![]() These drugs are administered intravenously in continuous infusions. The dose of adrenaline in anaphylactic shock is 0.25 – 1 mg, while when used as a supplement to local anaesthetics the dose is only 10 – 20 µg. ![]() This makes it useful in haemodynamic instability due to bradycardia. Isoprenaline has β1 effect and β2 effect, giving it a predominantly chronotropic effect. This makes it especially useful in acute heart failure and cardiogenic shock. This makes it increase the CO while causing peripheral vasodilation. Its use has mostly fallen out of favour as other cathecolamines are preferred instead.ĭobutamine has strong β1 effect and small α and β2 effects. It can also be added to local anaesthetic solutions to increase their effect and topically to stop bleeding.ĭopamine acts on D1 and D2 receptors, as well as β and α receptors. In higher doses however, the alpha-adrenergic receptor effect predominates, causing vasoconstriction in addition to an increased CO.Īdrenaline is also the main treatment in anaphylactic shock. In low doses the β1 activity predominates, causing inotropic and chronotropic effects but no vasoconstriction (as the β2-mediated vasodilation outweighs the α1-mediated vasoconstriction. Noradrenaline acts on mainly α1 and β1 receptors, producing vasoconstriction and positive heart effects.Īdrenaline has strong β1 activity and moderate β2 and α1 activity. The exact drug to use depends on the type of shock and the desired effect, and is mostly the work of a specialised in intensive care. Noradrenaline, adrenaline, dopamine, dobutamine, and isoprenaline are all used in the treatment of haemodynamic instability or shock. Noradrenaline, adrenaline, dopamine, and isoprenaline (as well as vasopressin and phenylephrine) are vasopressors, but also inotropes to some degree. Drugs of both types are important in haemodynamic instability, where there can be severe hypotension and the cardiac output may be insufficient. Inotropes are drugs which increase cardiac contractility. Vasopressors are drugs which induce peripheral vasoconstriction, thereby increasing systemic vascular resistance (SVR), which in turn increases blood pressure. Catecholamines in clinical practice Compounds ![]() Not written in the table is the fact that β1 receptors stimulate renin release. Activation of α2 receptors decreases sympathetic outflow by decreasing noradrenaline (NE) transmission, thereby causing negative heart effects and vasodilation. The most important takeaway from this table is that α1 receptors mainly cause vasoconstriction, β1 receptors mainly cause positive heart effects (chronotropy, inotropy) which increases cardiac output, and that β2 receptors mainly cause vasodilation and bronchodilation. D1 activates vasodilation of renal, splanchnic, coronary and cerebral vessels. D2 is Gi coupled and therefore inactivates protein kinase A. D1 is Gs coupled as well and therefore activates protein kinase A. Hint: An easy way to remember the G-proteins of α and β receptors is to remember the mnemonic “qiss”, which sounds almost like “kiss”. α1 has Gq, α2 has Gi, β1 has Gs and β2 has Gs.ĭ1 and D2 are the receptors for dopamine. Recall from the previous topic that α2 receptor is part of the negative feedback, so it makes sense that it is inhibitory.Īll β receptors are Gs coupled, meaning that they activate adenylyl cyclase and therefore increase the level of cAMP and activates protein kinase A. Α2 receptor has Gi type G-protein, meaning it reduces the activity of adenylyl cyclase and therefore reduces the level of cAMP in the cell and inhibits protein kinase A. The result will be activation of protein kinase C. Α1 receptor has a Gq type G-protein, meaning that when an agonist binds to it will phospholipase C be activated. Gs-type G-protein activates adenylyl cyclase, Gi type inhibits it and Gq type activates phospholipase C. Recall that depending on the type of G-protein on the inside of the cell will the activity of the receptor be different. Overview of drugs CatecholaminesĪdrenergic receptors, or adrenoceptors are the receptors that catecholamines can bind to. Now we’re going to look at some directly acting ones. In the previous topic we saw some indirectly acting sympathomimetics.
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