Figure 1

(a) Shows the scheme of purinergic neurotransmission in rat atria. ATP and/or UTP are co-released with noradrenaline (NOR) or acetylcholine (ACh). At the neuroeffector junction, ATP is degraded by nucleotidases, until adenosine (ADO) interacts with P1 receptors that are followed by an inhibition of adenylyl cyclase (AC) and, causing a decrease in the cAMP levels, whereas PKA activity diminish Ca²⁺ concentration, promoting a NIE. Moreover, ATP or UTP may activate the P2X or P2Y receptors followed by an increase of Ca²⁺ influx or phospholipase C/inositol triphosphate (PLPC/IP3) pathway, respectively, leading to PIE. (b) Shows the time course effect of a single concentration of ATP or UTP in atria. The latter exposure produced a biphasic effect represented by an initial NIE followed by a PIE. Individual vertical lines show atrial contractions elicited by field stimulation with pulses of 5 ms at 2 Hz. The basal contraction is known as baseline contraction amplitude (BCA). (c) Shows that NIE and PIE were calculated according to the formulas 1 and 2, respectively. (Figure based on Gergs et al.²⁸).