scholarly journals Adrenergic and Cholinergic Receptors of Cerebral Microvessels

1981 ◽  
Vol 1 (3) ◽  
pp. 329-338 ◽  
Author(s):  
Sami I. Harik ◽  
Virendra K. Sharma ◽  
John R. Wetherbee ◽  
Robert H. Warren ◽  
Shailesh P. Banerjee
Keyword(s):  
Adrenergic Receptors ◽  
Specific Binding ◽  
Cholinergic Receptors ◽  
Biologically Active ◽  
Adrenergic Agonists ◽  
Muscarinic Cholinergic Receptors ◽  
Cerebral Microvessels ◽  
Binding Characteristics ◽  
Muscarinic Cholinergic ◽  
Β Adrenergic Receptors

The presence of α- and β-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 α2- and β-adrenergic receptors but no appreciable specific binding to α1-adrenergic or muscarinic cholinergic receptors. β-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 β-adrenergic agonists. Further evidence derived from the differential potency of binding displacement by the various β-adrenergic agonists and selective β1- and β2-adrenergic antagonists indicates that β-adrenergic receptors of pig cerebral microvessels are mostly of the β2-subtype.

Contraction and [3H]QNB binding in collagenase isolated fundic smooth muscle cells

1983 ◽  
Vol 245 (2) ◽  
pp. G270-G276
Author(s):  
E. R. Seidel ◽  
L. R. Johnson
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Cholinergic Receptor ◽  
Gastric Fundus ◽  
Cholinergic Receptors ◽  
Muscarinic Agonists ◽  
Muscarinic Cholinergic Receptors ◽  
Binding Characteristics ◽  
Muscarinic Cholinergic

Smooth muscle cells from the guinea pig gastric fundus were isolated by successive collagenase digestions. Tritiated quinuclidinyl benzilate [( 3H]QNB) was used to study the binding characteristics of the muscarinic cholinergic receptors on these cells. Each cell bound 8.3 X 10(-19) mol of QNB, and a concentration of QNB of 0.19 nM was required to label one-half of the binding sites. This suggests a concentration of about 500,000 muscarinic cholinergic receptors per smooth muscle cell. The muscarinic cholinergic receptor antagonists atropine and scopolamine inhibited QNB binding with a 50% inhibiting concentration (IC50) in the nanomolar range, whereas the agonists acetylcholine (ACh), oxotremorine, and carbamylcholine had IC50S in the micromolar range. Hill coefficients (nH) for antagonists approached unity, but agonists displayed fractional nH. Exposure of cells to cholinergic muscarinic agonists resulted in dose-dependent decreases in cell length. The concentration of agonist required to induce half-maximal contractions (ED50) was 8.3 X 10(-12) M for ACh and 6.3 X 10(-13) M for oxotremorine. Atropine (10(-9) M) decreased the sensitivity to ACh, increasing the ED50 for ACh-induced contractions to 1.2 X 10(-10) M. These results suggest the existence of muscarinic receptor heterogeneity for cholinergic agonists but not for antagonists.

Isolated parietal cells: [3H]QNB binding to putative cholinergic receptors

1980 ◽  
Vol 239 (3) ◽  
pp. G204-G209
Author(s):  
R. Ecknauer ◽  
W. J. Thompson ◽  
L. R. Johnson ◽  
G. C. Rosenfeld
Keyword(s):  
Specific Binding ◽  
Cholinergic Receptors ◽  
Parietal Cells ◽  
Cholinergic Antagonists ◽  
Single Population ◽  
Muscarinic Cholinergic Receptors ◽  
Cholinergic Antagonist ◽  
Muscarinic Cholinergic ◽  
Quinuclidinyl Benzilate

The tritiated muscarinic cholinergic antagonist quinuclidinyl benzilate, [3H]QNB, was used as a direct probe for the detection and characterization of muscarinic cholinergic receptors associated with the particulate fraction of isolated and purified rat gastric muscosal parietal cells. Specific binding is saturable (Bmax = 55 fmol/mg protein, KD = 0.78 nM), shows a single population of binding sites, and has appropriate pharmacological specificity. Nanomolar concentrations of muscarinic cholinergic antagonists, such as atropine and scopolamine, inhibit [3H]QNB binding by 50%, whereas micromolar concentrations are needed for agonists, such as acetylcholine, oxotremorine, and carbamylcholine. Binding is also stereoselective as shown by the more than 1,000-fold difference in inhibitory potencies of the stereoisomers of benzetimide. Noncholinergic agents, including pentagastrin, histamine, and the H2-receptor antagonists cimetidine and metiamide, have little or no effect on [3H]QNB binding at concentrations of 100 microM. These data support the existence of specific parietal cell muscarinic cholinergic receptors with which the secretagogue acetylcholine may directly interact to initiate gastric acid secretion.

Alpha-adrenergic regulation of secretion by tracheal glands

1990 ◽  
Vol 259 (4) ◽  
pp. L198-L205 ◽  
Author(s):  
D. J. Culp ◽  
R. K. McBride ◽  
L. A. Graham ◽  
M. G. Marin
Keyword(s):  
Adrenergic Receptors ◽  
Specific Binding ◽  
Receptor Subtypes ◽  
Adrenergic Agonists ◽  
Beta Adrenergic ◽  
Adrenergic Regulation ◽  
Binding Characteristics ◽  
Low Concentrations ◽  
Adrenergic Antagonist ◽  
Uk 14,304

The purpose of the present study was to begin to characterize, pharmacologically, the alpha-adrenergic regulation of glycoconjugate secretion from airway glands. Using isolated gland cells from cat trachea, we determined the binding characteristics of [3H]dihydroergocryptine ([3H]DHE), an alpha-adrenergic antagonist, with equal affinities for alpha 1- and alpha 2-adrenergic receptors. Specific binding of [3H]DHE to gland cell homogenates was saturable, of high affinity (KDapp = 4.2 nM) and inhibited with greater efficacy by epinephrine much greater than isoproterenol. Competition experiments with alpha 1- and alpha 2-adrenergic selective antagonists (prazosin and yohimbine, respectively) demonstrated high- and low-affinity sites for each antagonist, indicating the presence of both receptor subtypes. In studies of glycoconjugate secretion by cat tracheal explants, secretion was stimulated by adrenergic agonists with the rank potency: norepinephrine greater than or equal to phenylephrine greater than epinephrine much greater than clonidine. alpha-Adrenergic-stimulated secretion (epinephrine + propranolol) was inhibited by low concentrations of prazosin, but was unaffected by 100 nM yohimbine. The alpha 2-adrenergic agonists, clonidine and UK-14,304, each markedly inhibited beta-adrenergic-stimulated secretion. Collectively, these results demonstrate alpha 1-adrenergic regulation of glandular glycoconjugate secretion and suggest alpha 2-adrenergic receptors may modulate beta-adrenergic-stimulated secretion.

Rat lung cholinergic receptor: characterization and regulation by corticosteroids

1982 ◽  
Vol 53 (3) ◽  
pp. 731-736 ◽  
Author(s):  
D. L. Marquardt ◽  
H. J. Motulsky ◽  
S. I. Wasserman
Keyword(s):  
Adrenergic Receptors ◽  
Radioligand Binding ◽  
Cholinergic Receptor ◽  
Cholinergic Receptors ◽  
Hill Coefficient ◽  
Scatchard Analysis ◽  
Rat Lung ◽  
Muscarinic Cholinergic Receptors ◽  
Muscarinic Cholinergic

Muscarinic cholinergic receptors have been implicated in the regulation of bronchomotor tone, bronchial mucus secretion, and lung mast-cell mediator release. Rat lung membranes prepared by homogenization, sonication, and sedimentation of 37,000 g in sucrose have been demonstrated to possess muscarinic cholinergic receptors as assessed by radioligand binding employing l-quinuclidinyl[phenyl-413;3H]benzilate ([3H]QNB). QNB binding was saturable, stereoselective, and reversible in the presence of 1 microM atropine. The rat lung muscarinic receptor demonstrated a Kd of 0.268 +/- 0.126 (+/- SD) nM and a density of 35.4 +/- 4.6 fmol/mg protein by Scatchard analysis. The Hill coefficient was 1.015 +/- 0.085, indicating noncooperative binding. Muscarinic cholinergic receptors in the rat lung were equal in number to alpha 1-adrenergic receptors, but beta-adrenergic receptors are 14 times more prevalent as defined by [3H]prazosin and l-[propyl-2, 3–3H]dihydroalprenolol ([3H]DNA) binding. Dexamethasone (140 micrograms) administration in vivo caused an increase in all three receptor types by 24–48 h, suggesting steroids regulate not only the number of beta-receptors but also that of alpha- and cholinergic receptors. These data suggest new avenues by which steroids may regulate lung function.

Human M1-, M2- and M3-muscarinic cholinergic receptors: Binding characteristics of agonists and antagonists

1990 ◽  
Vol 97 (1) ◽  
pp. 67-80 ◽  
Author(s):  
Patrick Vanderheyden ◽  
Jean-Pierre Gies ◽  
Guy Ebinger ◽  
Jacques De Keyser ◽  
Yves Landry ◽  
...  
Keyword(s):  
Cholinergic Receptors ◽  
Muscarinic Cholinergic Receptors ◽  
Binding Characteristics ◽  
Muscarinic Cholinergic
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