Fig. 3.

Agonist concentration encoding of Ca²⁺-dynamics, (a) [Ca_c²⁺]-oscillations in a single rat hepatocyte induced by the stimulation of the vasopressin receptor (G_αq pathway). An increase in drug dose shows an increase in the frequency of [Ca_c²⁺]-spikes. (b) Modulation of amplitude and area under the curve (AUC) of [Ca_c²⁺]-spikes by increasing the drug dose of acetylcholine (G_αq pathway). (c)-(e) Frequency and amplitude modulation of [Ca_c²⁺]-oscillation in a single representative HeLa cell by stimulation of α₂-adrenergic receptor (G_αi/o pathway). Various dosesof norepinephrine were used. (f) Increase in Ca²⁺-release (amplitude modulation) by treatment of β-adrenergic receptor (G_αs pathway) using isoprenaline in rat atrial and ventricular myocytes. (g) Frequency modulation of [Ca_c²⁺]-oscillation by treatment of β₂-adrenergic receptors (G_αs pathway) with increasing doses of salbutamol in porcine airway smooth muscle cells. Over a concentration range of 1 nM to 100 nM, salbutamol progressively decreased the frequency of acetylcholine-induced [Ca_c²⁺]-transients but did not alter the amplitude of the spike train. At salbutamol concentration of 1 μM, the oscillations were completely inhibited. Adapted with permission from [50,[53], [54], [55], [56]]. Copyright (2020).