An analysis of central adrenoceptors for control of cardiovascular function

Bhargava, K. P.; Mishra, Niraj; Tangri, K.K.

doi:10.1111/j.1476-5381.1972.tb08117.x

Cited by 57 publications

(18 citation statements)

References 16 publications

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“…However, the number of neurons which elicited excitatory responses to NE was larger in ATn sensitive neurons than in AT], non-sensitive neurons, as determined statistically. Considerable evidence has accumulated for the hypotensive action of a adrenergic stimulants and Q-adrenergic blockers as the result of central mechanisms (22)(23)(24).…”

Section: Discussionmentioning

confidence: 99%

Effects of Angiotensin Ii on the Medullaryneurons and Their Sensitivity to Acetylcholine and Catecholamines

Suga

Suzuki

1979

Japanese Journal of Pharmacology

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Abstract-In order to elucidate the mechanism of the central hypertensive action of angiotensin II (ATzi), the effects of ATII on the medullary neurons of rabbits were studied by the technique of electrophoretic application.ATII gave rise to excitatory effect on some neurons of medulla and this effect was antagonized by a specific AT,, antagonist, 1-sarcosine-8-alanine-ATi1.The ATII sensitive medullary neurons showed no specific response to acetylcholine, norepinephrine or isoproterenol, but there was a significant increase in the excitatory response to norepinephrine in comparison with the ATrr non-sensitive neurons. The excitatory effect of AT,, was not blocked by atropine, phentolamine and propranolol.The ATII sensitive neurons in the medulla apparently do not have a topograhically or functionally characteristic distribution related to the central vasomotor control mechanisms. The neurons in the area postrema did not respond to electrophoretically applied ATII, while microinjection of ATII in this region produced remarkable hypertensive responses. These results suggest that the mechanism of the central hypertensive action of ATI i administered into the vertebral artery is primarily mediated by the chemoreception of the area postrema. The mecha nism of central cardiovascular effect of ATrr and of the effects of acetylcholine and catecholamines on the medullary neurons are discussed.Since the first observation of a central effect of angiotensin II (AT,,) in dogs (1), con siderable evidence has accumulated that at least some of the hypertensive effects of AT,, are mediated by an action on the central mechanisms of the autonomic nervous system (2).The lower medulla is considered by several investigators to be one of the sites of central

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Section: Discussionmentioning

confidence: 99%

Effects of Angiotensin Ii on the Medullaryneurons and Their Sensitivity to Acetylcholine and Catecholamines

Suga

Suzuki

1979

Japanese Journal of Pharmacology

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“…Intracerebroventricular (i.c.v. ) injections of noradrenaline or adrenaline evoked hypotension and bradycardia in cats and dogs (Nashold, Mannarino & Wunderlich, 1962;Bhargava, Misra & Tangri, 1972). On the other hand, both excitatory and inhibitory cardiovascular responses, blocked by propranolol and phentolamine respectively, were reported with i.c.v.…”

Section: Introductionmentioning

confidence: 99%

Central Adrenoceptors and Cholinoceptors in Cardiovascular Control

Bhargava

Jain

Saxena

et al. 1978

British J Pharmacology

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1 In cats anaesthetized with chloralose, adrenoceptor and cholinoceptor agonists and antagonists were localized to the posterior hypothalamus (PH), lateral medullary pressor area (LMPA) and spinal autonomic loci to delineate the role of central cholinoceptors and adrenoceptors in cardiovascular control.2 All along the neuroaxis, the a-adrenoceptors seem to subserve an inhibitory and the f-adrenoceptors a facilitatory role in cardiovascular control. There appears to be a predominance of a-adrenoceptors at the medullary level and f-adrenoceptors at the hypothalamic level.3 The nicotinic cholinoceptors at the hypothalamic, medullary and spinal levels were facilitatory, whereas muscarinic cholinoceptors were inhibitory for cardiovascular control. However, muscarinic receptors were undetectable at the posterior hypothalamus. 4 The central cardiovascular effects of nicotine are attributed to nicotinic receptor activation and release of central catecholamines. 5 There appears to be a relationship between central cholinergic and adrenergic mechanisms in cardiovascular control.

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“…In this, the situation resembles that reported for noradrenaline by Cowell & Davey (1968) where, however, central and peripheral actions opposed each other whereas those of isoprenaline are similar. Gagnon & Melville (1967) and Bhargava et al (1972) have shown that intracerebroventricular isoprenaline stimulated central,-adrenoceptors since,-adrenoceptor blocking agents injected by the same route blocked the effects. It may be presumed that the central components of the actions of isoprenaline in the mouse are similarly mediated, though leakage of ,B-adrenoceptor blocking agents after intracerebroventricular injection in mice would preclude a decisive experiment along these lines, since the circulating agent could affect a tachycardia of central origin by blocking peripherally.…”

Section: Discussionmentioning

confidence: 99%

“…From this evidence it was suggested that sympathetic receptors exist in central regions paralleling those postulated in the periphery by Ahlquist (1948). Bhargava, Mishra & Tangri (1972) have shown these effects of intracerebroventricular isoprenaline to be central in origin in anaesthetized dogs by experiments in which bilateral removal of the stellate ganglion or transection of the upper spinal cord was carried out. Using conscious cats Day & Roach (1972) showed that intracerebroventricular isoprenaline produced tachycardia and hypertension, the latter being due to an increased systolic pressure.…”

Section: Introductionmentioning

confidence: 99%

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An Investigation of the Tachycardia Produced by Intracerebro‐ventricular Injections of Isoprenaline in Mice

Burden

Parkes

1975

British J Pharmacology

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I Isoprenaline, 3.5-20 ng, injected intracerebroventricularly in atropinized mice under pentobarbitone anaesthesia produced a dose-dependent tachycardia. 2 Pretreatment with either reserpine or pempidine blocked nervously-mediated tachycardia as shown by marked reduction of that due to stimulation of the spinal outflow in pithed mice. After pretreatment with these drugs, intracerebroventricular isoprenaline caused tachycardia of a similar degree and time course to that in mice not so pretreated. 3 Pretreatment with either reserpine or pempidine caused supersensitivity to the tachycardia due to intravenous isoprenaline. 4 When allowance was made for this supersensitivity in the effect of intracerebroventricular isoprenaline in pretreated mice, a small dose-dependent residual effect remained that could be attributed to leakage of isoprenaline into the peripheral circulation. 5 This was confirmed by the appearance of a late-developing tachycardia on intracerebroventricular injection of isoprenaline in spinal mice. 6 It is therefore concluded that the tachycardia caused by intracerebroventricular isoprenaline in mice is, at least initially, of central origin.Introduction.

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An analysis of central adrenoceptors for control of cardiovascular function

Cited by 57 publications

References 16 publications

Effects of Angiotensin Ii on the Medullaryneurons and Their Sensitivity to Acetylcholine and Catecholamines

Effects of Angiotensin Ii on the Medullaryneurons and Their Sensitivity to Acetylcholine and Catecholamines

Central Adrenoceptors and Cholinoceptors in Cardiovascular Control

An Investigation of the Tachycardia Produced by Intracerebro‐ventricular Injections of Isoprenaline in Mice

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