Modulation of Noradrenaline Release by Peripheral Presynaptic α2-Adrenoceptors in Humans

Kang, Jie; Brummelen, P. Van; Vermey, P.; Timmermans, Pieter B.M.W.M.; Zwieten, P. A. van

doi:10.1097/00005344-198704000-00005

Cited by 31 publications

(28 citation statements)

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“…A similar increase in circulating noradrenaline was reported for the a2-adrenoceptor antagonist, idazoxan (Elliott et al, 1983) and a recent investigation by Jie et al (1987) has lent further support for the concept that prejunctional a2-adrenoceptors are involved in the regulation of noradrenaline release in man.…”

Section: C Cdsupporting

confidence: 71%

“…There is some evidence that pre-junctional a2-adrenoceptors are involved in the regulation of noradrenaline release in man (Brown et al, 1985;Jie et al, 1987) and that post-junctional a2-adrenoceptors may contribute to the regulation of human peripheral vascular tone (van Brummelen et al, 1986). In addition it has been reported that post-junctional a2-adrenoceptor mediated vasoconstriction is enhanced in essential hypertension (Bolli et al, 1984).…”

Section: Introductionmentioning

confidence: 99%

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An evaluation of the alpha‐adrenoceptor antagonism produced by SK&F 86466 in healthy normotensive males.

Schafers

Elliott

Howie

et al. 1990

Brit J Clinical Pharma

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SK&F 86466 is a novel, potent a-adrenoceptor antagonist which, in animal experiments, is reported to show a high selectivity for a2-adrenoceptors at both pre-and postjunctional sites. The effects of two intravenous doses of 80 and 200 pLg kg-' of SK&F 86466were assessed in a placebo-controlled, double-blind, randomised study in eight young, healthy, normotensive males. Two indices of a-adrenoceptor activity were investigated: i) Pressor responsiveness to the relatively selective ox-adrenoceptor agonist phenylephrine and to the preferential ot2-adrenoceptor agonist oa-methylnoradrenaline. ii) Circulating levels of noradrenaline. SK&F 86466 at a dose of 200,ug kg-1 produced rightward shifts of the pressor dose-response curves to both agonists: a 1.4 fold shift for phenylephrine (P = 0.023) and a 1.6 fold shift for a-methylnoradrenaline (P = 0.051). Erect plasma noradrenaline sampled at 105 min into the infusion was significantly increased from 2.9 to 5.0 nmol 1-1 by SK&F 86466 200 ,ug kg-' (P = 0.002). The change in the phenylephrine responses indicates post-junctional al-adrenoceptor blockade and the rise in noradrenaline is consistent with pre-junctional a2-adrenoceptor antagonist activity. Overall the results of this study suggest that SK&F 86466, at a dose of 200 jig kg-', causes both oxl-and aL2-adrenoceptor antagonism in human subjects.

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Section: C Cdsupporting

confidence: 71%

Section: Introductionmentioning

confidence: 99%

An evaluation of the alpha‐adrenoceptor antagonism produced by SK&F 86466 in healthy normotensive males.

Schafers

Elliott

Howie

et al. 1990

Brit J Clinical Pharma

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“…less than expected for this level of NA spillover (Jie et al 1987). Thus, some vasodilating mechanisms, perhaps hypoxia-mediated, must have opposed the action of NA (Weisbrod et al 2001), and/or the responsiveness of the vascular smooth muscle fibres to the action of vasoconstrictor agents is partly blunted in chronic hypoxia (Heistad et al 1972;Doyle &Walker, 1991).…”

Section: Figure 1 Blood Pressure and Vascular Conductancesmentioning

confidence: 91%

Chronic hypoxia increases blood pressure and noradrenaline spillover in healthy humans

Calbet¹

2003

J Physiology

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“…From studies on human forearm blood flow, it has been proposed that the postjunctional a 1 -adrenoceptors are activated only by neurally released NA, whereas a 2 -adrenoceptors are selectively stimulated by circulating catecholamines (Jie et al, 1984;1987). Later results from investigations on human isolated resistance arteries disputed this hypothesis, indicating that both a 1 -and a 2 -adrenoceptors are activated postjunctionally by neurally released NA (Stevens & Moulds, 1985;Parkinson et al, 1992;Stephens et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

Neurogenic double‐peaked vasoconstriction of human gastroepiploic artery is mediated by both α₁‐ and α₂‐adrenoceptors

Fukui

Yang

Chiba

2005

British J Pharmacology

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1 The contribution of postjunctional P2X receptors and subtypes of a-adrenoceptors to vasoconstrictor responses following periarterial electrical nerve stimulation (PNS, 30 s trains of pulses at a frequency of 2, 4 or 8 Hz) was investigated in human gastroepiploic arteries. 2 The vasoconstrictor response to PNS at a stimulation of 4 or 8 Hz was a two-peaked response, whereas at a frequency of 2 Hz it appeared only as a late peak. All vasoconstrictions evoked by PNS were abolished by phentolamine, a nonselective a-adrenoceptor inhibitor, but not by a,b-methylene ATP, a P2X receptor-desensitizing agent. 3 The early peak to PNS at 4 or 8 Hz was abolished by prazosin, an a 1 -adrenoceptor antagonist, while the late one still remained, although it was markedly inhibited. The responses remaining after prazosin were blocked by rauwolscine. The vasoconstrictor response to PNS at 2 Hz was not affected by prazosin (0.1 mM), but was abolished by rauwolscine (0.1 mM), an a 2 -adrenoceptor antagonist. 4 OPC-28326(10 mM), a newly developed vasodilator, which preferentially exerts its antagonistic actions on the a 2B -and a 2C -adrenoceptors, significantly reduced the noradrenaline-induced vasoconstriction in the absence or presence of prazosin. OPC-28326 had a greater inhibitory effect on the late peak evoked by PNS than the early one. The neurogenic responses remaining after OPC-28326 were abolished by prazosin. 5 The present results suggest that sympathetic vasoconstriction of the human gastroepiploic artery is mediated by both a 1 -and a 2 -adrenoceptors postjunctionally, but not by P2X receptors. The a 2 -adrenoceptors may be preferentially activated at a low frequency of stimulation, which induces a constriction more slowly than that by a 1 -adrenoceptors. The existence of a 2 -adrenoceptors may cause an enhancement of a 1 -adrenoceptor-induced responses.

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Modulation of Noradrenaline Release by Peripheral Presynaptic α2-Adrenoceptors in Humans

Cited by 31 publications

References 0 publications

An evaluation of the alpha‐adrenoceptor antagonism produced by SK&F 86466 in healthy normotensive males.

An evaluation of the alpha‐adrenoceptor antagonism produced by SK&F 86466 in healthy normotensive males.

Chronic hypoxia increases blood pressure and noradrenaline spillover in healthy humans

Neurogenic double‐peaked vasoconstriction of human gastroepiploic artery is mediated by both α₁‐ and α₂‐adrenoceptors

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Modulation of Noradrenaline Release by Peripheral Presynaptic α2-Adrenoceptors in Humans

Cited by 31 publications

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An evaluation of the alpha‐adrenoceptor antagonism produced by SK&F 86466 in healthy normotensive males.

An evaluation of the alpha‐adrenoceptor antagonism produced by SK&F 86466 in healthy normotensive males.

Chronic hypoxia increases blood pressure and noradrenaline spillover in healthy humans

Neurogenic double‐peaked vasoconstriction of human gastroepiploic artery is mediated by both α1‐ and α2‐adrenoceptors

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Neurogenic double‐peaked vasoconstriction of human gastroepiploic artery is mediated by both α₁‐ and α₂‐adrenoceptors