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Biomedical subjects

A Mukherjee

Publications and source records attributed to A Mukherjee.

At least 271 records · Page 15Linked to original sources
PubMed1982

Reserpine-induced supersensitivity and the proliferation of cardiac beta-adrenoceptors.

Chronic reserpine pretreatment resulted in an increase in the basal developed force generated by papillary muscles isolated from the right ventricle of the rabbit. In addition, supersensitivity to the inotropic effects of isoproterenol and a concomitant increase in beta-adrenoceptor number were demonstrated. These results indicate that reserpine-induced supersensitivity is not only associated with alterations at sites beyond the level of receptor activation but also at the level of specific postjuctional membrane receptors.

Adrenergic beta-Agonists↗
PubMed1982

Relationship between beta-adrenergic receptor numbers and physiological responses during experimental canine myocardial ischemia.

In the present study, we evaluated the physiological responsiveness of the increased numbers of beta-adrenergic receptors in ischemic canine myocardium to in vivo stimulation by (-)-isoproterenol and epinephrine. After 1 hour of temporary proximal left anterior descending coronary artery occlusion and during a 15-minute period of reflow, dogs received (1)-isoproterenol intravenously at a rate sufficient to increase their heart rates 20--40 beats/min. Following the infusion of isoproterenol, myocardial tissue was obtained from the LV ischemic and nonischemic regions for measurement of beta-adrenergic receptor numbers, cyclic AMP content, and phosphorylase b to a conversion. beta-Adrenergic receptor numbers were significantly increased in the left ventricular (LV) ischemic tissue. The administration of (-)-isoproterenol was associated with significant increases in cyclic adenosine monophosphate content and phosphorylase b to a conversion in the LV ischemic tissue. Also, the administration of (-)-epinephrine significantly increased the phosphorylase b to a conversion in ischemic tissue over the nonischemic tissue and this conversion was blocked by pretreatment with (+/-)-propranolol. These data suggest that, in this experimental model, the increased numbers of beta-adrenergic receptors in canine LV ischemic tissue are capable of translating physiological responses when they are activated with an appropriate agonist in vivo.

Animals↗
PubMed1982

Evidence for the presence and characterization of angiotensin II receptors in rat anterior pituitary membranes.

Previous work from this laboratory (1) indicates that angiotensin II (AII) can affect release of several anterior pituitary hormones, both in vivo and in vitro. To ascertain whether specific receptors mediate the effects of AII on the anterior pituitary, specific binding as well as the kinetics of [125I] AII binding to rat anterior pituitary membranes were analyzed. Binding of [125I] AII was rapid, reaching equilibrium within 4 min at 37 C. Specific binding was approximately 90%. Increasing concentrations of ligand resulted in saturation of binding, with equilibrium attained at [125I] AII = 2 nM. Scatchard analysis of the data indicated a single class of binding sites, with an equilibrium dissociation constant, Kd = 0.49 nM, and a maximum binding capacity of 40 fmol/mg protein. Specific binding was directly proportional to membrane protein concentration (range 20-240 micrograms protein). Binding was competitively inhibited on an equimolar basis by (Sar1, Ala8) AII (Saralasin), a specific AII receptor antagonist. The decapeptide Angiotensin I was about 10-20-fold less potent in inhibiting specific AII binding. These studies demonstrate and characterize specific receptor sites for AII in the anterior pituitary gland and offer additional evidence for a role of AII in the regulation of anterior pituitary hormone secretion.

Angiotensin II↗
PubMed1982

Assessment of Dharmendra antigen. (V) attempts for purification of specific skin delayed hypersensitivity (DH) inducing antigen (S) from lepromin.

After electrophoresis (in pyrogen-free conditions) of Dharmendra antigen sonicates on agarose gel slides, the components (anionic and cationic) were eluted in pyrogen-free normal saline. On skin testing, it was found that only anionic component produced specific skin DH reactions in tuberculoid leprosy patients. The significance of the observations is discussed.

Antigens↗
PubMed1981

Characterization of alpha 2-adrenergic receptors in human platelets by binding of a radioactive ligand [3H]yohimbine.

[3H]Yohimbine, a potent alpha 2-adrenergic antagonist, was used to label the alpha-adrenergic receptors in membranes isolated from human platelets. Binding of [3H]yohimbine to platelet membranes appears to have all the characteristics of binding to alpha-adrenergic receptors. Binding reached a steady state in 2-3 min at 37 degrees C and was completely reversible upon the addition of excess phentolamine or yohimbine (both at 10(-5) M; t1/2 = 2.37 min). [3H]Yohimbine bound to a single class of noncooperative sites with a dissociation constant of 1.74 nM. At saturation, the total number of binding sites was calculated to be 191 fmol/mg protein. [3H]Yohimbine binding was stereo-specifically inhibited by epinephrine: the (-) isomer was 11-times more potent that the (+) isomer. Catecholamine agonists competed for the occupancy of the [3H]yohimbine-binding sites with an order of potency: clonidine greater than (-)-epinephrine greater than (-)-norepinephrine much greater than (-)-isoproterenol. The potent alpha-adrenergic antagonist, phentolamine, competed for the sites whereas the beta-antagonist, (+/-)-propranolol, was very weak inhibitor. 0.1 mM GTP reduced the binding affinity of the agonists, while producing no change in antagonist-binding affinity. Dopamine and serotonin competed only at very high concentrations. Similarly, muscarinic cholinergic ligands were also poor inhibitors of [3H]yohimbine binding. These results suggest that [3H]yohimbine binding to hunan platelet membranes is specific, rapid, saturable, reversible and, therefore, can be successfully used to label alpha 2-adrenergic receptors.

Adrenergic alpha-Agonists↗
PubMed1981

Metabolism of sitosterol by a Pseudomonas species.

Fermentation of sitosterol by a Pseudomonas species (SK-25) resulted in the formation of 5-stigmastene-3 beta, 7 alpha-diol; 5,6 alpha-epoxy-5 alpha-stigmastan-3 beta-ol; 5,6 beta-epoxy-5 beta-stigmastan-3 beta-ol and 5 alpha-stigmastan-3 beta, 5,6 beta-triol. The metabolites were characterized by a variety of conventional chemical and spectrometric techniques.

Chemical Phenomena↗
PubMed1981

Agonist specific effects of guanine nucleotides on muscarinic cholinergic receptors in rat anterior pituitary membranes.

The effects of guanine nucleotides on the binding affinity of muscarinic cholinergic receptors for muscarinic agents were studied in rat anterior pituitary membranes using direct ligand binding methods with [3H]quinuclidinyl benzylate, GTP and Gpp(NH)p at a concentration of 0.1 mM markedly decreased the binding affinity of the agonist, oxotremorine, for the receptors but had no effect on the binding of the antagonist, atropine. Mg2+ (1 mM) on the other had markedly increased the binding affinity of oxotremorine but not that of atropine. Thus, it is conceivable that the release of the growth hormone or the inhibition of prolactin release by acetylcholine, which we and others have previously shown, is modulated by the opposite actions of guanine nucleotides and divalent metal ions such as Mg2+.

Animals↗
PubMed1981

Glycoprotein synthesis in colonic epithelial cells from rats.

Viable colonic epithelial cells from rats were isolated by a non-enzymatic procedure using EDTA. The isolated cells were fractionated by sedimentation through at 15% to 35% discontinuous Ficoll gradient to yield cells differing in proliferative capacity from three different density regions of the gradient. Glycoprotein synthesis of these fractionated cells was examined in terms of their ability to absorb and incorporate labeled glucosamine and fucose into trichloracetic acid precipitable material. Glycoprotein synthesis was highest among cells with intermediate densities, banding in the middle of the gradient (Fraction II). Cytomorphological examination showed that these cells were predominantly goblet type.

Animals↗
PubMed1981

Effect of reserpine on Mg++-induced calcium fluxes and reactivity of the rat aorta.

The effect of reserpine on 45Ca++ fluxes and reactivity of the rat aorta in Mg++-free and Mg++ (1.2 or 3.6 mM) media to various agonists was examined to gain further insight into mechanism(s) responsible for the altered sensitivities in vascular smooth muscle. Incubation of rat aorta in Mg++-free and high Mg++ (3.6 mM) media containing ethylene diamine tetra-acetic acid (EDTA 0.03 mM), respectively, increased and decreased the sensitivity to noradrenaline (NA), 5-hydroxytryptamine (5-HT) and KCl. Mg++-free medium significantly enhanced maximal response to 5-HT whereas high Mg++ (3.6 mM) medium reduced the maximal responses to KCl and 5-HT but not to NA. Mg++-free medium had no effect on 45Ca++ uptake, while it enhanced 45Ca++ efflux from the aorta. Reserpine treatment induced supersensitivity in the aorta to KCl, but not to either NA or 5-HT in normal medium, whereas in Mg++-free medium, it induced partial contraction and inhibited both maximal responses and sensitivity to NA and 5-HT but not to KCl. Reserpine in high Mg++ (3.6 mM) medium had no effect on sensitivity and maximal responsiveness to all these agents. Reserpine reduced 45Ca++ uptake by aorta in either Mg++-free or normal Mg++ medium and it reduced 45Ca++ efflux for aorta in Mg++-free but not in normal Mg++ medium. These observations suggest that reserpine may promote membrane permeability rather nonspecifically to divalent ions. However, the presence of EDTA in the media may have partially reduced the antagonistic effects of Mg++ due to reserpine treatment in this tissue.

Animals↗