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

Abstract

We have assessed the effect of bradykinin and histamine on the cytosolic free calcium concentration ([Ca(2+)]i ) of bovine adrenal medulla capillary endothelial cells (BAMCECs). To measure [Ca(2+)]i changes in BAMCECs the intracellular fluorescent probe, fluo-3 AM, was used. Bradykinin (3 µM) produced a transient monophasic increase in [Ca(2+)]i , which was depressed by B1650 (0.1 µM), a B2-bradykinin receptor antagonist (D-Arg-[Hyp(3), Thi(5,8) , D-Phe(7)]-Bradykinin). Similarly, increase in [Ca(2+)]i induced by histamine was also depressed by tripolidine (0.1 µM), an H1-histamine receptor antagonist. [Ca(2+)]i increase induced by both agonists was unaffected in the absence of extracellular Ca(2+) or presence of antagonists of voltage operated Ca(2+) channels (VOCCs). Thapsigargin (1 µM) did not abolish the increase of [Ca(2+)]i produced by bradykinin, but abolished that of histamine. In contrast, caffeine (100 µM), abolished the [Ca(2+)]i response induced by bradykinin (3 µM), but did not affect the [Ca(2+)]i increase induced by histamine (100 µM). The results indicate the presence of B2 bradykinin- and H1 histamine-receptors in BAMCECs. Liberation of Ca(2+) induced by both agonists occurs through 2 different intracellular mechanisms. While bradykinin activates a sarco(endo) plasmic reticulum (SER) containing a SER Ca(2+) -ATPase (SERCA) thapsigargin-insensitive, histamine activates a SER containing a SERCA thapsigargin-sensitive. We suggest that the increase in [Ca(2+)]i induced by bradykinin and histamine could be of physiological relevance, modulating adrenal gland microcirculation.

Ca2+ signals in human umbilical endothelial cells derived from pregnancy with fetal growth restriction associated with hypertensive disorder

“…Our previous studies demonstrated that bradykinin, histamine, ATP and α-7 nicotinic acetylcholine receptors agonists increase [Ca 2+ ] i in endothelial cells (16)(17)(18). In human umbilical vein endothelial cells (HUVECs), ATP-induced Ca 2+ signal typically consists of an initial transient phase followed by a prolonged sustained phase (18).…”

Connexin and Pannexin Large-Pore Channels in Microcirculation and Neurovascular Coupling Function

“…GJ channels could contribute to the hyperpermeability mechanism because of their proximity and interactions with other junction proteins [170][171][172][173]. GJ channels and a hemichannel opening could be involved in hyperpermeability because the development of hyperpermeability is associated with an agonist-induced increment in the endothelial intracellular calcium concentration ([Ca 2+ ] i ), and maintaining hyperpermeability over time depends on an extracellular Ca 2+ influx [174][175][176][177][178][179][180], while ATP signaling is related to hyperpermeability mainly through purinergic receptor activation [181,182].…”

Calcium Mobilization in Endothelial Cell Functions

“…Supporting these studies, Vinet et al, demonstrated that bradykinin and histamine induced calcium increase in ECs by means of different intracellular mechanisms based on the different sensitivity to thapsigargin. These authors claimed that bradykinin- and histamine-induced intracellular Ca 2+ increase are of physiological relevance in modulating adrenal gland microcirculation [91]. The physiological role of a number of agonist-induced Ca 2+ mobilization in ECs, such as angiotensin II, serotonin and acetylcholine has previously been extensively reviewed [8,92].…”