Role of Acetylcholine in Central Vasomotor Regulation

Sinha, J. N.; Dhawan, K.N.; Chandra, O; Gupta, Garima

doi:10.1139/y67-059

Cited by 34 publications

(14 citation statements)

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“…carbachol is not significantly influenced by sectioning of the bilateral cervical vagal nerves. On the other hand, it has been reported that a pressor response can be produced by the central application of a muscarinic or nicotinic agent, and that the pressor responses to the central applications of cholinomimetic agents originate in either the central muscarinic or nicotinic mechanism (4,9,10,16). In the present experiments, a pressor response was observed with both i.e.…”

Section: Effectssupporting

confidence: 46%

“…As carbachol has both muscarinic and nicotinic actions, it is considered that the pressor response to the central application of carbachol originates in either muscarinic or nicotinic, or both mecha nisms. Actually this pressor response originating in either muscarinic or nicotinic mecha nism has already been reported (7,16). In the present experiments, however, we considered that the pressor response to i.e.…”

Section: Effectsmentioning

confidence: 69%

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Centrally Mediated Cardiovascular Effects of Intracisternal Application of Carbachol in Anesthetized Rats

Ozawa

Uematsu

1976

Japanese Journal of Pharmacology

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Abstract-The pressor response to the intracisternal (i.e.) injection of carbachol (1 µg) in anesthetized rats was analyzed. This response was significantly reduced by the intravenous (i.v.) injection of guanethidine (5 mg), hexamethonium (10 mg) or phen tolamine (5 mg), and conversely, potentiated by i.v. desmethylimipramine (0.3 mg), while propranolol (0.5 mg) i.v. selectively inhibited the enlargement of pulse pressure and the tachycardia following i.e. carbachol (I ug). On the other hand, the pressor response to i.e. carbachol (1 ,g) was almost completely blocked by i.e. atropine (3 µg) or hexamethonium (500 µg), and significantly reduced by i.e. chlorpromazine (50 lag) but significantly potentiated by i.e. desmethylimipramine (30 µg). The pressor response to i.e. carbachol (I yg) remained unchanged after sectioning of the bilateral cervical vagal nerves but disappeared after sectioning of the spinal cord (C7-C8). From the above result it is suggested that the pressor response to i.e. carbachol originates in the central muscarinic mechanism, is exerted through the central and peripheral adren ergic mechanisms, and that the sympathetic trunk is the main pathway.

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Section: Effectssupporting

confidence: 46%

Section: Effectsmentioning

confidence: 69%

Centrally Mediated Cardiovascular Effects of Intracisternal Application of Carbachol in Anesthetized Rats

Ozawa

Uematsu

1976

Japanese Journal of Pharmacology

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“…Later Bhawe (1958) obtained both pressor and depressor responses with large doses of ACh injected into the lateral ventricles of anaesthetized cats and dogs. Pressor responses after intraventricular injection of carbachol and ACh in the anaesthetized dog were also reported by Dhawan, Gupta, Dixit & Chandra (1965) and Sinha, Dhawan, Chandra & Gupta (1967). According to Srimal, Jaju, Sinha, Dixit & Bhargava (1969) intraventricular choline in anaesthetized dogs produces first a rise and then a prolonged fall in arterial blood pressure, and Sinha et al (1967) suggested that cholinomimetic substances stimulate the vasomotor centre.…”

Section: Introductionmentioning

confidence: 59%

Cardiovascular responses to injections of cholinomimetic drugs into the cerebral ventricles of unanaesthetized dogs

Lang

Rush

1973

British J Pharmacology

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Summary1. The cardiovascular and behavioural effects of cholinomimetic drugs injected through a cannula chronically implanted into a lateral cerebral ventricle were examined in unanaesthetized dogs.2. Acetylcholine (ACh) (10-20 pg) produced an increase in arterial pressure and heart rate, the dogs became more alert, moved their heads, licked and swallowed and then became drowsy. 3. The responses to ACh were potentiated by intraventricular physostigmine (5 ,ug), were abolished by intraventricular atropine (100 ,ug) but were unaffected by intraventricular mecamylamine (250 ,g). The responses to ACh were reproducible on any one day if injections were given again after a 30 min interval but tolerance developed when ACh was injected repeatedly over periods of several days. 4. Methacholine (40 ,ug) produced similar behavioural and cardiovascular effects to ACh but of a longer duration. The responses to methacholine were abolished by intraventricular atropine (100 ,ug). 5. Nicotine (20-60 ,g) produced a biphasic cardiovascular response of an initial brief pressor response and tachycardia followed by a secondary increase in arterial pressure and heart rate which was greater in magnitude and duration. The secondary cardiovascular effects were associated with restlessness and vomiting.6. The responses to nicotine were abolished by prior injection of mecamylamine (250 ,ug) but were unaffected by atropine (100 ,ug). The responses to nicotine were not reproducible if injections were repeated on the same day but could be again produced if a few days were allowed to elapse between injections.7. An increased heart rate occurred during the pressor response to the cholinomimetic drugs but when a comparable pressor response was produced by intravenous infusion of noradrenaline in the same unanaesthetized dogs pronounced reflex bradycardia resulted. 8. The results indicate that the activation of both muscarinic and nicotinic cholinergic mechanisms leads to cardiovascular and behavioural effects in the conscious dog although the site of action and peripheral mechanisms have not been determined.

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“…Existence of vasoactive neurones in the spinal cord, which can function independent of the supra spinal influences has also been re ported (1). We have earlier demonstrated that acetylcholine acts as an excitatory transmitter in the medul lary vasomotor loci (2). The purpose of the present investigation was to throw some light on the nature of the neurohumor in spinal vasomotor neurones by observing the effect of alleged neurohumors on the spinal compression vasomotor response (3).…”

mentioning

confidence: 78%

Effect of Neurohumors on Spinal Vasomotor Neurones

Sinha

Gupta

Dhawan

1968

Japanese Journal of Pharmacology

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The role of central nervous system in the regulation of blood pressure is now well established. The loci concerned in the regulation of blood pressure are situated all along the neuraxis. Vasomotor center situated in the medulla oblongata plays the key role in the regulation of the vascular tone. Existence of vasoactive neurones in the spinal cord, which can function independent of the supra spinal influences has also been re ported (1). We have earlier demonstrated that acetylcholine acts as an excitatory transmitter in the medul lary vasomotor loci (2). The purpose of the present investigation was to throw some light on the nature of the neurohumor in spinal vasomotor neurones by observing the effect of alleged neurohumors on the spinal compression vasomotor response (3).The present study was carried out on 18 adult mongrel dogs of either sex, anaesthetized with pentobar bitone sodium (35 mg/kg i.v.). The animals were routinely vagotomized and maintained on artificial posi

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Role of Acetylcholine in Central Vasomotor Regulation

Cited by 34 publications

References 0 publications

Centrally Mediated Cardiovascular Effects of Intracisternal Application of Carbachol in Anesthetized Rats

Centrally Mediated Cardiovascular Effects of Intracisternal Application of Carbachol in Anesthetized Rats

Cardiovascular responses to injections of cholinomimetic drugs into the cerebral ventricles of unanaesthetized dogs

Effect of Neurohumors on Spinal Vasomotor Neurones

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