Drugs online research references
J Cardiovasc Pharmacol. 1985;7 Suppl 6:S137-43.
In vivo and in vitro studies of alpha 2-adrenoceptor responses in human vascular smooth muscle.
Thom S, Hayes R, Calvete J, Sever PS.
To assess the role of alpha 2-receptor mechanisms in the control of vascular tone in humans, the pharmacological activities of RX 781094, an alpha 2-antagonist, and UK 14304, an alpha 2-agonist, have been investigated with the additional use of an alpha 1-antagonist, doxazosin. The effects of these agents on human forearm blood flow have been studied. In addition, some preliminary observations on the effects of these alpha 2-selective agents on isolated human arterial segments have been made. The alpha 2 agonist, UK 14304, produced a dose-dependent reduction in forearm blood flow, but the antagonism of this response by both doxazosin and RX 781094 at a dose which must be regarded as nonselective casts doubt on the hypothesis that alpha 2-receptors may be located postsynaptically in human vascular smooth muscle. These observations may be explained by UK 14304 having partial alpha 1-agonist activity. RX 781094 infused at low doses produced a dose-dependent reduction in forearm blood flow, which is interpreted as evidence for a presynaptic alpha 2 autoregulatory mechanism in the vasculature. Observations on isolated arterial segments (mesenteric, renal, splenic, gastric, and brachial) obtained during surgical procedures and mounted under tension in tissue baths did not provide evidence for a postsynaptic alpha 2-receptor mediating vasoconstriction. In contrast, the potentiation of the adrenaline response in the presence of the alpha 2 antagonist, RX 781094, supports the possibility that, in humans, an extrajunctional alpha 2-receptor may serve as the adrenergic mechanism for the release of an endothelial derived relaxing factor.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2414576&dopt=Abstract
J Cardiovasc Pharmacol. 1985;7 Suppl 6:S149-52.
Postjunctional alpha-adrenoceptors and the regulation of arteriolar tone in humans.
van Brummelen P, Jie K, Timmermans PB, van Zwieten PA.
The highly selective alpha-adrenoceptor agonists methoxamine (alpha 1) and azepexole (alpha 2), the less selective alpha-adrenoceptor agonists clonidine (alpha 2 greater than alpha 1) and guanfacine (alpha 2 greater than alpha 1), and the highly selective antagonists doxazosin (alpha 1) and yohimbine (alpha 2) were used to study post-junctional alpha-adrenoceptor subtypes in human blood vessels. Studies were done in healthy volunteers. All drugs were given intraarterially, and changes in forearm blood flow were measured by plethysmography. All agonists produced a significant and dose-dependent vasoconstriction. The effect of azepexole was abolished by yohimbine but hardly influenced by doxazosin. The reverse was found for methoxamine. The clonidine and guanfacine-induced vasoconstriction was partly prevented by both antagonists. Single infusions of doxazosin and yohimbine gave significant vasodilation. It is concluded that post-junctional alpha 1-and alpha 2-adrenoceptors are present in human blood vessels and contribute to basal vascular tone. In a second study, it was shown that both alpha-adrenoceptor subtypes are involved in the vasoconstrictor effect of exogenous adrenaline and noradrenaline. No preference was found of either catecholamine for the postjunctional alpha 1-and alpha 2-adrenoceptor.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2414578&dopt=Abstract
J Cardiovasc Pharmacol. 1987 Apr;9(4):407-13.
Modulation of noradrenaline release by peripheral presynaptic alpha 2-adrenoceptors in humans.
Jie K, van Brummelen P, Vermey P, Timmermans PB, van Zwieten PA.
The existence of a functional presynaptic alpha 2-adrenoceptor that modulates noradrenaline release was studied in 15 volunteers. Noradrenaline spillover was measured in the forearm under basal conditions, during single intraarterial infusions of the alpha-adrenoceptor antagonists yohimbine (alpha 2, 1.0 micrograms/kg/min) and doxazosin (alpha 1, 0.1 microgram/kg/min), and during intraarterial infusion of tyramine (1.25 microgram/kg/min) alone and in combination with either and both alpha-adrenoceptor antagonists. Forearm blood flow (FBF) was measured by plethysmography. Noradrenaline spillover was calculated as the product of FBF and the difference in arterial and venous plasma noradrenaline. The various infusions did not induce systemic hemodynamic effects. Tyramine induced a dose-dependent decrease in FBF (p less than 0.001) which was reduced by yohimbine (p less than 0.01), as well as by doxazosin (p less than 0.01), and abolished by the combination of both alpha-adrenoceptor antagonists (p less than 0.001). During basal conditions noradrenaline spillover was virtually zero, and this was not changed by yohimbine or doxazosin. Local infusion of tyramine increased noradrenaline spillover (p less than 0.05). This tyramine-induced noradrenaline spillover was further increased by yohimbine (p less than 0.01) and by the combination of yohimbine and doxazosin (p less than 0.001). The single infusion of doxazosin only enhanced the tyramine-induced noradrenaline spillover significantly when it was preceded by yohimbine. The present investigation supports the concept of a presynaptic alpha 2-adrenoceptor modulating noradrenaline release from sympathetic nerve endings via a negative feedback mechanism in humans. Stimulation of noradrenaline release might help to reveal this mechanism.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2438503&dopt=Abstract
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