Isoprenaline

Isoprenaline is a non-selective beta adrenergic receptor agonist. Agonism of beta-1 and beta-2 adrenergic receptors causes the alpha subunit of G-protein coupled receptors to exchange GMP for GTP, activating them, and allowing the alpha subunit to dissociate from the beta and gamma subunits. Dissociation of the alpha subunit activates adenylate cyclase, converting ATP to cyclic AMP. Cyclic AMP activates protein kinase A (PKA), which phosphorylates cardiac L-type calcium channels such as Cav1.2. These channels depolarize cells by inward active transport of calcium ions.

Agonism of beta-1 adrenergic receptors lead to increased strength of contractility, conduction of nerve impulses, speed of relaxation, and rate in the heart.

Agonism of beta-2 adrenergic receptors leads to glycogenolysis in the liver, glucagon release from the pancreas, and activation of the renin-angiotensin-aldosterone system.

In the alveoli, agonism of beta-2 adrenergic receptors, activates similar pathways to the heart, however the end result is regulation of sodium channels, the cystic fibrosis transmembrane conductance regulator (CFTR), and sodium potassium ATPase. PKA phosphorylates scaffolding proteins and sodium channels, increasing the number of sodium channels on the apical side of alveolar cells and increasing active transport of sodium ions into cells. Agonism of beta-2 adrenergic receptors can also increase chloride ion transport across CFTR. Together, these actions lead to passive transport of water out of the alveoli, and the clearance of alveolar fluid.