Evidence for an α-sympathomimetic component in the effects of catapresan on vasomotor centres: Antagonism by piperoxane

Schmitt, Henri; Schmitt, Mme Hélène; Fénard, S

doi:10.1016/0014-2999(71)90130-0

Cited by 263 publications

(45 citation statements)

References 13 publications

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“…We considered that clonidine has both hypotensive and bradycardiac effects originated in the central nervous system, since a central application of the drug showed only a fall in blood pressure with a bradycardia, and that even a very small dose of the drug was sufficient to cause such responses in this experiment. It is reasonable to consider that the cardiovascular effects of a central application of clonidine are due to a stimulation of central a-adrenoceptors in agreement with other reports (Schmitt et al 1971;Bucher et al 1973;Finch 1974;Bogaievsky et al 1974), since the effects to i.e. clonidine are completely reduced after a treatment with i.e.…”

Section: Discussionsupporting

confidence: 90%

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Peripherally and Centrally Mediated Bradycardiac Effects of Clonidine in Anesthetized or Spinal Rats

Ozawa¹,

Uematsu²

1976

Tohoku J. Exp. Med.

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Section: Discussionsupporting

confidence: 90%

“…These cardiovascular effects of clonidine are thought to be due to a stimulation of central a-adrenoceptors (Schmitt et al 1971(Schmitt et al , 1973bBucher et al, 1973;Finch 1974;Bogaievsky et al 1974). The attention of many investigators has been recently focused on the peripheral mechanism of bradycardia inducing effect of clonidine.…”

mentioning

confidence: 99%

Peripherally and Centrally Mediated Bradycardiac Effects of Clonidine in Anesthetized or Spinal Rats

Ozawa¹,

Uematsu²

1976

Tohoku J. Exp. Med.

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“…The experiments show that the effect of clonidine on the heart has a peripheral component in addition to its known central component (Schmitt, Schmitt & Fenard, 1971). Similar peripheral effects were shown by both clonidine and BS 100-141 and they can be explained by assuming that these drugs stimulate presynaptic a-adrenoceptors that inhibit transmitter release as postulated by Kirpekar & Puig (1971).…”

Section: Discussionmentioning

confidence: 99%

Inhibitory Effects of Clonidine and Bs 100‐141 on Responses to Sympathetic Nerve Stimulation in Cats and Rabbits

Pacha¹,

Salzmann²,

Scholtysik³

1975

British J Pharmacology

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1 In pithed cats, the spinal sympathetic outflow was stimulated preganglionically at segments C7 and TI and heart rate responses and nictitating membrane tone were measured in parallel.2 Clonidine and a related drug, BS 100-141 (N-amidino-2-(2,6-dichlorophenyl)acetamide hydrochloride), caused a dose-dependent inhibition of the stimulation-induced tachycardia but did not inhibit responses of the nictitating membrane. The inhibition of heart rate was antagonized by the oa-adrenoceptor blocking drug, phentolamine. 3 In isolated hearts of rabbits, noradrenaline release in response to adrenergic nerve stimulation was reduced by clonidine and BS 100-141 and the effect was antagonized by phentolamine. 4 The results support the view that presynaptic ci-adrenoceptors are involved in the regulation of transmitter release from adrenergic nerves. Cardiac adrenergic nerves appear more sensitive to a-adrenoceptor-mediated inhibition of impulse transmission than the sympathetic nerves to the nictitating membrane.

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“…2 "- 27 The marked decrease in circulating catecholamine levels observed after CLND could be explained by such a central mechanism. However, the action of CLND on peripheral presynaptic a-receptors, as observed in the present study, also may be an important factor in the reduction of circulating catecholamines and in the hypotensive action of that drug.…”

Section: Figure 3 Percent Change In the Release Of Norepinephrine In mentioning

confidence: 99%

Regulation of norepinephrine release from cardiac sympathetic fibers in the dog by presynaptic alpha- and beta-receptors.

Yamaguchi¹,

Champlain²,

Nadeau³

1977

Circulation Research

152

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SUMMARY The effect of pbenoxybenzamine (PBA), desmethylimipramine (DMI), donidine (CLND), sotalol (STL), and isoproterenol (ISPR) on the release of endogenous norepinephrine (NE) from the heart on right cardioaccelerator nerve stimulation was studied in anesthetized dogs. Under control conditions, the catecholamine levels in coronary sinus blood increased linearly with increasing frequencies of stimulation up to 10 Hz and did not increase further at 30 Hz. The release of NE was markedly enhanced after PBA (1 mg/kg, iv) and OMI (1 mg/kg, iv). The enhanced release of NE after DMI, bat not after PBA, was associated with a prolonged response in heart rate. In contrast, NE release was reduced after CLND (15 /xg/kg, iv) at stimulation frequencies of 1 and 2 Hz and this was associated with reduced responses in heart rate and left ventricular dP/dt. STL (5 mg/kg, iv) reduced significantly the release of NE at stimulation frequencies of 1-5 Hz, whereas ISPR enhanced NE outflow at frequencies of 1-4 Hz. These results support the existence of both negative and positive feedback mechanisms on the release of norepinephrine by cardiac sympathetic fibers mediated through presynaptic a-and /3-adrenoreceptors, respectively. The functional significance of these mechanisms is also suggested by the correlation found between changes in NE release and variations in cardiac responses under the various drug treatments.

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Evidence for an α-sympathomimetic component in the effects of catapresan on vasomotor centres: Antagonism by piperoxane

Cited by 263 publications

References 13 publications

Peripherally and Centrally Mediated Bradycardiac Effects of Clonidine in Anesthetized or Spinal Rats

Peripherally and Centrally Mediated Bradycardiac Effects of Clonidine in Anesthetized or Spinal Rats

Inhibitory Effects of Clonidine and Bs 100‐141 on Responses to Sympathetic Nerve Stimulation in Cats and Rabbits

Regulation of norepinephrine release from cardiac sympathetic fibers in the dog by presynaptic alpha- and beta-receptors.

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