33 The effect of eserine on the activity of adrenergic nerves in the rat

Varagić, V.M.; Lešić, R.; Vučo, J.; Stamenović, B.

doi:10.1016/0006-2952(61)90200-3

Cited by 8 publications

(2 citation statements)

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“…The pressor response to physostigmine is presumed to involve a central cholinergic link, with an activation of central cholinergic mechanisms, which subsequently trigger the peripheral sympathetic activation (Varagi6 & Krstic, 1966;Varagic et al, 1969). Two possible sites of cholinergically-mediated pressor response to physostigmine are nucleus tractus solitarius and the locus coeruleus (Brezenoff & Giuliano, 1982).…”

Section: Discussionmentioning

confidence: 99%

The effect of enkephalins and of β‐endorphin on the hypertensive response to physostigmine in the rat

Varagić

Stojanović

1987

British J Pharmacology

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1 Intracarotid injection of [Leu]enkephalin and [Met]enkephalin produced a dose-dependent biphasic change in blood pressure of the rat consisting of an initial shortlasting fall followed by a longlasting increase of blood pressure. Naloxone consistently depressed or abolished the effects of enkephalins on blood pressure. Intracarotid injection of P-endorphin only occasionally produced a hypotension, or did not produce any change in the blood pressure of the rat.3 All three opioids ([Leu]enkephalin, [MetJenkephalin and P-endorphin) significantly depressed or abolished the hypertensive response to intravenous injection of physostigmine. This depressive action of opioids was easily reversed by naloxone. 5 It is concluded that opioids depress the central cholinergic link implicated in the hypertensive response to physostigmine most probably by inhibiting acetylcholine and/or noradrenaline release in the structures relevant for the action of physostigmine on blood pressure of the rat. This interaction is realized through the activation of opioid receptor(s).

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Section: Discussionmentioning

confidence: 99%

The effect of enkephalins and of β‐endorphin on the hypertensive response to physostigmine in the rat

Varagić

Stojanović

1987

British J Pharmacology

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“…It has been well documented that IV injection of physostigmine produces a hypertensive response in anaesthetized rats. This effect is due to cholinergically mediated activation of adrenergic mechanisms in the central nervous system (CNS) (VaragiC, 1955 ;VaragiC et al, 1969; Brezenoff and Giuliano, 1982;VaragiC, 1985).…”

Section: Introductionmentioning

confidence: 99%

Effects of Bestatin and Phosphoramidon on the Hypertensive Response to Physostigmine in the Rat

Džoljić

Varagić

1987

Fundamemntal Clinical Pharma

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Intracarotid (IC) injection of bestatin produced a dose-dependent biphasic change in blood pressure (BP) of the rat, consisting of an initial short-lasting fall followed by a long-lasting increase. This effect was regularly depressed or abolished by IV injection of naloxone. IC injection of Leu-enkephalin also produced a biphasic BP response, with the same characteristics as that produced by IC injection of bestatin. This effect was also easily blocked by IV injection of naloxone. IC injection of bestatin significantly potentiated the BP response to IC injection of Leu-enkephalin. This potentiated response was blocked by naloxone. IC injection of both bestatin and phosphoramidon, whether separately or in combination, significantly depressed the hypertensive response to physostigmine. This depressive action of bestatin and phosphoramidon on physostigmine hypertension can be significantly antagonized or even reversed by IV injection of naloxone. IC injection of both bestatin and phosphoramidon did not affect the BP response to either acetylcholine or catecholamines. It is concluded that bestatin and phosphoramidon, injected into the carotid artery, inhibit the activity of aminopeptidase and "enkephalinase", thus producing an accumulation of enkephalins in the central nervous system. These enkephalins activate opioidergic receptors in the brain, but concomitantly produce a depression of the cholinergic-adrenergic interaction in the central nervous system, which is known to be a prerequisite for the hypertensive response to physostigmine in the rat.

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