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J. Pablo Huidobro-Toro

Researcher at Pontifical Catholic University of Chile

Publications -  83
Citations -  2746

J. Pablo Huidobro-Toro is an academic researcher from Pontifical Catholic University of Chile. The author has contributed to research in topics: Receptor & Vas deferens. The author has an hindex of 30, co-authored 82 publications receiving 2610 citations. Previous affiliations of J. Pablo Huidobro-Toro include Andrés Bello National University & University of Chile.

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Activation and Regulation of Purinergic P2X Receptor Channels

TL;DR: Data obtained from numerous site-directed mutagenesis experiments accumulated during the last 15 years are discussed with reference to the crystal structure, allowing a structural interpretation of the molecular basis of orthosteric and allosteric ligand actions.
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Anandamide elicits an acute release of nitric oxide through endothelial TRPV1 receptor activation in the rat arterial mesenteric bed.

TL;DR: It is proposed that low concentrations of anandamide, devoid of vasorelaxing effects, elicit an acute release of NO mediated predominantly by the activation of endothelial TRPV1 receptors whose physiological significance remains elusive.
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P2Y1 and P2Y2 receptors are coupled to the NO/cGMP pathway to vasodilate the rat arterial mesenteric bed

TL;DR: Endothelial P2Y1 and P2y2 receptors coupled to the NO/cGMP cascade suggest that extracellular nucleotides are involved in endothelial‐smooth muscle signalling.
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Zinc and copper modulate differentially the P2X4 receptor

TL;DR: The present results are compatible with the working hypothesis that trace metals, such as copper and zinc, are physiological modulators of the P2X4 receptor, and hypothesize the existence of metal binding site(s), which are most likely localized in the extracellular domain of thePN4 receptor structure.
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Clonidine-induced nitric oxide-dependent vasorelaxation mediated by endothelial α2-adrenoceptor activation

TL;DR: Clonidine and congeners activate endothelial α2D‐adrenoceptors coupled to the L‐arginine pathway, suggesting that the antihypertensive action of clonidine involves an endothelial vasorelaxation mediated by NO release, in addition to presynaptic mechanisms.