Ion channels and excitatory transmission in the smooth muscle of the urinary bladder.

The bladder of most non-human species receives dual purinergic and cholinergic excitatory innervation. Activation of P2x-purinoceptors depolarizes the cells, increases the spike frequency and causes contraction. Addition of agonists rapidly activates non-selective cation channels, which underly the excitatory junction potentials seen on simulation of the intrinsic nerves. In all species studied including humans the detrusor possesses well developed post-junctional purinergic mechanisms, and interspecies differences here cannot account for the large difference in the potency of the purinergic innervation seen. Muscarinic receptor activation causes contraction through pharmacomechanical coupling, using inositol trisphosphate as a second messenger. Increase in intracellular calcium results in outward currents through Ca activated K channels. In most species little depolarization or increase in spike frequency is seen, although in some, a slowly developing inward current mechanism is activated, which might account for the small delayed muscarinic depolarization seen following the purinergic excitatory junction potential.