Relaxation of Arterial Smooth Muscle by Calcium Sparks

TLDR

Activation of ryanodine‑sensitive calcium‑release channels in smooth muscle raises local intracellular calcium, which triggers arterial dilation. Ca²⁺ sparks in smooth muscle cells activate KCa channels, causing hyperpolarization and arterial dilation, while exerting only a minor direct effect on overall intracellular calcium levels.

Abstract

Local increases in intracellular calcium ion concentration ([Ca 2+ ] i ) resulting from activation of the ryanodine-sensitive calcium-release channel in the sarcoplasmic reticulum (SR) of smooth muscle cause arterial dilation. Ryanodine-sensitive, spontaneous local increases in [Ca 2+ ] i (Ca 2+ sparks) from the SR were observed just under the surface membrane of single smooth muscle cells from myogenic cerebral arteries. Ryanodine and thapsigargin inhibited Ca 2+ sparks and Ca 2+ -dependent potassium (K Ca ) currents, suggesting that Ca 2+ sparks activate K Ca channels. Furthermore, K Ca channels activated by Ca 2+ sparks appeared to hyperpolarize and dilate pressurized myogenic arteries because ryanodine and thapsigargin depolarized and constricted these arteries to an extent similar to that produced by blockers of K Ca channels. Ca 2+ sparks indirectly cause vasodilation through activation of K Ca channels, but have little direct effect on spatially averaged [Ca 2+ ] i , which regulates contraction.