Centrally mediated decrease in sympathetic tone induced by 2(2,6-dichlorophenylamino)-2 imidazoline (S.T. 155, Catapresan)

Schmitt, Henri; Schmitt, Mme Hélène; Boissier, J.R.; Jf, Giudicelli

doi:10.1016/0014-2999(67)90041-6

Cited by 161 publications

(47 citation statements)

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“…To our knowledge, the effect of clonidine on MSA has not been studied previously but in recordings from cervical sympathetic trunk, cardiac, splanchnic, and renal nerves, clonidine always caused a reduction of sympathetic activity. 6 '•• 20 ' 21 The reason for the difference is not clear, but several factors may contribute. Our experiments were conducted on conscious patients who received doses of 1.4 to 3.3 Mg/kg body weight, whereas previous studies were carried out on animals subjected to general anesthesia and surgery, and given higher doses (10 to 30 Mg/kg body weight).…”

Section: Discussionmentioning

confidence: 99%

The antihypertensive mechanism of clonidine in man. Evidence against a generalized reduction of sympathetic activity.

Wallin¹,

Frisk-Holmberg²

1981

Hypertension

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SUMMARY Recordings of multi-unit sympathetic activity were made from muscle branches of the peroneal nerve during i.v. bolus injection of 100 to 275 pg clonidine in seven hypertensive patients. Blood pressure was reduced in all patients, but sympathetic activity and heart rate could either increase or decrease. When plasma levels of clonidine were low, sympathetic activity tended to Increase, and when plasma levels were high, activity tended to decrease. A CUTE and chronic administration of clonidine lowers blood pressure (BP) in humans and is used in the treatment of hypertension. The effect is concentration-dependent, and after intravenous bolus injections, the BP reduction is linearly related to the logarithm of the plasma concentration of clonidine.1 The mechanism for the BP reduction is only incompletely understood. Clonidine is a partial pre-and postsynaptic a-adrenoreceptor agonist.2 From animal experiments, it has been postulated that the hypotensive effect is elicited centrally, 3 since the drug is active after intracisternal administration 4 and induces a BP reduction in baroreceptor-denervated animals.' The mechanism has been suggested to be a stimulation of central aadrenoreceptors, causing a reduction in peripheral sympathetic outflow.3 ' *"" The arterial baroreflex may be potentiated by clonidine, 9 " 11 but since the BP reduction remains after baroreceptor denervation, this cannot be the main hypotensive mechanism of the drug. 6 ' 9 In patients, no direct information is available on the effect of clonidine on sympathetic activity, but renal

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Section: Discussionmentioning

confidence: 99%

The antihypertensive mechanism of clonidine in man. Evidence against a generalized reduction of sympathetic activity.

Wallin¹,

Frisk-Holmberg²

1981

Hypertension

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“…Therefore, a possible interaction was excluded with clonidine on the chemosensitive zones at the ventral surface of the brain stem on which atropine itself has an action (Guertzenstein, 1973). Both the depressor and cardio-inhibitory effects of clonidine thus appear to result mainly or wholly from the same mechanism of action, a decrease in sympathetic discharge, which was found by Schmitt (1970) to be particularly pronounced in the cardiac nerves.…”

Section: Discussionmentioning

confidence: 99%

“…The fall is preceded by a transient rise which is a peripheral effect due to vasoconstriction. But the fall is central in origin and has been obtained with minute doses of clonidine injected into the vertebral arteries (Sattler & van Zweiten, 1967;Constantine & McShane, 1968;Katic, Lavery & Lowe, 1972) into the cisterna magna (Kobinger, 1967;Kobinger & Walland, 1967; Dollery & Reid, 1973), and into the lateral or third cerebral ventricle (Schmitt, 1970). The fall is not abolished by vagotomy and is due to a decrease in sympathetic vasomotor tone.…”

Section: Introductionmentioning

confidence: 99%

Localization of the central cardiovascular action of clonidine

Bousquet¹,

Guertzenstein²

1973

British J Pharmacology

111

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Summary The fall in arterial blood pressure with bradycardia that occurs on injection of clonidine into the cerebral ventricles and into the cisterna magna is attributed to an action on ‘chemosensitive zones’ situated at the ventral surface of the brain stem. This conclusion is based on the following results obtained in cats anaesthetized with pentobarbitone sodium. The fall in blood pressure no longer occurs on injection of clonidine (10 to 100 μg) into the cerebral ventricles when the passage of clonidine into the subarachnoid space is prevented by cannulation of the aqueduct. In this condition, the injections produce instead a rise in blood pressure. Applied bilaterally, by means of perspex rings, to the ventral surface of the brain stem, clonidine (10 μl of a 50 to 1,000 μg/ml solution placed in each ring) produces a fall in blood pressure with bradycardia, but only when the perspex rings cover the ‘chemosensitive zones’ from which changes in blood pressure and heart rate are obtained with various drugs.

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“…adrenaline (Day & Roach, 1974) and isoprenaline (Gagnon & Melville, 1967;Day & Roach, 1974). Moreover, centrally administered clonidine, an a-adrenoceptor agonist, decreased blood pressure, heart rate and sympathetic discharges (Schmitt, Schmitt, Boissier & Giudicelli, 1968).…”

Section: Introductionmentioning

confidence: 97%

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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Centrally mediated decrease in sympathetic tone induced by 2(2,6-dichlorophenylamino)-2 imidazoline (S.T. 155, Catapresan)

Cited by 161 publications

References 1 publication

The antihypertensive mechanism of clonidine in man. Evidence against a generalized reduction of sympathetic activity.

The antihypertensive mechanism of clonidine in man. Evidence against a generalized reduction of sympathetic activity.

Localization of the central cardiovascular action of clonidine

Central Adrenoceptors and Cholinoceptors in Cardiovascular Control

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