An essential role of Cav1.2 L‐type calcium channel for urinary bladder function

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Abstract
Mice deficient in the smooth muscle Cav1.2 calcium channel (SMACKO, smooth muscle α1c‐ subunit calcium channel knockout) have a severely reduced micturition and an increased bladder mass. L‐type calcium current, protein, and spontaneous contractile activity were absent in the bladder of SMACKO mice. K+ and carbachol (CCh)‐induced contractions were reduced to 10‐ fold in detrusor muscles from SMACKO mice. The dihydropyridine isradipine inhibited K+‐ and CCh‐induced contractions of muscles from CTR but had no effect in muscles from SMACKO mice. CCh‐induced contraction was blocked by removing extracellular Ca2+ but was unaffected by the PLC inhibitor U73122 or depletion of intracellular Ca2+ stores by thapsigargin. In muscles from CTR and SMACKO mice, CCh‐induced contraction was partially inhibited by the Rho‐ kinase inhibitor Y27632. These results show that the Cav1.2 Ca2+ channel is essential for normal bladder function. The Rho‐kinase and Ca2+‐release pathways cannot compensate the lack of the L‐type Ca2+ channel.
Funding Information
  • Deutsche Forschungsgemeinschaft

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