Role of Ca²⁺entry and Ca²⁺stores in atypical smooth muscle cell autorhythmicity in the mouse renal pelvis

Abstract

ASMCs generated Ca2+ transients and cation-selective STDs via mechanisms involving Ca2+ release from IP3-dependent Ca2+ stores, STD stimulation of TSMCs was supported by Ca2+ entry through L type Ca2+ channels and Ca2+ release from ryanodine-sensitive stores.