The central action of antihypertensive drugs, mediated via central α -receptors
12 Apr 2011-Journal of Pharmacy and Pharmacology (Blackwell Publishing Ltd)-Vol. 25, Iss: 2, pp 89-95
About: This article is published in Journal of Pharmacy and Pharmacology.The article was published on 2011-04-12 and is currently open access. It has received 158 citations till now.
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TL;DR: A division of adrenergic receptors into alpha and beta types could conceivably lead to the development of powerful agents even more selective for inhibition of renin release, control of blood pressure by a central site of action, reduction of fever, and possible other scientific or therapeutic applications.
796 citations
TL;DR: Clonidine was less potent in stimulating the hindlimb flexor reflex activity of spinal rats than in inhibiting the α-methyltyrosine-induced disappearance of noradrenaline in the spinal cord and brain of rats and in the brain of mice.
Abstract: The influence of clonidine on α-adrenoreceptors in the central nervous system of rats and mice has been investigated. Both functional events due to postsynaptic receptor stimulation (flexor reflex activity, motor activity) and biochemical changes have been considered.
1.
Clonidine was less potent in stimulating the hindlimb flexor reflex activity of spinal rats than in inhibiting the α-methyltyrosine-induced disappearance of noradrenaline in the spinal cord and in the whole brain of rats.
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The increase in flexor reflex activity due to clonidine (0.4 mg/kg) was virtually completely inhibited by phenoxybenzamine (20 mg/kg) and haloperidol (10 mg/kg), was partially inhibited by yohimbine (10 mg/kg) and piperoxan (60 mg/kg) and was not significantly inhibited by yohimbine (3 mg/kg) and tolazoline (50 mg/kg).
3.
The potentiation by clonidine of the apomorphine-induced locomotor stimulation of reserpinetreated mice was almost completely inhibited by phenoxybenzamine (20 mg/kg) but was not significantly affected by yohimbine (10 or 3 mg/kg) and only slightly inhibited by tolazoline (50 mg/kg).
4.
Clonidine (0.1 mg/kg) caused a considerable inhibition of the α-methyltyrosine-induced disappearance of noradrenaline in the spinal cord and brain of rats and in the brain of mice. This effect of clonidine was completely antagonized by yohimbine (10 mg/kg). It was markedly antagonized by yohimbine (3 mg/kg), piperoxan (60 mg/kg) or tolazoline (50 mg/kg) but not by phenoxybenzamine (20 mg/kg) or haloperidol (10 mg/kg).
5.
Clonidine (0.1 mg/kg) caused an inhibition of the accumulation of Dopa after decarboxylase inhibition in the noradrenaline-rich regions of the rat central nervous system. This effect was counteracted by yohimbine (10 mg/kg), piperoxan (60 mg/kg) or tolazoline (50 mg/kg) but not by phenoxybenzamine (20 mg/kg).
6.
The postsynaptic functional effects and the biochemical effects of clonidine may be due to stimulation of different α-adrenoreceptors since the two effects were inhibited differently by various α-adrenoreceptor blocking agents and since the two effects were produced by different doses of clonidine. The α-adrenoreceptors mediating the biochemical changes might be located on the noradrenergic neurones.
363 citations
TL;DR: Sympathetic nervous activity and the ability of the sympathetic nervous system to respond to a uniform stimulus are studied in hypertensive and normotensive subjects and a survey of the plasma levels of norepinephrine in a variety of neurologic disorders is given.
Abstract: Plasma norepinephrine derives from sympathetic nerves, but the proportion reaching the circulation before being metabolized varies with the type of nerve ending-effector junctions in the tissue. Plasma levels of norepinephrine also will fluctuate because of rapid metabolism rates and environmental, emotional, and endogenous stimuli provoking a sympathetic response. The responses of plasma catecholamines in spontaneously hypertensive rats and in normotensive rats of the same strain were compared after exposure to a variety of stressors. Drugs that inhibit monoamine oxidase, catechol-O-methyl transferase, or neuronal uptake were administered to show the effects of metabolic enzymes and neuronal uptake on the amounts of catecholamines reaching the circulation. Sympathetic nervous activity and the ability of the sympathetic nervous system to respond to a uniform stimulus are studied in hypertensive and normotensive subjects. A survey of the plasma levels of norepinephrine in a variety of neurologic disorders is given.
205 citations
References
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TL;DR: Clonidine increased the flexor reflex of spinal rats also after depletion of all known noradrenaline stores, indicating a stimulation of also central noradRenaline receptors.
545 citations
TL;DR: In 78 anaesthetized cats the lower brain stem was explored with microelectrodes for localization of the secondary neurones of the carotid sinus primary afferents by stimulation of the CSN these neurones were located exclusively in the nucleus tractus solitarius (NTS) at the level of the obex.
Abstract: In 78 anaesthetized cats the lower brain stem was explored with microelectrodes for localization of the secondary neurones of the carotid sinus primary afferents. By means of recording single unit activities and evoked potentials (E.P.) by stimulation of the carotid sinus nerve (CSN) these neurones were located exclusively in the nucleus tractus solitarius (NTS) at the level of the obex.
221 citations
TL;DR: In most animals the infusion of 1 μg/kg 2-(2, 6-dichlorophenylamino)-2-imidazoline-hydrochloride into the verterbral artery reduced the carotid occlusion reflex considerably, probably also via a central mechanism.
163 citations
162 citations
01 Jan 1965
158 citations
"The central action of antihypertens..." refers background in this paper
...The changes in noradrenaline storage and release induced by these compounds only occur in the peripheral nervous system and not in the cns (Boura & Green, 1965)....
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