Question

. When introduced to salivary gland cells, acetylcholine promotes exocytosis. When introduced to heart pacemaker cells, acetylcholine causes a decrease in heart rate. Why does acetylcholine not also cause exocytosis in heart pacemaker cells?

Answer 1

Salivary glands are innervated by cholinergic parasympathetic neurons. This neurons release the neurotransmitter acetylcholine. Acetylcholine (Ach) binds to muscarinic receptors (M3 or M1) on salivary gland and activates release of calcium form intracellular stores via voltage gated calcium channels. There is increased depolarization induced by Ach binding to its receptor. This results in release of saliva from the acinar cells. The cAMP and calcium intracellular pathways crosstalk is involved in this secretion. This acetylcholine promotes exocytosis in salivary gland.

SA pacemaker cells undergo spontaneous depolarization as they lack true resting potentials. Spontaneous depolarization occurs in Phase 4 of action potential, which is through slow sodium currents and activation of T type calcium channels. Phase 0 is depolarization phase, while phase 3 is repolarization phase. Phase 0 is caused by increase calcium conductance through L type calcium channels. In phase, K+ channels open, causing repolarization.

The sinoatrial node is innervated by the vagus nerve. Activation of vagus nerve causes release of acetylcholine via parasympathetic stimulation. This parasympathetic Ach binds to its receptors and decreases the phase O of nodal action potential. ACh binds to pacemaker muscarinic receptors and decrease cAMP. There is less activation of the calcium channels, leading to decrease in phase O. Hence, there is decreased heart rate due to less stimulation of pacemaker cells, thereby not causing exocytosis.