bluuebunny/crossref_metadata_2025_split huggingface dataset:
THE ACTION OF GENERAL ANAESTHETICS ON ACETYLCHOLINE‐INDUCED INHIBITION IN THE CENTRAL NERVOUS SYSTEM OF Helix
Authors: JUDGE SUSAN E. , NORMAN J. 
Published: July 2012

The effects of general anaesthetics, thiopentone, etomidate, minaxolone and ketamine were studied on identified voltage‐clamped neurones of Helix aspersa.
At concentrations of 0.1–0.5 mm, thiopentone, etomidate and minaxolone had no effect on the resting conductance of identified cells, D1 and D2. Ketamine at a concentration of 0.1–0.5 mm depolarized and excited the cells.
All four anaesthetics tested depressed a chloride‐dependent inhibitory response to acetylcholine (ACh) in cells D1 and D2 at concentrations of 0.1–0.5 mm in a dose‐dependent and reversible manner with no change in the reversal potential of the response.
These results show that general anaesthetics can block the transmitter‐evoked chloride‐mediated increases in membrane conductance in Helix neurones.
CHOLINERGIC ACTION IN THE NUCLEUS ACCUMBENS: MODULATION OF DOPAMINE AND ACETYLCHOLINE RELEASE
Authors: DE BELLEROCHE J.S. , GARDINER I.M. 
Published: July 2012

The action of oxotremorine and acetylcholine on the release of dopamine and acetylcholine from tissue slices of the rat nucleus accumbens was studied.
Oxotremorine significantly enhanced the release of [14C]‐dopamine evoked by 34 mmK+ and the EC50 for this action was 1.5 × 10−7 m. A maximal enhancement (30%) for this effect was reached at 2 × 10−7 m oxotremorine. A further enhancement of dopamine release occurred at concentrations of oxotremorine greater than 10−4 m.
The action of oxotremorine on [14C]‐dopamine release was calcium‐dependent and blocked by atropine (10−4 m) but not mecamylamine (up to 10−4 m).
Oxotremorine affected [3H]‐acetylcholine release differentially, inhibiting the K+‐evoked release of [3H]‐acetylcholine at concentrations greater than 10−5m. The IC50 for this process was 4.3×10−5m.
Acetylcholine (8 × 10−4 m) showed a similar pattern of action to oxotremorine: it enhanced the K+‐evoked release of [14C]‐dopamine (50%) and inhibited the K+‐evoked release of [3H]‐acetylcholine (30%).
The mechanism of action of oxotremorine on dopamine release is discussed in terms of a presynaptic receptor‐mediated process.
EVIDENCE FOR THE PHARMACOLOGICAL SIMILARITY BETWEEN THE CENTRAL PRESYNAPTIC MUSCARINIC AUTORECEPTOR AND POSTSYNAPTIC MUSCARINIC RECEPTORS
Authors: BOWEN D.M. , MAREK K.L. 
Published: July 2012

Twenty antagonist substances with varying potencies for central and peripheral postsynaptic muscarinic receptors have been examined for effects on the central presynaptic muscarinic autoreceptor. This has been monitored by measuring the stimulating effects of the substances on acetylcholine synthesis by rat neocortical tissue prisms.
Dose‐response curves for selected agents showed that maximal stimulation of synthesis was to 136–140% of the value without an antagonist.
At a concentration of 1 μm, 17 of the substances caused a significant increase in synthesis, whilst at 0.01 μm significant stimulation occurred with only atropine, dexetimide, N‐methyl‐piperdin‐4‐yl (R)‐2‐cyclohexyl‐2‐hydroxyl‐2‐phenylacetate, quinuclidinyl benzilate (QNB) and scopolamine.
Linear regression analysis between synthesis values obtained with the substances and published data for the effects on either cholinoceptor‐agonist induced contraction of guinea‐pig ileum or the binding of [3H]‐QNB to rat forebrain membranes gave correlation coefficients of r = 0.84 (P<0.01), and r = 0.75 (P<0.02) respectively.
The results provide no indication of a pharmacological difference between the central presynaptic muscarinic autoreceptor and central and peripheral postsynaptic muscarinic receptors.
LOW CONCENTRATIONS OF PROSTAGLANDIN E2 INHIBIT THE PROSTACYCLIN‐INDUCED ELEVATION OF CYCLIC ADENOSINE 3′,5′‐MONOPHOSPHATE IN ELICITED POPULATIONS OF RAT PERITONEAL MACROPHAGES
Authors: ADOLFS MARTIN J.P. , BONTA IVAN L. 
Published: July 2012

Elevation of cyclic adenosine 3′,5′‐monophosphate (cyclic AMP) in elicited populations of rat peritoneal macrophages was used as a parameter to examine the influence of prostaglandin E2 (PGE2) on the effects of prostacyclin (PGI2) and (±)‐5E‐13,14‐didehydro‐carbo‐prostacyclin (DDH‐carbo‐PGI2) in vitro.
PGE2, within the range of 1.4 × 10−9 to 1.2 × 10−8 m, caused a concentration‐dependent inhibition of the rise in cyclic AMP induced by 2.8 × 10−6 m PGI2 or DDH‐carbo‐PGI2.
With higher concentrations of PGE2 the inhibition was either non‐existent or masked by the effect of PGE2 per se on cyclic AMP levels.
The present findings suggest that the earlier observed low responsiveness of granuloma macrophages to PGI2, in terms of rise in cyclic AMP, is possibly due to permanent exposure of these cells to environmental endogenous PGE2.
[3H]‐GUANFACINE: A RADIOLIGAND THAT SELECTIVELY LABELS HIGH AFFINITY α2‐ADRENOCEPTOR SITES IN HOMOGENATES OF RAT BRAIN
Authors: JARROTT BEVYN , LOUIS WILLIAM J. , SUMMERS ROGER J. 
Published: July 2012

[3H]‐guanfacine (N‐amidino‐2‐(2,6‐dichloro 3[3H] phenyl) acetamide hydrochloride; 24.2 Ci/mmol) has been used as a radioligand in homogenates of rat cerebral cortex.
Specific binding of [3H]‐guanfacine was linear with respect to tissue concentration (2.5–15 mg/ml), saturable and not markedly affected in the pH range 6.5–8.0.
Analysis of the saturation of [3H]‐guanfacine binding using an iterative least squares fitting procedure gave best fits to a single site model.
[3H]‐guanfacine binding was of high affinity (Kd 1.71 ± 0.24 nm; n = 8) to a population of non interacting sites (nH 0.99 ± 0.02; n = 8) with a density of 118.2 ± 8.4 fmol/mg protein (n = 8).
Highest levels of binding were achieved in cerebral cortex followed by thalamus > hypothalamus > medulla/pons > spinal cord > striatum > cerebellum.
Binding was stereoselective with regard to the (—)‐isomer of noradrenaline and the order of potency for displacement of [3H]‐guanfacine by agonists was naphazoline > clonidine > (—)‐adrenaline > (—)‐α methylnoradrenaline > (—)‐noradrenaline > (±)‐α‐methylnoradrenaline > (+)‐noradrenaline > methoxamine > (+)‐adrenaline > phenylephrine and by antagonists was phentolamine > dihydroergocryptine > piperoxane > yohimbine > prazosin > labetalol > indoramin suggested binding to α2‐adrenoceptors.
The monovalent cations Na+ and K+ and also guanosine 5′‐triphosphate (GTP) produced concentration‐dependent inhibition whereas the divalent cations Ca2+, Mg2+, and Mn2+ first enhanced, then inhibited [3H]‐guanfacine binding.
Na+ (150 mm) or GTP (100 μm) produced marked reductions and Mn2+ (5 mm) marked increases in the number of receptor sites labelled by [3H]‐guanfacine.
It is concluded that [3H]‐guanfacine preferentially labels a high affinity state of the α2‐adrenoceptor in homogenates of rat cerebral cortex.
INTERACTIONS AMONG THE EFFECTS OF NORMORPHINE, CALCIUM AND MAGNESIUM ON TRANSMITTER RELEASE IN THE MOUSE VAS DEFERENS
Authors: MILNER J.D. , NORTH R.A. , VITEK L.V. 
Published: July 2012

Excitatory junction potentials (e.j.ps) were recorded with intracellular electrodes from smooth muscle cells of the mouse vas deferens.
The dependence of the e.j.p. amplitude on the extracellular calcium ion concentration was determined in the absence or presence of normorphine (50 nm‐1 μm) or magnesium (1.2–4.8 mm).
The interaction between normorphine and calcium was non‐competitive beyond a dose‐ratio of 1.5, whereas the interaction between magnesium and calcium was competitive up to the highest dose‐ratio investigated (1.9).
It is suggested that inhibition by normorphine occurs at least partly by a mechanism different from that of magnesium.
EFFECTS OF MELATONIN ON SLEEP AND NEUROCHEMISTRY IN THE RAT
Authors: HOLMES S.W. , SUGDEN D. 
Published: July 2012

The effects of intraperitoneally administered melatonin on sleep and brain neurochemistry in the rat were studied by use of EEG recording and standard fluorescence techniques.
Melatonin, 10 mg/kg, reduced time to sleep onset and time spent awake but increased both slow wave and paradoxical sleep. Qualitatively similar but smaller effects were produced by a dose of 2.5 mg/kg.
Neither dose of melatonin altered normal EEG patterns or disrupted normal sleep behaviour.
Melatonin, 20 mg/kg, did not significantly alter concentrations of tryptophan, 5‐hydroxytryptamine, 5‐hydroxyindoleacetic acid, noradrenaline or dopamine in any part of the brain.
It is concluded that the sleep promoting activity of melatonin cannot be related to gross changes in brain indoleamine and catecholamine levels.
EFFECTS OF SOME ORGANIC CALCIUM ANTAGONISTS AND OTHER PROCEDURES AFFECTING Ca2+ TRANSLOCATION ON KCl‐INDUCED CONTRACTIONS IN THE RAT VAS DEFERENS
Authors: HAY D.W.P. , WADSWORTH R.M. 
Published: July 2012

Both phasic and tonic responses to KCl 160 mm were reduced by Ca2+ deprivation. After 90 min, the phasic response was abolished but 13 ± 1.5% of the tonic response remained. This resistant component was still present if the Ca2+‐free solution contained EGTA 0.1 mm. The tonic response was more resistant to deprivation in the prostatic half, while the phasic was more resistant in the epididymal half. KCl‐induced contractions were completely restored 5 min after readmission of Ca2+.
Both the phasic and the tonic responses were reduced on lowering, and increased on raising [Ca2+]o. In 0.1 mm Ca2+, the phasic response was abolished, but 23 ± 4% of the tonic response remained (mainly attributable to the prostatic half). These resistant contractions indicate that some of the extracellular Ca2+, especially in the prostatic half, is bound with high affinity, probably to the plasma membrane.
Incubation with LaCl3 (0.3–10 mm) for 15 min inhibited the phasic response more than the tonic. After incubation for 1 h, 3 mm LaCl3 abolished both phases. It is concluded that La3+ blocks Ca2+ channels most readily when they are opened during the spike. Hydralazine (0.76–5.1 mm) resembled LaCl3 in that it reduced the phasic response with little effect on the tonic.
MnCl2 (0.3–10 mm) reduced the phasic but increased the tonic response at all concentrations. The augmenting effect may be due to release of intracellular Ca2+ or to inhibition of Ca2+ efflux.
The tonic response was inhibited more than the phasic response by nifedipine (0.002–0.01 μm), methoxyverapamil (0.06–2 μm), verapamil (0.2–1 μm), flunarizine (0.2–100 Iμm)and diazoxide (22–650 μm). With higher concentrations, only flunarizine remained selective for the tonic response. It is concluded that flunarizine blocks Ca2+ channels most readily when opened during sustained spike‐free depolarization.
Methoxyverapamil 48 μm and verapamil 100 μm virtually abolished both phases of the contraction to KCl 160 mm, but no more than 80% inhibition could be produced with nifedipine. It is concluded that voltage‐sensitive Ca2+ channels exist in two sub‐types, one of which is blocked by nifedipine, and both are blocked by verapamil, methoxyverapamil and flunarizine. Nitroprusside 17 μm had no effect on the phasic response but inhibited the nifedipine‐resistant component of the tonic response.
Increasing [Ca2+]o reversed the effects of verapamil, methoxyverapamil, nifedipine and MnCl2, but not the effects of LaCl3.
Dantrolene sodium (1.25–25 μm) had no effect on KCl‐induced contractions.
THE ACTIONS OF LEUKOTRIENES C4 AND D4 ON GUINEA‐PIG ISOLATED HEARTS
Authors: LETTS L.G. , PIPER PRISCILLA J. 
Published: July 2012

Infusions of leukotrienes C4 (LTC4) and LTD4 (5 min; 4 × 10−10‐2 × 10−8 m) produced dose‐dependent decreases in coronary flow in Langendorff preparations of guinea‐pig isolated hearts.
LTC4 was more active than LTD4 and produced a greater reduction in coronary flow.
LTC4 and LTD4 also caused reduction in contractility in perfused hearts but not in isolated atria or driven ventricular strips.
There was a greater reduction in contractility to LTD4 compared with LTC4 at doses which produced approximately 50% reduction in coronary flow.
Indomethacin (1.4 × 10−5 m) inhibited the effects of LTC4 but only reduced the initial LTD4‐induced effects.
The effects of FPL 55712 (3.8 × 10−6 m) were similar to those of indomethacin.
LTC4 and LTD4 may therefore contribute to the abnormalities of cardiac function that occur in immediate hypersensitivity reactions, particularly reduction in coronary flow.
THE EFFECTS OF NORADRENERGIC DENERVATION ON MUSCARINIC RECEPTORS OF SMOOTH MUSCLE
Authors: BENNETT T. , LOT T.Y. , STRANGE P.G. 
Published: July 2012

Changes in the response to acetylcholine of expansor secundariorum muscles from chicks have been analysed by pharmacological techniques and by [3‐3H]‐quinuclidinyl benzilate ([3‐3H]‐QNB) binding to quantify the muscarinic receptor population.
The expansor secundariorum muscle responded to acetylcholine up to the age of 30 days; the response declined thereafter. This developmental decrease in response to acetylcholine was prevented by surgical denervation.
In chicks aged less than 25 days, denervation did not affect the sensitivity of the expansor muscle to acetylcholine. In older chicks (above 40 days) denervation gradually restored the sensitivity of the expansor muscle to acetylcholine. Responses of the expansor muscle were always abolished by atropine (1 μm) indicating they were mediated by muscarinic receptors.
Binding studies with [3‐3H]‐QNB showed that changes in response of expansor muscles to acetylcholine were primarily due to changes in the muscarinic receptor population.
It is suggested that the noradrenergic innervation of the expansor muscle influences the number of muscarinic receptors expressed in the tissue.
THE INFLUENCE OF DRUGS ON THE OVERFLOW OF NORADRENALINE AND THE IDENTIFICATION OF RECEPTORS IN GUINEA‐PIG ATRIA
Authors: HAYES R. , HOWARD J.C. , NASMYTH P.A. 
Published: July 2012

Salbutamol (1.0 μm) and isoprenaline (1.2 nm) significantly increased the fractional release of tritiated noradrenaline from driven left atria but phentolamine (10 μm) failed to do so. Butoxamine (4.0 μm) blocked the increase in overflow produced by isoprenaline. Isoprenaline (1.2 nm), phentolamine (10.0 μm) and salbutamol (1.0 μm) failed to increase the overflow of tritiated noradrenaline from spontaneously beating atria.
Spontaneously beating atria were therefore used to identify the receptors mediating chronotropism and inotropism.
There was no clear relationship between inotropism and chronotropism.
The inotropic effects of both dobutamine (0.04–4.0 μm) and isoprenaline (0.11–9.0 nm) were inhibited by practolol (4.0 μm) and by butoxamine (4.0 μm). The chronotropic effects were inhibited only by practolol (4.0 μm).
Both inotropic and chronotropic effects of noradrenaline (3.0–200 nm) were antagonized by practolol (4.0 μm), but not by butoxamine (4.0 μm). Thus both functions appeared to be mediated by β1‐adrenoceptors when noradrenaline was the agonist.
Inotropic responses to salbutamol (0.45–7.5 μm) were inhibited by both practolol (4.0 μm) and by butoxamine (4.0 μm), but chronotropic responses were anatgonized only by butoxamine (4.0 μm). Thus salbutamol acts on both β1‐ and β2‐adrenoceptors to produce an inotropic response but only on β2‐adrenoceptors to produce its chronotropic response.
It is concluded that both β1‐ and β2‐adrenoceptors can mediate chronotropism and inotropism in guinea‐pig isolated atria. Determination of the postsynaptic effects of drugs should be carried out on spontaneously beating rather than driven atria to obviate modification of the responses by noradrenaline released from sympathetic neurones.
DESENSITIZATION BY NORADRENALINE OF RESPONSES TO STIMULATION OF PRE‐ AND POSTSYNAPTIC ADRENOCEPTORS
Authors: BALL N. , DANKS J.L. , DORUDI S. , NASMYTH P.A. 
Published: July 2012

The effect of exposing isolated preparations of rat aortic strip, rat atria and mouse vas deferens to perfusions of Krebs solution containing various concentrations of noradrenaline on their sensitivity to the drug has been determined.
The responses evoked by stimulation of postsynaptic adrenoceptors in all the tissues and presynaptic α‐adrenoceptors in the mouse vas deferens were diminished by the perfusion of noradrenaline through the organ bath for 30 min.
The concentration of noradrenaline required to produce desensitization was higher in the mouse vas deferens than in the other tissues and more was required to desensitize the chronotropic responses than the inotropic responses in rat isolated atria.
The inclusion of cocaine (10−5m) in the bathing solution to block uptake1 increased the sensitivity of most tissues to noradrenaline. With the possible exception of the response to stimulation of presynaptic receptors in the mouse vas deferens, desensitization was somewhat increased in its presence.
When uptake2 was blocked by oestradiol (10−5m), it was not possible to desensitize the contractor responses of the aortic strip and vas deferens to exogenous noradrenaline, nor the inotropic response of the atria to the drug. However, oestradiol failed to block the desensitization of chronotropic responses and responses to stimulation of presynaptic receptors in the vas deferens.
Blockade of monoamine oxidase (MAO) with iproniazid (7.2 × 10−4m) or with pargyline (5 × 10−4 m) did not affect the desensitization process in the aortic strip.
Blockade of catechol‐O‐methyltransferase (COMT) with U‐0521 (5.3 × 10−5m) greatly increased desensitization in the aortic strip and desensitization of inotropic responses in the atria. It had no effect on desensitization of chronotropic responses. Its effect on responses in the mouse vas deferens was not determined.
The perfusion of methoxamine at concentrations about 1000 times higher than those of noradrenaline also produced desensitization in the aortic strip.
The desensitization of presynaptic receptors in the mouse vas deferens was shown to be specific and that of the responses to postsynaptic receptor stimulation to be non‐specific.
It is concluded that responses to adrenoceptor stimulation may be desensitized by accumulation of noradrenaline inside the cells bearing the receptors and that the desensitization is caused by noradrenaline itself not by a metabolite. Desensitization may also be caused without accumulation of noradrenaline in uptake2 and for some receptors these may not be alternative mechanisms.
A COMPARATIVE STUDY OF β‐ADRENOCEPTORS IN HUMAN AND PORCINE LUNG PARENCHYMA STRIP
Authors: GOLDIE ROY G. , PATERSON JAMES W. , WALE JANET L. 
Published: July 2012

Responses to (±)‐isoprenaline (Iso), (−)‐adrenaline (Adr) and (−)‐noradrenaline (NA) were compared in isolated preparations of human and porcine lung parenchyma strip.
The order of relaxant potencies of these catecholamines in both human and porcine lung parenchyma was Iso > Adr > NA (1:0.24:0.01, human; 1:0.21:0.01, pig). These results suggest that β2‐adrenoceptors predominate in both types of lung parenchyma strip.
pA2 values for the β‐adrenoceptor antagonist, propranolol (non‐selective), with Iso as the agonist, in human and porcine lung strips were 7.84 and 7.83 respectively and for atenolol were 6.50 and 5.35 respectively. Taken as a whole, results indicate the existence of an apparently homogeneous population of β2‐adrenoceptors in porcine parenchyma strip, while both β1 and β2‐adrenoceptors were revealed in human lung parenchyma.
DEVELOPMENT OF MOTOR RESPONSE TO INTRAMURAL NERVE STIMULATION AND TO DRUGS IN RAT SMALL INTESTINE
Authors: MIYAZAKI H. , OHGA A. , SAITO K. 
Published: July 2012

The onset and development of functional innervation and transmitter reactivity in the small intestine, isolated from foetal and neonatal rat, was examined in relation to the development of two muscle layers.
About half of the preparations tested at embryonic day 15 responded to electrical field stimulation, although both acetylcholine (ACh, 1 μm) and excess K (50 mm) evoked a response in all preparations. The response to these stimuli was the extension of the preparation longitudinally. All six preparations examined at embryonic day 16 extended in response to electrical field stimulation.
The extension response to electrical field stimulation was observed up to embryonic day 19. Then, the response changed to a biphasic one and finally to shortening after 4‐days postnatal. The responses to electrical field stimulation were blocked by tetrodotoxin (TTX, 0.3 μm) or atropine (0.3 μm). The response to ACh and excess K similarly changed and became only a shortening at embryonic day 21 and 6‐days postnatal, respectively.
The extension and biphasic responses produced by these stimuli were invariably converted to shortening after the preparation had been opened longitudinally.
The pD2 value for ACh was 6.74–7.37 during the period embryonic day 15–6‐days postnatal.
These results suggest that in the rat intestine, functional cholinergic innervation is established at least by embryonic day 16. In the early stages, the development of the circular muscle layer precedes that of the longitudinal muscle layer in causing contraction. This results in longitudinal extension of the preparation in response to stimuli. The reverse takes place following the development of the longitudinal muscle layer.
RELEASE OF β‐LIPOTROPIN‐ AND β‐ENDORPHIN‐LIKE MATERIAL INDUCED BY ANGIOTENSIN IN THE CONSCIOUS RAT
Authors: BEUERS U. , HERTTING G. , KNEPEL W. 
Published: July 2012

The influence of the renin‐angiotensin system on plasma β‐endorphin‐like immunoreactivity (β‐EI) was investigated in the conscious rat by use of a radioimmunoassay for β‐endorphin without prior extraction.
Intravenous infusion of angiotensin I, II or (des‐1‐Asp)angiotensin II (angiotensin III) caused a dose‐dependent increase in plasma β‐EI, angiotensin III infusion being less effective than angiotensin I or II. The plasma adrenocorticotrophin (ACTH) levels too were elevated by angiotensin II. The receptor antagonist, saralasin, prevented the angiotensin II‐induced β‐EI release as did dexamethasone pretreatment.
Both the release of β‐EI and the pressor response to angiotensin I were abolished by the converting enzyme inhibitor, captopril (SQ 14225). In contrast, captopril did not affect the action of angiotensin II.
In view of the appreciable cross‐reactivity of β‐lipotropin (β‐LPH) in our assay, plasma β‐EI was analysed by Sephadex G‐50 chromatography. In plasma extracts of angiotensin II‐infused rats, immunoreactivity corresponding to human β‐endorphin comprised about 49% of the total immunoreactivity, whereas 51% co‐migrated with human β‐LPH.
The increase in plasma levels of β‐EI elicited by angiotensin II was diminished by about 35% in rats with a hereditary absolute lack of vasopressin (Brattleboro rats), when compared to normal rats.
These results suggest that the renin‐angiotensin system can stimulate the secretion of β‐LPH and β‐endorphin with ACTH from rat anterior pituitary. One link in mediating the response appears to be vasopressin. The physiological function remains to be defined.
α1‐ADRENOCEPTOR ACTIVATION CAN INCREASE HEART RATE DIRECTLY OR DECREASE IT INDIRECTLY THROUGH PARASYMPATHETIC ACTIVATION
Authors: FLAVAHAN N.A. , McGRATH J.C. 
Published: July 2012

The chronotropic effects of α‐ and β‐adrenoceptor agonists were investigated in the pithed rat.
The β‐adrenoceptor agonist, isoprenaline, produced only a positive chronotropic response. α1‐Adrenoceptor agonists, phenylephrine and amidephrine, produced positive and negative chronotropic effects. Part of the response to phenylephrine was β‐mediated.
A positive chronotropic response to amidephrine and phenylephrine was mediated directly through cardiac α1‐adrenoceptors and had a different time course from β‐adrenoceptor‐mediated responses.
A negative chronotropic response to α‐agonists was potentiated by neostigmine and blocked by atropine, tetrodotoxin or hexamethonium as well as by α1‐adrenoceptor antagonists. This may indicate α1‐adrenoceptors on preganglionic parasympathetic nerves, stimulation of these receptors causing release of acetylcholine.
The α2‐adrenoceptor agonist, xylazine, produced a direct negative chronotropic effect on the heart, independent of α‐adrenoceptors. No evidence was found for functional post‐junctional α2‐adrenoceptors. At high doses xylazine stimulated cardiac α1‐adrenoceptors.