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Bradykinin and histamine-induced cytosolic calcium increase in capillary endothelial cells of bovine adrenal medulla

Authors

  • Raúl Vinet,

    Corresponding author
    1. Laboratory of Pharmacology, Faculty of Pharmacy, Universidad de Valparaíso, Gran Bretaña 1093, 2360102 Valparaíso, Chile
    2. Centro Regional de Estudios en Alimentos Saludables (CREAS), Región de Valparaíso, Avda. Universidad 330, 2360102 Valparaíso, Chile
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  • Magdalena P. Cortés,

    1. Department of Biochemistry, Faculty of Pharmacy, Universidad de Valparaíso, Gran Bretaña 1093, 2360102 Valparaíso, Chile
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  • Rocío Álvarez,

    1. Laboratory of Pharmacology, Faculty of Pharmacy, Universidad de Valparaíso, Gran Bretaña 1093, 2360102 Valparaíso, Chile
    2. Department of Pharmaceutical Sciences, Faculty of Pharmacy, Universidad de Valparaíso, Gran Bretaña 1093, 2360102 Valparaíso, Chile
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  • Marco A. Delpiano

    1. Department of Physiology, Faculty of Sciences, Universidad de Valparaíso, Gran Bretaña 1111, 2360102 Valparaíso, Chile
    2. Max-Planck-Institute for Molecular Physiology, Otto-Hahn-Str. 11, 44227 Dortmund, Germany
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Abstract

We have assessed the effect of bradykinin and histamine on the cytosolic free calcium concentration ([Ca2+]i) of bovine adrenal medulla capillary endothelial cells (BAMCECs). To measure [Ca2+]i changes in BAMCECs the intracellular fluorescent probe, fluo-3 AM, was used. Bradykinin (3 µM) produced a transient monophasic increase in [Ca2+]i, which was depressed by B1650 (0.1 µM), a B2-bradykinin receptor antagonist (D-Arg-[Hyp3, Thi5,8, D-Phe7]-Bradykinin). Similarly, increase in [Ca2+]i induced by histamine was also depressed by tripolidine (0.1 µM), an H1-histamine receptor antagonist. [Ca2+]i increase induced by both agonists was unaffected in the absence of extracellular Ca2+ or presence of antagonists of voltage operated Ca2+ channels (VOCCs). Thapsigargin (1 µM) did not abolish the increase of [Ca2+]i produced by bradykinin, but abolished that of histamine. In contrast, caffeine (100 µM), abolished the [Ca2+]i response induced by bradykinin (3 µM), but did not affect the [Ca2+]i increase induced by histamine (100 µM). The results indicate the presence of B2 bradykinin- and H1 histamine-receptors in BAMCECs. Liberation of Ca2+ induced by both agonists occurs through 2 different intracellular mechanisms. While bradykinin activates a sarco(endo) plasmic reticulum (SER) containing a SER Ca2+-ATPase (SERCA) thapsigargin-insensitive, histamine activates a SER containing a SERCA thapsigargin-sensitive. We suggest that the increase in [Ca2+]i induced by bradykinin and histamine could be of physiological relevance, modulating adrenal gland microcirculation.

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