Norepinephrine responses in rat renal and femoral veins are reinforced by vasoconstrictor prostanoids
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Data
2015
Autores
Souza Rossignoli, Patrícia de [UNESP]
Yamamoto, Fernanda Zocatelli
Pereira, Oduvaldo Câmara Marques [UNESP]
Chies, Agnaldo Bruno
Título da Revista
ISSN da Revista
Título de Volume
Editor
Elsevier B. V.
Resumo
Norepinephrine (NE) responses are larger in renal and femoral veins compared to phenylephrine (PE). These differences may be due to the subtypes of adrenoceptor involved in these responses or to the involvement of local modulatory mechanisms. Therefore, the present study investigated in organ bath the adrenoceptor subtypes involved in the NE and PE responses in both renal and femoral veins as well as the influence of local mechanisms related to NO and to prostanoids upon these responses. The obtained data showed that the NE responses in these veins were not significantly modified by the selective inhibition of β1 or β2-adrenoceptors as well as AT1 or AT2 receptors. However, yohimbine reduced the NE Rmax in renal veins and, in parallel, right shifted the NE concentration-response curves in femoral veins. In both veins, prazosin reduced the NE Rmax and the clonidine induced a measurable contraction. The endothelium removal attenuated the NE responses in femoral veins, thereby abolishing the differences of NE and PE responses. Furthermore, the NE responses in renal and femoral veins were attenuated by indomethacin, which suppressed the statistical difference in relation to the PE response. In conclusion, a synergism between α1- and α2-adrenoceptors is essential to assure full NE contractile responses in both renal and femoral veins. Thus, by acting simultaneously in these adrenoceptors, NE induces more pronounced contractile responses, in comparison to PE, not only in renal but also in femoral veins. Moreover, this pronounced NE response in both renal and femoral veins appears to involve endothelium-derived vasoconstrictor prostanoids.
Descrição
Palavras-chave
(r)-(−)-phenylephrine hydrochloride (pubchem cid: 5284443), (±)-isoproterenol hydrochloride (pubchem cid: 5807), Acetylcholine chloride (pubchem cid: 6060), Adrenoceptor, Atenolol (pubchem cid: 2249), Clonidine hydrochloride (pubchem cid: 20179), Endothelin 1 (pubchem cid: 44284481), Ici 118,551 hydrochoride (pubchem cid: 46704341), Indomethacin (pubchem cid: 3715), Losartan potassium (pubchem cid: 11751549), N(ω)-nitro-l-arginine methyl ester hydrochloride (pubchem cid: 39836), Norepinephrine, Pd 123,319 di(trifluoroacetate) salt hydrate (pubchem cid: 5311345), Phenylephrine, Prazosin hydrochloride (pubchem cid: 68546), Prostanoid, Vein, Yohimbine hydrochloride (pubchem cid: 6169), L-(−)-norepinephrine (+)-bitartrate salt monohydrate (pubchem cid: 24847757)
Como citar
Vascular Pharmacology, v. 72, p. 93-100, 2015.