Search PubMed⌕ Search

Biomedical subjects

B N Manukhin

Publications and source records attributed to B N Manukhin.

At least 55 records · Page 3Linked to original sources
PubMed1986

[Desensitization of alpha-adrenoreceptors of the small intestine of the rat].

A study performed on the isolated section of the rat small intestine has shown that at a slow increase in the concentration of the specific alpha-adrenomimetic phenylephrine in the incubation medium 1.0 X 10(-8) M/sec) adrenoreceptors pass into a state of desensitization without excitation, and no reaction takes place. At 2.5 X 10(-8)-10 X 10(-8) M/sec the reaction develops depending on the rate of phenylephrine introduction and is stabilized at 5.5-5.8 X 10(-6) M. Apparently, under these conditions an equilibrium is set up between activation and desensitization of adrenoreceptors. The role of desensitization of alpha-adrenoreceptors in the regulation of adrenergic reaction is discussed.

Animals↗
PubMed1986

[Relation between adrenoreceptor desensitization and their specific sensitivity].

In isolated parts of the rat small intestine, the relationship between desensitization of alpha- and beta-adrenoreceptors and change of their specific sensitivity was studied upon a decrease in noradrenaline content and increase of the incubation medium temperature. An enhancement of the adrenomimetics affinity was always followed by an increase in their ability for desensitization, thus entailing an increased effect of adrenomimetics as the autoinhibitors of adrenergic responses. The dependence of the adrenoreceptors ability for desensitization of their affinity for noradrenaline seems to ensure the control of adrenergic response upon a change in activity of adrenoreceptors.

Animals↗
PubMed1985

[Changes in Na, K-ATPase activity following adrenoreceptor blockade].

A regulatory factor released from the effector cell during blockade of postsynaptic alpha- and beta-adrenoreceptors with phentolamine and propranolol (5 X 10(7)-1 X 10(-6) M) and activating norepinephrine neuronal uptake and synthesis, was shown to activate, Na, K-ATPase of the rat isolated organs as well as the preparation of partly purified Na, K-ATPase extracted from the rat brain. Ouabain (1 X 10(-3) M) eliminated completely the activating effect of the regulatory factor on the ATPase.

Adrenergic Fibers↗
PubMed1985

[Functional interaction between alpha- and beta-adrenoreceptors of the small intestine].

Effect of desensitization of alpha-adrenoreceptors on the functional state of beta-receptors and vice versa was studied in isolated sections of the rat small intestine. Neither blockade, nor desensitization of alpha-receptors produced any effect on the sensitivity of beta-receptors to isopropyl-noradrenaline (IPN) whereas desensitization of beta-receptors to IPN resulted in the increase of alpha-receptors sensitivity to phenylephrine with a decreased maximal reaction. In the presence of GTP (0.02 mM) and propranolol (2.00 x 10(-7) M) IPN acts as a competitive reversible auto-inhibitor, GTP fully removing the inhibitory effect of IPN on both alpha- and beta-adrenoreceptors. Existence of functional interrelationship between alpha- and beta-adrenoreceptors is suggested.

Animals↗
PubMed1985

[Effect of temperature on the adrenoreactivity of the small intestine in the rat].

In isolated sections of the rat small intestine, adrenergic responses to phenylephrine (P), noradrenaline (NA) and isopropylnoradrenaline (IN) were studied at various temperatures of the incubation medium. Raise of the temperature from 33 to 37 degrees C increased the sensitivity of adrenoreceptors to P and NA 3.2-and 2.1-fold but did not change the sensitivity to IN. This change of adrenoreactivity was eliminated by phentolamine blockade of alpha-adrenoreceptors, and the raise of temperature always produced a decrease in maximal reaction of the small intestine. The change of adrenoreceptors of the small intestine smooth muscles seems to be related primarily to the rearrangement of alpha-adrenoreceptors.

Adrenergic Fibers↗
PubMed1985

[Effect of the short term exposure to heat on the adreno- and cholinosensitivity of the small intestine in the rat].

A 10-day study of the dynamics of adreno- and cholinosensitivity of isolated fragments of the small intestine of Wistar rats exposed to temperature of 45 degrees C for 30 and 60 min, revealed an increase in adreno- and cholinosensitivity in hyperthermia. A significant correlation exists between the body temperature and adrenoreactivity. Normalizing of body temperature is followed by reciprocal changes in adreno- and cholinosensitivity.

Acetylcholine↗
PubMed1985

[Changes in the level of eosinophils, corticosterone and catecholamine metabolism in the dynamics of emotional-painful stress].

A correlation has been established between changes in blood eosinophil content, corticosterone level and catecholamine metabolism during emotional painful stress. The authors assume that the differences in the functions of the adrenergic and pituitary-adrenal systems permit an objective determination of the parameters of stress formation in extremal exposures.

Adrenal Glands↗
PubMed1984

[Effector cell adrenoreceptors--local regulators of the intensity of the adrenergic reaction].

An activation of adrenoreceptors initiates both the specific adrenergic response and the process aiming at its limitation. Catecholamines induce a desensitization of adrenoreceptors acting as competitive autoinhibiting agents on the adrenergic response. A mechanism of feedback transsynaptic regulation becomes involved which inhibits accumulation of noradrenaline in the adrenergic neuron. A deficit of adrenergic effect activates the above steps of adrenergic process.

Animals↗
PubMed1983

[Patterns in the inhibition of adrenergic response by catecholamines].

Alterations of adrenergic reaction under the effect of norepinephrine (NE), epinephrine (E), phenylephrine (Ph) and isopropylnorepinephrine (ISO) were studied in isolated segments of the rat small intestine. The dissociation constants of adrenoreceptors with NE, E, Ph and ISO were found to be 5.1 +/- 0.70 X 10(-7) M, 1.20 +/- 0.30 X 10(-7) M, 7.60 +/- 1.40 X 10(-7) M, 1.40 +/- 0.02 X 10(-7) M, resp. Ph, NE, E, were shown to begin to function in 10-20 sec as competitive inhibitors of the adrenergic reaction with Ki 2.20 +/- 0.80 X 10(-7) M, 6.80 +/- 1.20 X 10(-7) M, 0.30 +/- 0.09 X 10(-7) M, resp., and ISO as an inhibitor of a mixed type with Ki of competitive inhibition 1.80 +/- 0.05 X 10(-7) M and Ki of the noncompetitive one 0.37 +/- 0.04 X 10(-7) M. The autoinhibition seems to take part in adrenergic process control chiefly through a considerable catecholamine release from nerve endings and adrenals in extreme conditions.

Animals↗
PubMed1983

[Reverse transsynaptic regulation of noradrenaline-H3 uptake in chronic sympathetic denervation].

A change in the functional state of adrenoreceptors in conditions of chronic sympathectomy with guanethidine produces constant spontaneous release of chemical factors regulating the intensity of neuronal uptake of noradrenaline-H3 by an adrenergic neuron. In the first two months when adrenoreceptors experience constant deficit of excitation, the factors are released increasing by half the neuronal uptake of noradrenaline-H3 in atrium and v. deferens. Some increase of NA concentration in peripheral organs during the 3rd month seemingly creates conditions providing for constant activation of sensitized adrenoreceptors which results in the release of factors inhibiting the rate of NA--H3 uptake in atrium by 65%, in v. deferens by 38%. The release from effector cell of chemical agents regulating the intensity of neuronal NA uptake, is one of the local peripheral mechanisms regulating the adrenergic transmitter process.

Animals↗
PubMed1982

Reverse trans-synaptic regulation of catecholamine synthesis in adrenergic neurones.

It was established that the blocking agent of beta-adrenoceptors, propanolol (1 X 10(-6)M), activates [3H] catecholamine synthesis from [3H] tyrosine in isolated rat organs (vas deferens and atrium) by 40-80%. The blocking agent of alpha-adrenoceptors, phentolamine (1 X 10(-6)M) activates [3H] catecholamine synthesis by 30-60% only in the organ possessing postsynaptic alpha-adrenoceptors (vas deferens). The activator of beta-adrenoceptors, isopropylnoradrenaline (1 X 10(-6)M), was shown to produce a decrease in [3H] catecholamine synthesis by 30-40% in both organs investigated. The substance activating alpha-adrenoceptors, phenylephrine (1 X 10(-5)M), inhibits [3H] catecholamine synthesis in the organ with postsynaptic alpha-adrenoceptors by 40-50%. Activation and inhibition of [3H] catecholamine synthesis induced by adrenotropic drugs is due to the release of chemical factors from he effector cell and their influence on the adrenergic neurone. The formation of chemical factors changing the intensity of catecholamine synthesis is related to the activation of protein synthesis in the effector cell. The processes which proceed in the adrenergic neurone are not connected with protein synthesis de novo. Existence of the common mechanism for trans-synaptic regulation of noradrenergic synthesis and uptake via the adrenoceptors of the effector cell is discussed.

Adrenergic Fibers↗
PubMed1982

[Age-related changes in the sympathetic innervation of effector organs in the rat after partial sympathectomy with guanethidine].

Guanethidine (30 mg/kg daily for first 15 days of life) decreased by 85% the amount of cells in the rat upper cervical sympathetic ganglion for 4 months. In ageing, the volume of the ganglion's cells, the density of adrenergic fibers and the noradrenaline content in the heart, intestine and ductus deferens increased in the desympathized animals. The neural cells remaining after desympathization seem to develop a growth of axons and to restore to some extent the density of sympathetic innervation of the periphery. The firing rate of single preganglionic fibers of the cervical sympathetic nerve is increased in the desympathized animals. The increased firing rate seems to be the cause of changes in the surviving neurons.

Adrenergic Fibers↗
PubMed1981

Growth of sympathetic postganglionic axons after partial chemical destruction with guanethidine.

Partial sympathectomy of neonatal rats was produced by treatment with guanethidine. The number of neurons of the superior cervical ganglion decreased to 15% of control values and remained constant throughout the subsequent observation period of 4 months. The volume of the remaining neuronal perikarya increased faster than that of control animals during the observation period, and the density of adrenergic innervation of the iris and the noradrenaline content of the heart were found to partially recover after the initial decrease produced by the guanethidine treatment, reaching 33% and 30% of control values, respectively, after 4 months. The noradrenaline content of the duct of the vas deferens was greatly reduced by guanethidine treatment, but almost recovered after 4 months. The frequency of sympathetic preganglionic impulses was elevated throughout the 4 months observation period, and it is suggested that this increase is responsible for the compensatory changes in cell volume, terminal density and terminal noradrenaline content of the remaining neurons.

Aging↗
PubMed1981

Biogenic monoamines in early embryos of sea urchins.

Indolylalkylamine determination was performed on the eggs and embryos of six species of sea urchins, using several fluorometric techniques, including the fluorescence of a substance itself and the fluorescence of its condensation products after treatment with orthophthaldialdehyde and ninhydrin. The serotonin-like substance of sea urchin embryos as well as of adults was shown to consist of at least two components, of which the major one is tryptamine or its derivative with a substituting group at aminonitrogen. Further, serotonin was found to be present at all developmental stages investigated. although at much lower concentrations. The results of this study suggest a regulatory role of 'prenervous' tryptamine in the early embryogenesis of the sea urchin.

Animals↗
PubMed1981

[Functional status of the sympatho-adrenal system of rats during emotional-painful stress].

Within 2-24 hrs after cessation of the 5-hr emotional-nociceptive stress the content of noradrenaline decreases in myocardium, small intestine, striatum, hypothalamus. The neuronal uptake of H3-NA and its synthesis decreased in atria. The compensatory response of small intestine to the lack of the adrenergic transmitter involves an increase of its sensitivity to NA and simultaneous decrease of its sensitivity to acetylcholine. Starting from the 2nd day after cessation of the stress the sympatho-adrenal system begins its normalizing and practically restores by the 5th day.

Adrenal Medulla↗