+ Organ Effects Heart Increases heart rate; contractility; conduction across AV node Lungs Increases respiratory rate; bronchodilation Liver Stimulates glycogenolysis Muscle Stimulates glycogenolysis and glycolysis Brain Systemic Vasoconstriction and vasodilation Triggers lipolysis Muscle contraction 7x speed timelapse video of fish melanophores responding to 200µM<unk>  As a hormone,<unk>  acts on nearly all body tissues by binding to adrenergic receptors. Its effects on various tissues depend of the type of tissue and expression of specific forms of adrenergic receptors. For example, high levels of<unk>  causes smooth muscle relaxation in the airways but causes contraction of the smooth muscle that lines most arterioles.<unk>  is a nonselective agonist of all adrenergic receptors, including the major subtypes α1, α2, β1, β2, and β3.<unk> 's binding to these receptors triggers a number of metabolic changes. Binding to α-adrenergic receptors inhibits insulin secretion by the pancreas, stimulates glycogenolysis in the liver and muscle, and stimulates glycolysis and inhibits insulin-mediated glycogenesis in muscle. β adrenergic receptor binding triggers glucagon secretion in the pancreas, increased adrenocorticotropic hormone (ACTH) secretion by the pituitary gland, and increased lipolysis by adipose tissue. Together, these effects lead to increased blood glucose and fatty acids, providing substrates for energy production within cells throughout the body.<unk>  causes liver cells to release glucose into the blood, acting through both alpha and beta adrenergic receptors to stimulate glycogenolysis.<unk>  binds to β2 receptors on liver cells, which changes conformation and helps Gs, a heterotrimeric G protein, exchange GDP to GTP. This trimeric G protein dissociates to Gs alpha and Gs beta/gamma subunits. Gs alpha stimulates adenylyl cyclase, thus converting adenosine triphosphate into cyclic adenosine monophosphate (AMP). Cyclic AMP activates protein kinase A. Protein kinase A phosphorylates and partially activates phosphorylase kinase.<unk>  also binds to α1 adrenergic receptors, causing an increase in inositol trisphosphate, inducing calcium ions to enter the cytoplasm. Calcium ions bind to calmodulin, which leads to further activation of phosphorylase kinase. Phosphorylase kinase phosphorylates glycogen phosphorylase, which then breaks down glycogen leading to the production of glucose.<unk>  also has significant effects on the cardiovascular system. It increases peripheral resistance via α1 receptor-dependent vasoconstriction and increases cardiac output by binding to β1 receptors. The goal of reducing peripheral circulation is to increase coronary and cerebral perfusion pressures and therefore increase oxygen exchange at the cellular level. While<unk>  does increase aortic, cerebral, and carotid circulation pressure, it lowers carotid blood flow and end-tidal CO2 or ETCO2 levels. It appears that<unk>  may be improving macrocirculation at the expense of the capillary beds where actual perfusion is taking place.
Adrenaline
Synephrine
Norepinephrine
Norepinephrine 
Adrenomedullin
Dobutamine
Dopamine
Dopamine 