphatase ((Na+ + K+)-ATPase), these results provide evidence for an increase in number of (Na+ + K+)-ATPase macromolecules during chronic alcoholism. 3 The importance of the increase in number of (Na+ + K+)-ATPase molecules in the adaptive increase in ethanol metabolism and cardiac myopathy in chronic alcoholism is discussed.

Adenosine Triphosphatases↗