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B N Manukhin

Publications and source records attributed to B N Manukhin.

At least 19 recordsLinked to original sources
PubMed2006

[Changes of alpha1-adrenergic and muscarinic cholinergic responses of arterial blood pressure in the rabbit during adaptation to cold].

Changes in major parameters of alpha1-adrenergic and muscarinic cholinergic responses of arterial blood pressure (EC50 and P(m)) were studied in rabbits adapted to cold for 1-30 days (daily cold exposures for 6 hours at -10 degrees C). It was shown that responses to noradrenaline, adrenaline (agonists of alpha1-adrenoceptors) and acetylcholine (agonist of muscarinic cholinoreceptors) could be expressed by equation p = (Pm- A(n))/(EC50(n) + A(n)) with n = 1. Adaptation to cold induced radically different changes in the major parameters of adrenergic and cholinergic responses. In the noradrenergic responses, the parameters EC50 and Pm gradually decreased within 1-30 days of adaptation. In the adrenaline responses, Pm increased from 1 to 30 days of adaptation, EC50 decreased to 10 day and increased on the 30th day. In the muscarinic cholinergic response, the Pm value decreased from 1 and 10 days but returned to control values on the 30th day. IC5O did not differ from the control 1 day, decreased to 10 days and increased on the 30th day.

Acetylcholine↗
PubMed2005

[Influence of carbachol on the kinetic parameters of the contractile response to noradrenaline in the rat vas deferens].

Graphic and mathematical analysis of kinetics of the rat vas deferens contractile response to noradrenaline showed that alpha1-adrenoceptors mediating the contraction were in different functional states. In some organs, these receptors were homogeneous with the Hill coefficient n = 1 (the linear mode of the Scatchard plot), in the others--not homogeneous, with n > 1 (not linear mode of the Scatchard plot). Carbachol increased the contractile response to noradrenaline. As in the control, two types of response were revealed: 1. The Hill coefficient n < 1 (biphasic mode of the Scatchard plot) with two pools (high and low affinity) of alpha1-adrenoceptors, and 2. The Hill coefficient n = 1 (the linear mode of the Scatchard plot). These results suggest that the influence of carbachol is caused by the local interaction of M-cholinergic and alpha1-adrenergic systems.

Adrenergic alpha-1 Receptor Agonists↗
PubMed2004

[Carbachol effect on kinetics of the alpha1-adrenergic contractile response of the rat vas deferens].

Analysis of the control kinetics of the rat vas deferens contractile response to phenylephrine showed that alpha 1-adrenoceptors mediating the contraction could be in different functional states. In some organs these receptors represented a single pool with Hill coefficient n = 1 (the linear mode of the Scatchard plot), in others--not a single pool, n > 1 (not linear mode of the Scatchard plot). Activation of muscarinic cholinergic receptors by carbachol exerted a stimulating effect on the alpha 1-adrenergic contractile response especially to low adrenomimetic concentrations and the maximum response was increased. The action of cholinomimetic was accompanied by a decrease of Hill coefficient. When the control represented a single pool of alpha 1-adrenoceptors in the presence of carbachol Scatchard plot became biphasic with Hill coefficient n < 1, in addition to the low affinity pool the high affinity appeared. In case of not homogeneous control pool, in the presence of carbachol a single pool was revealed and n was close to 1. These findings suggest that the stimulatory effect of carbachol is caused by its modulator action on the alpha 1-adrenoceptors states and activating influence on the intracellular effector's system.

Adrenergic alpha-1 Receptor Agonists↗
PubMed2003

[Effect of adaptation to cold on the alpha1- and beta-adrenergic reactions of arterial vessels of the small intestine in rabbits].

Changes in major paraments of alpha 1- and beta-adrenergic responses (EC50 and Pm) were studied in the intestine arterial blood vessels of rabbits adapted to cold for 1-30 days (daily cold exposures for 6 hours at -10 degrees C). It was shown that responses to phenylephrine, noradrenaline, adrenaline (alpha 1-agonists), isopropylnoradrenaline (beta-agonist) corresponded to the equation p = (Pm.An)/(EC50n + An) with n = 1 and n = 2, respectively. Adaptation to cold induced radically different changes in the major parameters of alpha- and beta-adrenergic responses. In the alpha-adrenergic responses, the parameters EC50 and Pm changed reciprocally. In the beta-adrenergic response, only Pm value changed while EC50 did not differ from the control over the entire period of adaptation to cold. The pronounced differences from the control gradually decreased within 1-30 days of adaptation.

Adaptation, Physiological↗
PubMed2001

[Changes in alpha1-, alpha2-, and beta-adrenergic responses of blood pressure in blood vessels of the rabbit hindlimbs during cold adaptation].

Changes in major parameters of alpha 1-, alpha 2- and beta-adrenergic responses (EC50 and Pm) were studied in hind-limb arterial vessels of the rabbits adapted to cold for 1-30 days (daily cold exposures for 6 hours at -10 degrees C). It was shown that responses to phenylephrine, noradrenaline, adrenaline (alpha 1-agonists), clondine (alpha 2-agonist), isopropylnoradrenaline (beta-agonist) corresponded to the equation p = (Pm.An)/(EC50n = An) with n = 1 and n = 2, respectively. Adaptation to cold induced radically different changes in the major parameters of alpha- and beta-adrenergic responses. In the alpha-adrenergic responses, the parameters EC50 and Pm changed reciprocally. In the beta-adrenergic response, only the Pm value changed while EC50 did not differ from the control over the entire period of adaptation to cold. The pronounced differences from the control gradually decreased within 1-5 days of adaptation but remained significant until the 30th day.

Adaptation, Physiological↗
PubMed2000

Interactions of radiolabelled ligands with specific receptors: an analysis.

The binding and displacement of beta-adrenoceptor blockers, [3H]propranolol ([3H]PRP) and [3H]dihydroalprenolol ([3H]DHA), were studied on isolated rat erythrocytes, their membranes and ghosts; the binding of [3H]DHA and a M-cholinoceptor blocker, [3H]quinuclidinylbenzylate ([3H]QNB), on cerebral cortex membranes. In all experiments, ligand-receptor interactions conformed to a model of two pools of receptors in the same effector system and the binding of two ligand molecules to the receptor. The results were similar for the displacement of [3H]PRP, [3H]DHA and [3H]QNB with propranolol, dihydroalprenolol and quinuclidinyl-benzylate, respectively. The parameters of [3H]PRP to beta-adrenoceptor binding for intact erythrocytes were: Kd1 = 0.74+/-0.07 nM, Kd2 = 14.40+/-0.41 nM, B1 = 24+/-2 unit/cell, B2 = 263+/-5 unit/cell; for ghosts, Kd1 = 0.70+/-0.17 nM, Kd2 = 19.59+/-2.59 nM, B1 = 9+/-1 fmol/mg protein, B2 = 39+/-4 fmol/mg protein. Receptor affinities were similar in erythrocytes and ghosts; on the ghost membrane, the number of receptors was considerably lower (B1 = 2 unit/cell, B2 = 6 unit/cell). The parameters of [3H]QNB to M-cholinoceptor binding of the cerebral cortex membrane were the following: Kd1 = 0.43 nM, Kd2 = 2.83 nM, B1 = 712 fmol/mg, B2 = 677 fmol/mg.

Adrenergic beta-Antagonists↗
PubMed2000

[Analysis ligand-receptor interactions from the molecular to the organism levels].

A system of quantitative analysis is proposed for evaluation of ligand-receptor interaction on models of different levels of complexity. For two discrete receptor pools, binding of radio-labelled ligands to specific receptors and the magnitude of physiological response for an effector system with two discrete pools of receptors with different affinities are described with the aid of developed respective equations. The equations' parameters characterise properties of the effector system under study: the number of receptor pools differing in their affinity to a ligand; the number of active receptors of the maximum response magnitude; and the number of ligand's molecules bound to the receptor. The derived parameter's efficiency provides a general characteristic of affinity for the effector system under study. The described method of analysis of the ligand-receptor interactions is applicable to studies of any biological responses yielding quantitative results.

Acetylcholine↗
PubMed2000

[Pharmacokinetic analysis of alpha- and beta-adrenoreceptors in the chick embryo amnion].

Following a stimulation with acetylcholine, the beta-adrenergic agonists adrenaline (A), noradrenaline (NA), isoproterenol (Iso) and salbutamol (Sal) induced a concentration-dependent decrease in the tone and (or) rate of amnion contraction with EC50 ISO < NA << A < Sal. Metaprolol, a specific beta 1-antagonist, induced a rightward shift in the dose-response curves of Iso, NA and A, whereas beta-antagonist butoxamine was ineffective. pA2 values for beta-antagonists were propranolol 8.3, metoprolol 7.0, butoxamine 5.6. EC50 values of alpha-adrenergic agonists form a sequence: clonidine < NA << methoxamine < phenylephrine. Specific alpha-antagonists yohimbine and idazoxan were found to antagonise competitively the effects of NA. The data obtained characterize the adrenergic receptors mediating stimulation of amniotic contractile activity as alpha 2-adrenergic receptors. Inhibition of contractile receptors in amnion is mainly mediated by beta 1-adrenergic receptor activation.

Adrenergic Agonists↗
PubMed1999

An approach to analysis of radiolabeled ligand interactions with specific receptors.

The aim of the study was to reveal general characteristics of the ligand-receptor interaction in the binding and displacement of radiolabeled ligands. The binding and displacement of DL-[3H]propranolol hydrochloride ([3H]propranolol) and L-[propyl-2,3, -3H]dihydroalprenolol ([3H]dihydroalprenolol), beta-adrenoceptor antagonists, were studied with isolated rat red blood cells, their membranes and ghosts. The binding of [3H]dihydroalprenolol and L-quinuclidinyl-[phenyl-4-3H]-benzylate ([3H]quinuclidinyl benzylate), a muscarinic acetylcholine receptor antagonist, was studied with cerebral cortex membranes. The ligand-receptor interaction corresponded to that for a model of two pools of receptors in the same effector system, with the binding of two ligand molecules to the receptors and was described by the following equation: b=[(B(m1)A(2))/(K(d1)(2)+A(2))]+[(B(m2)A(2))/(K(d2)(2)+A(2))]. The parameters of [3H]propranolol binding to beta-adrenoceptors were as follows: K(d1)=0.74 nM, K(d2)=14.40 nM, B(m1)=24 unit/cell, and B(m2)=263 unit/cell for native red blood cells from rats; K(d1)=0.70 nM, K(d2)=19.59 nM, B(m1)=9 fmol/mg protein, and B(m2)=39 fmol/mg protein for blood ghosts. The parameters of [3H]quinuclidinyl benzylate binding to muscarinic acetylcholine receptors of cerebral cortex membrane were as follows: K(d1)=0.43 nM, K(d2)=2.83 nM, B(m1)=712 fmol/mg, B(m2)=677 fmol/mg. The analysis of the equilibrium binding and displacement of [3H]propranolol and [3H]dihydroalprenolol at beta-adrenoceptors of membranes, ghosts and native red cells of rats, [3H]dihydroalprenolol at beta-adrenoceptors and [3H]quinuclidinyl benzylate at muscarinic acetylcholine receptors of synaptosomal membranes from rat cerebral cortex demonstrated that the receptors bound two ligand molecules each and consisted of two discrete pools of high- and low-affinity receptors. Similar results were obtained for the displacement of [3H]propranolol, [3H]dihydroalprenolol and [3H]quinuclidinyl benzylate by propranolol, dihydroalprenolol and quinuclidinyl benzylate.

Adrenergic beta-Antagonists↗
PubMed1999

[Effect of cocaine on the contractile response to noradrenaline in the epididymal and prostatic regions of the vas deferens].

In the prostatic half of the rat vas deferens, the response to noradrenaline under the cocaine effect revealed a phasic and a tonic components, whereas in the epididymal portion of the vas deferens there only occurred the tonic component. Cocaine increased the maximal tonic contractile response to noradrenaline in the epididymal portion and the maximal phasic response--in the prostatic one. Mechanisms of direct postsynaptic action of cocaine are discussed.

Animals↗
PubMed1998

[Quantitative analysis of ligand-receptor interactions in physiological experiments].

In isolated smooth muscles of the sea cucumber, the rat intestine, vas deferens and portal vein, and in chick embryonic amnion, contractile responses of smooth muscles to transmitters and their agonists were described with two equations: p = (Pm.A(n))/(EC50n + A(n)) [7] or p = [(Pm1.An1)/(EC50(1)n1 + An1)] + [(Pm2.An2)/(EC50(2)n2 + An2)] [8]. The findings reveal a possibility of ligand-receptor interaction according to several models: a single receptor pool with n = 1 or n not equal to 1; two receptor pools in the same effector system with n1 = n2 or n1 not equal to n2.

Acetylcholine↗
PubMed1997

The effect of heat shock on M-cholinoreceptors from rat cerebral cortex membranes.

The major parameters of binding the specific blocker [3H]quinuclidinyl benzylate were obtained for M-cholinoreceptors of rat cerebral cortex membranes. One receptor was shown to bind two molecules of the ligand; two discrete receptor pools were revealed, which differed in the sensitivity (Kd1 = 0.35 +/- 0.03; Kd2 = 1.79 +/- 0.21 nM) and the number of the ligand binding sites (B1 = 468 +/- 54; B2 = 864 +/- 81 fmol/mg protein). Heat shock decreased the number of receptors of the high-affinity pool (B1) by 16% (Kd1 did not differ from the control); the efficiency of the ligand binding to the receptors (E = B/2Kd) decreased by 26%, which suggests the decrease in the functional activity of the receptors of this pool. In the low-affinity pool (B2), the number of receptors increased by 39%, and Kd2 decreased by 22%; the efficiency (E2) increased by 14%.

Adrenal Glands↗
PubMed1994

[The kinetics of the reaction of the portal vein of the liver in the rat to catecholamines and acetylcholine].

The portal vein was shown to possess two pools of alpha-adrenoreceptors and m-cholinoreceptors, and one beta-adrenoreceptor pool, with functional interrelationships among them. Increase in the temperature of the incubation medium to 40.5 and 41.0 degrees C induced characteristic changes of adrenergic response which were reversed or considerably attenuated by specific agonists and antagonists. The role of changes in the conformational membrane induced by adrenotropic substances in modulating specific responses to neurotransmitters and their agonists, is discussed.

Acetylcholine↗