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At least 973 records · Page 54Linked to original sources
PubMed1996

Spinally-mediated behavioural responses evoked by intrathecal high-dose morphine: possible involvement of substance P in the mouse spinal cord.

Intrathecal (i.t.) administration of morphine in the spinal subarachnoid space of mice produced a severe hindlimb scratching followed by biting and licking. The onset of the scratching behaviour was observed 60-70 s after i.t. injection of morphine (60 and 90 nmol), and had a duration of 3-4 min. The morphine-induced behaviour was increased additively by i.t. co-administration of substance P (SP). This characteristic behavioural response was inhibited dose-dependently by i.t. co-administration of the tachykinin NK-1 receptor antagonists, sendide and CP-96,345. Significant antagonistic effects of SP (1-7), a putative antagonist for NK-1 receptors and [D-Phe7, D-His9]SP (6-11), a selective antagonist for SP receptors, were observed against the morphine-induced behaviour. Pretreatment with i.t. SP antiserum and i.t. capsaicin resulted in reduction of the response to morphine. I.t. administration of somatostatin (SOM) antiserum, cysteamine, a relatively selective depletor of SOM and cyclo-SOM, a SOM receptor antagonist, produced no inhibitory effect on the morphine-induced behaviour. These results demonstrate that a spinal system of neurones containing SP may be involved in elicitation of the behavioural episode following i.t. injection of morphine in mice.

Animals↗
PubMed1989

Variation in alpha-1-antitrypsin phenotypes associated with penicillamine therapy.

During a detailed study of alpha-1-antitrypsin (AAT) by isoelectric focusing, of 130 individuals of the PiZ phenotype and their families, an unusual alpha-1-antitrypsin protein pattern was identified which related directly to the effect of penicillamine therapy. The effect, believed to be mediated by reaction with the free cysteine of the alpha-1-antitrypsin molecule, was demonstrable by in vitro experiments. It was not apparently associated with loss of the anti-proteinase properties of alpha-1-antitrypsin and was not specific to the Z gene products. It is however, a source of possible confusion in the accurate assessment of Pi phenotypes.

Cystamine↗
PubMed1984

Reversible inhibition of neuronal uptake by benextramine, an irreversible presynaptic alpha-adrenoceptor antagonist.

Benextramine, a covalently binding alpha-adrenoceptor blocking agent, potentiated the action of noradrenaline but not isoprenaline in guinea pig isolated right atria. This potentiation was probably caused by inhibition of neuronal uptake. When the benextramine was washed from the tissues for 60 min, no potentiation of the action of noradrenaline was observed. This easily reversed inhibition of neuronal uptake by benextramine contrasts with the effects of desipramine and phenoxybenzamine because the potentiating effect of these drugs was unaffected by 60 min of washing. The presence of benextramine also caused a small tachycardia in both rabbit and guinea pig right atria which was probably due to the release of endogenous noradrenaline. Clonidine a presynaptic alpha 2-adrenoceptor agonist, inhibited the responses to electrical field stimulation. Pretreatment with benextramine greatly diminished the effect of clonidine. This alpha 2-adrenoceptor antagonism was not reversed by washing the benextramine from the tissue for 240 min. We conclude that benextramine is a readily reversible inhibitor of neuronal uptake and an irreversible antagonist of presynaptic alpha 2-adrenoceptors.

Adrenergic alpha-Antagonists↗
PubMed1984

N,N''-(dithio-2,1-ethanediyl)bis[N'-(pyrrol-2-ylmethyl)-1, 6,- hexanediamine] (pyrextramine), a new irreversible alpha 1-adrenoreceptor blocking agent of the tetramine disulfide class.

In an attempt to further improve the alpha-adrenoreceptor blocking activity of benextramine, the effect of heteroaromatic substituents on the terminal nitrogens was studied. In this communication we report on the newly synthetized N,N''-(dithio-2,1-ethanediyl)bis[N'-(pyrrol-2-ylmethyl)-1,6- hexanediamine] (pyrextramine) that displayed higher affinity (5-10-fold) and higher selectivity (about 12-fold) than benextramine. These preliminary results show that pyrextramine can replace benextramine in the elucidation and characterization of the peripheral alpha 1-adrenoreceptors.

Adrenergic alpha-Antagonists↗
PubMed1986

The relationship between alterations in alpha 1-adrenoceptor reserve by phenoxybenzamine and benextramine and the sensitivity of cirazoline-induced pressor responses to inhibition by nifedipine.

Nifedipine does not inhibit the alpha 1-adrenoceptor-mediated pressor response of cirazoline at a dose that significantly antagonizes the alpha 2-adrenoceptor-mediated pressor response of B-HT 933. After elimination of the alpha 1-adrenoceptor reserve with either phenoxybenzamine or benextramine, the response to cirazoline was rendered highly sensitive to antagonism by nifedipine. These results support the hypothesis that the resistance of alpha 1-adrenoceptor-mediated pressor responses to inhibition by calcium channel antagonists may be caused by a large alpha 1-adrenoceptor reserve.

Adrenergic alpha-Antagonists↗
PubMed1995

Neuronal mechanism of the inhibitory effect of calcitonin on N-methyl-D-aspartate-induced aversive behavior.

To elucidate the mechanism of antinociceptive effects of calcitonin, we investigated whether receptor antagonists for various neurotransmitter receptors alter the inhibitory effect of calcitonin on intrathecally injected N-methyl-D-aspartate-induced aversive behavior in mice. Neither naloxone, an opioid receptor antagonist, phentolamine and benextramine, alpha-adrenoceptor antagonists, nor ritanserin, a 5-HT2A receptor antagonist, inhibited the calcitonin-induced anti-aversive effects. Pindolol and (--)-propranolol, non-selective antagonists of beta-adrenoceptors and 5-HT1 receptors, 1-(2-methoxyphenyl)-4-[4-(2-phethalimido) butyl]-piperazine hydrobromide (NAN-190), a 5-HT1A receptor antagonist, 3-tropanyl-3,5-dichlorobenzoate (MDL72222) and metoclopramide, 5-HT3 receptor antagonists, significantly inhibited the calcitonin-induced anti-aversive effects. (--)-Bicuculline, a GABAA receptor antagonist, phaclofen and 5-aminovaleric acid, GABAB receptor antagonists, also attenuated the calcitonin-induced anti-aversive effects. These results suggest that beta-adrenoceptor, 5-HT1A, 5-HT3, GABAA and GABAB receptors, but not alpha-adrenoceptor, opioid nor 5-HT2A receptors, are involved in the inhibitory effect of calcitonin on intrathecally injected N-methyl-D-aspartate-induced aversive behavior in mice.

Adrenergic alpha-Antagonists↗
PubMed1994

Binding profile of benextramine at neuropeptide Y receptor subtypes in rat brain areas.

Binding studies in rat whole brain, frontoparietal cortex and brainstem membrane preparations revealed that benextramine displaced [3H]neuropeptide Y specific binding from a low and a high affinity site with IC50 values in the microM (36 +/- 2, 4.4 +/- 1.4 and 300 +/- 120 microM, respectively) and the pM (29.3 +/- 12.1, 0.35 +/- 0.11 and 0.42 +/- 0.03 pM, respectively) range, whereas in rat hippocampus benextramine displaced [3H]neuropeptide Y specific binding from one site only with an IC50 value of 22.8 +/- 5.7 microM. With the exception of frontoparietal cortex binding assay, benextramine was not able to completely inhibit [3H]neuropeptide Y specific binding revealing the presence of a benextramine nonsensitive third binding site. Benextramine pretreatment followed by membrane washing demonstrated that benextramine inhibited irreversibly both high and low affinity sites.

Adrenergic alpha-Antagonists↗