Calyculin-A inhibits nitrergic relaxations of the mouse anococcygeus.
The aim was to determine whether blockade of store-operated Ca(2+) entry, or inhibition of Ca(2+) sensitisation, is the predominant mechanism by which neuronally released nitric oxide mediates relaxation of the mouse anococcygeus. Nitrergic relaxations to field stimulation (10 Hz, 10 s trains) were unaffected by the sarcoplasmic reticulum Ca(2+) ATPase blocking agent thapsigargin (100 nM), known to prevent nitric-oxide-induced inhibition of store-operated Ca(2+) entry. Conversely, the myosin phosphatase inhibitor calyculin-A (1 microM) caused almost complete abolition of nitrergic relaxations. The results provide evidence that inhibition of Ca(2+) sensitisation is the major cellular mechanism underlying nitrergic relaxation of the mouse anococcygeus.
Gibson
Alan
A
School of Biomedical Sciences, King's College London, Room 2.12 Hodgkin Building, Guys Campus, London SE1 9RT, UK. alan.gibson@kcl.ac.uk
Wallace
Pat
P
McFadzean
Ian
I
D001003:Anal Canal / Q000187:drug effects* / Q000502:physiology; D000818:Animals; D008297:Male; D008387:Marine Toxins; D051379:Mice; D009126:Muscle Relaxation / Q000187:drug effects* / Q000502:physiology; D026602:Nitrergic Neurons / Q000187:drug effects* / Q000502:physiology; D010080:Oxazoles / Q000494:pharmacology*; D012445:Sacrococcygeal Region / Q000502:physiology
D008387:Marine Toxins; D010080:Oxazoles; C059041:calyculin A