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      Vasodilator Effect of Tertatolol in Isolated Perfused Rat Kidneys: Involvement of Endothelial 5-HT 1A Receptors

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          Abstract

          The aim of the studies was to examine the mechanism of the renal vasodilator action of the beta-adrenoceptor antagonist tertatolol. In isolated Tyrode perfused rat kidneys, constricted with norepinephrine, serotonin (5-HT) or BaCl<sub>2</sub>, tertatolol evokes dilatations; these vasodilator responses are not due to an interaction of tertatolol with alpha- or beta-adrenoceptors, muscarinic or nicotinic receptors, opioid receptors, dopamine or histamine receptors and they are independent of prostaglandin release. In the presence of ritanserin and ICS 205930, to block 5-HT<sub>2</sub> and 5-HT<sub>3</sub> receptors, tertatolol, 5-HT, 5-carboxamidotryptamine (5-CT) and 8-hydroxy-2 (di-n-propylamino) tetralin (8-OH-DPAT) all evoked renal vasodilator responses that were significantly reduced by the nonselective 5-HT antagonist metergoline and by the selective 5-HT<sub>1A </sub>antagonist BMY 7378 suggesting that 5-HT<sub>1</sub> receptors resembling the 5-HT<sub>1A</sub> subtype were involved. The nitric oxide (NO) inhibitors hemoglobin and nitro-L-arginine (L-NNA), as well as the guanylate cyclase inhibitor methylene blue also inhibited the vasodilator responses to tertatolol and to the serotonergic agonists, suggesting the involvement of the NO-cyclic GMP pathway. These data suggest that 5-HT receptors located on the vascular endothelium of the rat renal circulation are involved in the vasodilator responses caused by tertatolol and these receptors resemble the 5-HT<sub>1A</sub> subtype.

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          Author and article information

          Journal
          CRD
          Cardiology
          10.1159/issn.0008-6312
          Cardiology
          S. Karger AG
          978-3-8055-5869-3
          978-3-318-01965-0
          0008-6312
          1421-9751
          1993
          1993
          18 November 2008
          : 83
          : Suppl 1
          : 5-9
          Affiliations
          Division of Angiology, Institut de Recherche Servier, Suresnes, France
          Article
          176004 Cardiology 1993;83:5–9
          10.1159/000176004
          7903215
          © 1993 S. Karger AG, Basel

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          Pages: 5
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