Effects of pentobarbitone and decerebration on the clonidine-induced circulatory changes

Trolin, G.

doi:10.1016/0014-2999(75)90219-8

Cited by 41 publications

(18 citation statements)

References 21 publications

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“…These results are in accordance with the findings of other authors (Trolin 1975;Gurtu et al 1983;Kawasaki and Takasaki 1986;Kawasaki et al 1992). The pressor response has been shown to be mediated through the activation of α 2 -adrenoceptors in the central nervous system (Kawasaki and Takasaki 1986; Kawasaki et al 1992;Ricci et al 1992) probably located in the hypothalamus (Ebihara et al 1993), and the bradycardic response could be mediated through the activation of α 2 -adrenoceptors in the nucleus of the tractus solitarii (Van Zwieten 1980;Hamilton et al 1992;Chan et al 1996).…”

Section: Discussionsupporting

confidence: 96%

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Central benzodiazepine involvement in clonidine cardiovascular actions

Castro

Ricci²,

Taira³

et al. 1999

Can. J. Physiol. Pharmacol.

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It is well known that the GABAergic and noradrenergic systems play an important role in blood pressure and heart rate regulation. Benzodiazepines and beta-carbolines, respectively, increase or decrease the probability of chloride-channel opening induced by GABA. The aim of this study was to determine, in conscious rats, the interaction existing between the central alpha2-adrenoceptor stimulation induced by clonidine and the facilitation or impairment of benzodiazepine receptor activity through the administration of either diazepam, a benzodiazepine receptor agonist, or methyl 6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate (DMCM), an inverse benzodiazepine agonist. Clonidine (5-10 microg, intracerebroventricularly) reduced heart rate and increased mean blood pressure by activation of central alpha2-adrenoceptors. Diazepam (2 mg/kg, intravenously (i.v.)) induced an increase in heart rate, while DMCM (0.3 mg/kg, i.v.) elicited a bradycardic effect. The bradycardic effects induced by both clonidine and DMCM were antagonized by the prior administration of methylatropine (1.5 mg/kg, i.v.). DMCM (0.3 mg/kg, i.v.) prevented the clonidine effects on heart rate and mean blood pressure, while diazepam (2 mg/kg, i.v.) failed to modify these effects. Our results suggest that the bradycardic effects of clonidine are mediated by a vagal stimulation and are related to the activation of a GABAergic pathway.

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Section: Discussionsupporting

confidence: 96%

“…Trolin (1975) has postulated that clonidine increases blood pressure by an action on the forebrain, and Ebihara et al (1993) have postulated that the pressor response to clonidine is mediated by an activation of α 2 -adrenoceptors in the hypothalamus.…”

Section: Introductionmentioning

confidence: 99%

Central benzodiazepine involvement in clonidine cardiovascular actions

Castro

Ricci²,

Taira³

et al. 1999

Can. J. Physiol. Pharmacol.

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show abstract

“…This difference between anesthetized and unanesthetized animals has been previously observed after the i.v. injection of clonidine in normotensive rats (Trolin, 1975). Hypotensive responses to either peripheral or central administration of clonidine have been classically observed in hypertensive rats.…”

Section: Discussionmentioning

confidence: 99%

Interaction between glutamatergic and nitrergic mechanisms mediating cardiovascular responses to l-glutamate injection in the diagonal band of Broca in anesthetized rats

2007

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“…Clonidine was also reported -in high doses -to induce a pressor response when the drug was injected into the lateral ventricle of the brain of cats and prevented to reach the floor of the fourth ventricle by cannulation of the acqueduct of Sylvius (BOUSQUET and GUERTZENSTEIN, 1973), but in these experiments a leakage of the drug into the systemic circulation, leading to a stimulation of peripheral ex adrenoceptors and to hypertension, was not ruled out. The pressor effect of clonidine was increased in rats by prehypothalamic section (HENNING et aI., 1976;TROLIN, 1976). Superfusion of the posterior hypothalamus with a push-pull cannula was reported to increase the pressor response to stimulation of this structure (PmLrP-PU et aI., 1973a, b).…”

Section: Cardiac Nervementioning

confidence: 95%