Effects of α1- and α2-Adrenoceptor Blocking Drugs on Noradrenaline Release Rate in Anesthetized Rabbits

Majewski, H.; Lc, Rump; Hedler, L; Starke, Klaus

doi:10.1097/00005344-198309000-00001

Cited by 26 publications

(3 citation statements)

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“…The plasma noradrenaline levels, MAP and heart rate of rabbits anaesthetized with pentobarbitone 60-80mg kg-1, as measured at t = 49 min, are also shown in Table 1. The control values resemble those obtained previously (Majewski et al, 1983). As in pithed animals, NMN Figure 1 Interaction of opioid peptides and opioid antagonists on (a) plasma noradrenaline (NA) concentration, (b) mean arterial pressure (MAP) and (c) heart rate (HR) in pithed rabbits with electrically stimulated sympathetic outflow.…”

Section: Experiments In Anaesthetized Rabbitssupporting

confidence: 76%

Peripheral sympatho‐inhibitory cardiovascular effects of opioid peptides in anaesthetized rabbits

Szabó

Hedler

Schurr

et al. 1988

British J Pharmacology

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1 Opioid agonists influence isolated cardiovascular tissues from rabbits, as well as the cardiovascular system of pithed rabbits, through presynaptic receptors on postganglionic sympathetic nerve fibres. The present experiments were carried out in order to study effects which result from activation of these receptors in anaesthetized rabbits. 2 In pithed rabbits with electrically stimulated sympathetic outflow, infusion of [D-Ala2-D-Leu5]-enkephalin (DADLE) 10 yg kg-'min-1 and dynorphin-l-13) (dynorphin) 1 pgkg-1 min-1 decreased the plasma noradrenaline concentration, mean arterial pressure (MAP) and heart rate. The effects of dynorphin and, less completely, those of DADLE were antagonized by the peripherally selective opioid antagonists N-methyl naloxone bromide (NMN) 1.3mgkg-1 and N-methyl levallorphan methanesulphonate (NML) 1-3 mg kg-.3 In pentobarbitone-anaesthetized rabbits, DADLE 3-30ygkg-1 min-1 and dynorphin 0.3-3 g kg -1 min-1 decreased the plasma noradrenaline concentration and MAP. The highest dose of dynorphin also decreased heart rate, whereas DADLE l0ygkg-'min-' caused slight cardioacceleration. The effects of DADLE but not those of dynorphin decreased upon repeated administration. 4 The effects of dynorphin 10pgkg-'min-' were abolished or greatly attenuated by NMN 1.3mgkg-' and NML 3mgkg-'. In contrast, the antagonists reduced only slightly the blood pressure-lowering effect of DADLE 10pgkg-min-' and did not reduce significantly the effects of DADLE on the plasma noradrenaline level and heart rate. 5 It was concluded that systemically administered dynorphin produces sympatho-inhibition and an ensuing fall in blood pressure by an action at peripheral receptors, in all probability presynaptic K-receptors on postganglionic sympathetic nerve fibres. The effects of DADLE are more complex and may involve both central and peripheral components.

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Section: Experiments In Anaesthetized Rabbitssupporting

confidence: 76%

Peripheral sympatho‐inhibitory cardiovascular effects of opioid peptides in anaesthetized rabbits

Szabó

Hedler

Schurr

et al. 1988

British J Pharmacology

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“…Namely, while the effect of clonidine administered in a dose of 0.5 mg/kg is likely to be produced by activation of postsynaptic α 2 -adrenoceptors (32), the observed effect of yohimbine is probably due to the blockade of inhibitory presynaptic α 2 -adrenoceptors, resulting in increased noradrenaline release (44). However, as the action of clonidine and yohimbine could be mediated by the activation or by the blockade of α 2 -adrenoreceptors (32,41,45), and as the drugs used are not absolutely selective, other more receptor-distinctive agonists and/or antagonists might be useful in revealing the potential involvement of these receptors in diazepam-induced suppression of the HPA axis.…”

Section: Discussionmentioning

confidence: 99%

The involvement of noradrenergic mechanisms in the suppressive effects of diazepam on the hypothalamic-pituitary-adrenal axis activity in female rats

Štrac¹,

Mück‐Šeler²,

Pivac³

2012

Croat Med J

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AimTo elucidate the involvement of noradrenergic system in the mechanism by which diazepam suppresses basal hypothalamic-pituitary-adrenal (HPA) axis activity.MethodsPlasma corticosterone and adrenocorticotropic hormone (ACTH) levels were determined in female rats treated with diazepam alone, as well as with diazepam in combination with clonidine (α2-adrenoreceptor agonist), yohimbine (α2-adrenoreceptor antagonist), alpha-methyl-p-tyrosine (α-MPT, an inhibitor of catecholamine synthesis), or reserpine (a catecholamine depleting drug) and yohimbine.ResultsDiazepam administered in a dose of 2.0 mg/kg suppressed basal HPA axis activity, ie, decreased plasma corticosterone and ACTH levels. Pretreatment with clonidine or yohimbine failed to affect basal plasma corticosterone and ACTH concentrations, but abolished diazepam-induced inhibition of the HPA axis activity. Pretreatment with α-MPT, or with a combination of reserpine and yohimbine, increased plasma corticosterone and ACTH levels and prevented diazepam-induced inhibition of the HPA axis activity.ConclusionThe results suggest that α2-adrenoreceptors activity, as well as intact presynaptic noradrenergic function, are required for the suppressive effect of diazepam on the HPA axis activity.

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“…A series of experiments in rabbits were formulated to try and take these effects into account (Majewski et al 1982(Majewski et al , 1983a(Majewski et al , b, c, 1984 and these are discussed below. The drugs used in these series of experiments include the a,-adrenoceptor blocking drugs yohimbine and rauwolscine, the a,-adrenoceptor blocking drugs prazosin and corynanthine, the a,-adrenoceptor agonists clonidine and a-methylnoradrenaline, the a,-adrenoceptor agonist phenylephrine and the non-selective a-adrenoceptor agonist adrenaline.…”

Section: Prejunctional A-adrenoceptors and Animal Studiesmentioning

confidence: 99%

MODULATION OF NORADRENALINE RELEASE IN VIVO THROUGH PREJUNCTIONAL α‐ADRENOCEPTORS

Majewski

1987

Clin Exp Pharma Physio

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1. Extensive in vitro studies have suggested that noradrenaline release from sympathetic nerve endings is modulated by alpha 2-adrenoceptors on the terminal varicosities, activation of which by alpha-adrenoceptor agonists or neuronally released noradrenaline leads to inhibition of transmitter release. 2. Studies in intact animals support essentially the physiological operation of this mechanism, whereas human studies have reached mixed conclusions and more information is required.

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Effects of α1- and α2-Adrenoceptor Blocking Drugs on Noradrenaline Release Rate in Anesthetized Rabbits

Cited by 26 publications

References 0 publications

Peripheral sympatho‐inhibitory cardiovascular effects of opioid peptides in anaesthetized rabbits

Peripheral sympatho‐inhibitory cardiovascular effects of opioid peptides in anaesthetized rabbits

The involvement of noradrenergic mechanisms in the suppressive effects of diazepam on the hypothalamic-pituitary-adrenal axis activity in female rats

MODULATION OF NORADRENALINE RELEASE IN VIVO THROUGH PREJUNCTIONAL α‐ADRENOCEPTORS

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