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channels in corpus
cavernosum smooth muscle: a novel mechanism for control of penile
erection
1 Departments of Physiology and Pharmacology and 2 Surgery, The University of Western Ontario, London, Ontario, and 3 Lawson Health Research Institute, St. Joseph's Health Centre, London, Ontario, Canada N6A 5C1
Little is known of the excitatory
mechanisms that contribute to the tonic contraction of the corpus
cavernosum smooth muscle in the flaccid state. We used patch-clamp
electrophysiology to investigate a previously unidentified inward
current in freshly isolated rat and human corporal myocytes.
Phenylephrine (PE) contracted cells and activated whole cell currents.
Outward current was identified as large-conductance
Ca2+-activated K+ current. The inward current
elicited by PE was dependent on the Cl
gradient and was
inhibited by niflumic acid, indicative of a Ca2+-activated
Cl (ClCa) current. Furthermore, spontaneous
transient outward and inward currents (STOCs and STICs, respectively)
were identified in both rat and human corporal myocytes and derived
from large-conductance Ca2+-activated K+ and
ClCa channel activity. STICs and STOCs were inhibited by PE
and A-23187, and combined 8-bromoadenosine cAMP and 8-bromoadenosine cGMP decreased their frequency. When studied in vivo, chloride channel
blockers transiently increased intracavernosal pressure and prolonged
nerve-evoked erections. This report reveals for the first time
ClCa current in rat and human corpus cavernosum smooth
muscle cells and demonstrates its key functional role in the regulation
of penile erection.
chloride current; calcium sparks; penis
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