Involvement of Inositol 1,4,5-Trisphosphate Formation in the Voltage-Dependent Regulation of the Ca²⁺Concentration in Porcine Coronary Arterial Smooth Muscle Cells

Abstract

The involvement of inositol 1,4,5-trisphosphate (IP 3 ) formation in the voltage-dependent regulation of intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ) was examined in smooth muscle cells of the porcine coronary artery. Slow ramp depolarization from Ϫ90 to 0 mV induced progressive [Ca 2ϩ ] i increase. The slope was reduced or increased in the presence of Cd

Basal activity of voltage-gated Ca2+ channels controls the IP3-mediated contraction by α1-adrenoceptor stimulation of mouse aorta segments

“…The IC 50 of 2-APB was below the concentration of 50 mM, which is the highest concentration that avoided inhibition of Ca 2 þ uptake to the SR (SERCA), but caused a sevenfold decrease in IP 3 -sensitivity of the IP 3 receptor (Saleem et al, 2014). Therefore, the phenylephrineinduced phasic contraction in 0Ca is due to Ca 2 þ release through IP 3 receptor activation via IP 3 formation (Manolopoulos et al, 1991;Yamamura et al, 2012). Furthermore, the phasic contraction was not directly affected by the LCC blocker diltiazem, by membrane potential hyperpolarization with levcromakalim or by membrane potential depolarization with elevated K þ .…”

“…Similar results were obtained in isolated coronary SMC, where depolarization with slow ramp clamps elevated and hyperpolarization diminished intracellular Ca 2 þ signals. However, in these cells, it was described that with depolarization the continuous influx of Ca 2 þ via LCC caused activation of phospholipase C, IP 3 formation and subsequent SR Ca 2 þ release (Yamamura et al, 2012). In mouse aortic segments, however, we suggest that the background window Ca 2 þ influx via LCC, which was not only evident in isolated cells (Fleischmann et al, 1994;Yamamura et al, 2012), but also in multicellular preparations (Fransen et al, 2012a), contributed to filling of the contractile SR Ca 2 þ store and subsequent phenylephrine-induced and IP 3 -mediated phasic contractions.…”

“…However, in these cells, it was described that with depolarization the continuous influx of Ca 2 þ via LCC caused activation of phospholipase C, IP 3 formation and subsequent SR Ca 2 þ release (Yamamura et al, 2012). In mouse aortic segments, however, we suggest that the background window Ca 2 þ influx via LCC, which was not only evident in isolated cells (Fleischmann et al, 1994;Yamamura et al, 2012), but also in multicellular preparations (Fransen et al, 2012a), contributed to filling of the contractile SR Ca 2 þ store and subsequent phenylephrine-induced and IP 3 -mediated phasic contractions. It should be noted that contractile and non-contractile Ca 2 þ stores may be different and that (re)filling of the SR stores may occur via different pathways (Abe et al, 1996;Clark et al, 2010;van Breemen et al, 1995).…”

“…SR ryanodine receptor activation with caffeine (Wray and Burdyga, 2010) causes transient [Ca 2 þ ] i elevations and transient contractions, which are inhibited with ryanodine (Fransen et al, 2012a;. α 1 -Adrenoceptor stimulation with phenylephrine causes concentration-dependent IP 3 production (Eckert et al, 2000;Manolopoulos et al, 1991;Yamamura et al, 2012) and sustained contractions by the elevation of [Ca 2þ ] i via IP 3 receptor-mediated Ca 2þ release from SR Ca 2 þ stores and by Ca 2þ influx via Ca 2þ -permeable ion channels (Chiu et al, 1986;Eckert et al, 2000;Scarborough and Carrier, 1984;Villalba et al, 2007).…”

Potassium Channels in Regulation of Vascular Smooth Muscle Contraction and Growth

“…Y. Ganitkevich & Isenberg, 1993; Kukuljan, Rojas, Catt, & Stojilkovic, 1994; Q. H. Liu et al, 2009; Mahaut-Smith, Martinez-Pinna, & Gurung, 2008; Okada, Yanagisawa, & Taira, 1993; Urena, del Valle-Rodriguez, & Lopez-Barneo, 2007; Yamagishi, Yanagisawa, & Taira, 1992; Yamamura, Ohya, Muraki, & Imaizumi, 2012; Yanagisawa, Yamagishi, & Okada, 1993). Potassium channels also contribute to the regulation of proliferation of VSM cells through membrane potential-dependent (Bi et al, 2013; Miguel-Velado et al, 2005; Miguel-Velado et al, 2010) and membrane potential-independent mechanisms (Cidad et al, 2012; Cidad et al, 2015; Jimenez-Perez et al, 2016).…”