1983
DOI: 10.1007/bfb0031007
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Adrenergic mechanisms in blood vessels: Morphological and pharmacological aspects

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Cited by 61 publications
(21 citation statements)
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“…However, the b 2 AR is known to be the main isoform expressed in EC and in the skeletal muscles (Osswald and Guimarães, 1983;Guimarães and Moura, 2001;Lynch and Ryall, 2008), so we can assume that part of the effects of HI and bARKct gene therapy on total bAR density might be ascribed to changes in b 2 AR density. Moreover, our in vitro data in ECs have specifically investigated the effects of bARKct on b 2 AR signaling and function, clearly demonstrating a protective effect of bARKct on b 2 AR down-regulation.…”
Section: Discussionmentioning
confidence: 99%
“…However, the b 2 AR is known to be the main isoform expressed in EC and in the skeletal muscles (Osswald and Guimarães, 1983;Guimarães and Moura, 2001;Lynch and Ryall, 2008), so we can assume that part of the effects of HI and bARKct gene therapy on total bAR density might be ascribed to changes in b 2 AR density. Moreover, our in vitro data in ECs have specifically investigated the effects of bARKct on b 2 AR signaling and function, clearly demonstrating a protective effect of bARKct on b 2 AR down-regulation.…”
Section: Discussionmentioning
confidence: 99%
“…neuronal uptake can act as a dissipation mechanism for agonists acting on these 031-adrenoceptors. We have investigated whether responses of the f1-adrenoceptors in the left circumflex artery could be modulated by another dissipation mechanism, namely extraneuronal uptake, since extraneuronal uptake has been postulated to be more closely associated with 12-than with Pl-adrenoceptors (Bryan et al, 1981;Osswald & Guimaraes, 1983). In fact, potentiation, by ex-traneuronal uptake inhibitors, of responses known to be mediated exclusively by f1-adrenoceptors has not previously been described.…”
Section: Potencies and Relative Potencies Of Isoprenaline Noradrenalmentioning
confidence: 99%
“…In the present study, responses of the canine left circumflex artery to isoprenaline (mediated exclusively by 131-adrenoceptors, vide supra) were potentiated by corticosterone and by metanephrine. This suggests that modulation of f3-adrenoceptormediated responses by extraneuronal uptake is not confined to responses mediated by 32-adrenoceptors, as had previously been suggested (Bryan etal., 1981;O'Donnell & Wanstall, 1983;Osswald &Guimaraes, 1983).…”
Section: Potencies and Relative Potencies Of Isoprenaline Noradrenalmentioning
confidence: 99%
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“…Inactivation of norepinephrine release by sympathetic nerve stimulation in blood vessels is mainly carried out by neuronal (uptake-1) and extraneuronal uptake (uptake-2) of the transmitter and subsequent inactivation by MAO and catechol-O-methyltransferase (Osswald and Guimarã es, 1983). The uptake mechanisms for norepinephrine can thus regulate the amount of transmitter in the junctional cleft.…”
Section: Discussionmentioning
confidence: 99%