Ca²⁺ signaling in mouse mesenteric small arteries: myogenic tone and adrenergic vasoconstriction

Abstract

Zacharia J, Zhang J, Wier WG. Ca 2ϩ signaling in mouse mesenteric small arteries: myogenic tone and adrenergic vasoconstriction.

Inositol trisphosphate receptors in smooth muscle cells

“…Ca 2ϩ puffs arise from the synchronous opening of ϳ30 IP 3 R channels distributed within a ϳ400-nm diameter cluster in Xenopus oocytes (170,194 (10,18,29,111,190). In isolated retinal arteriole SMCs, ET-1 increased Ca 2ϩ oscillation frequency and this elevation was inhibited by blockers of IP 3 Rs and RyRs, indicating that IP 3 R-RyR cross talk stimulates Ca 2ϩ oscillations (190,218 (249). Similarly, ANG II receptor antagonists abolished Ca 2ϩ ripples and reduced myogenic tone in tail arteries (9).…”

“…It was concluded that ANG II produced locally within the arterial wall stimulates Ca 2ϩ ripples, which regulate myogenic tone (9). Therefore, IP 3 Rmediated Ca 2ϩ ripples may be a Ca 2ϩ signal by which the local renin-angiotensin system in the arterial wall contributes to myogenic constriction (9,249 sparks, albeit in a small number of SMC types (116,190,218,252). RyR-and IP 3 R-mediated SR Ca 2ϩ release both stimulated Ca 2ϩ sparks in SMCs of choroidal and retinal arterioles, pulmonary artery, and trachea (116,190,218,252).…”

“…U-73122, a PLC inhibitor, dilated pressurized cerebral and ophthalmic arteries, suggesting that DAG/PKC and/or IP 3 /IP 3 Rs contribute to myogenic tone (85,92,166,237 (231). Similarly, in pressurized mesenteric and tail arteries, IP 3 R-mediated Ca 2ϩ ripples were proposed to stimulate myogenic constriction (9,249). SR-dependent Ca 2ϩ waves contributed to myogenic tone at low intravascular pressure in cerebral artery SMCs, although the contribution of IP 3 Rs was not determined (151).…”

Marfan Syndrome Decreases Ca²⁺ Wave Frequency and Vasoconstriction in Murine Mesenteric Resistance Arteries without Changing Underlying Mechanisms

“…The characteristics of the spatial and temporal patterns of the changes in [Ca 2+ ] i are of fundamental importance in determining their efficacy in activating contraction, through Ca 2+ /calmodulin-dependent myosin light chain kinase. Confocal imaging of [Ca 2+ ] i within single smooth muscle cells in the arterial wall has shown that the spatiotemporal patterns of the agonist-stimulated Ca 2+ response are more complex than previously thought, as in many types of blood vessels activation of α 1 -adrenoceptors elicits propagating Ca 2+ waves that occur asynchronously in the individual smooth muscle cells [2,3,4,5,6,7]. Increasing concentrations of agonist are associated with graded contraction and recruitment of cells which produce asynchronous Ca 2+ waves of increasing frequency [5,8,9].…”

The Role of Actin Filament Dynamics in the Myogenic Response of Cerebral Resistance Arteries

“…6 However, pressure elevation also evokes asynchronous Ca 2 þ waves within individual vascular smooth muscle cells because of release of Ca 2 þ from the sarcoplasmic reticulum, 42,43 similarly to the Ca 2 þ waves observed during agonist-induced contraction. 44 Thus, myogenic constriction is suppressed by membrane hyperpolarization, block of voltagegated Ca 2 þ channels, removal of extracellular Ca 2 þ , or application of ML-7 (which inhibits MLCK activity). 2,6,43,45,46 The extent of myogenic depolarization must be precisely controlled to obtain an appropriate increase in [ 6,42 However, these changes are not sufficient to explain the phenomenon.…”