SNS receptors Flashcards
Alpha 1 receptors
Drugs: adrenaline, metaraminol, noradrenaline
Effect: systemic vasoconstrictor
Tissue: vascular smooth muscle and myocardial tissue
How they act: Gq protein-coupled – activating phospholipase enzymes
Alpha 2 receptors
Drug: clonidine
Effect: Reduce sympathetic tone
Tissue: Vascular smooth muscle
How they act: Gi protein-coupled – inhibits adenylyl cyclase
Beta 1 receptor
Drugs: Dobutamine, isoprenaline, noradrenaline
Effect: Positive chronotrope and inotrope
Tissue: Kidneys, heart
How they act: Gs protein-coupled - activates cAMP and protein kinase pathway
Beta 2 receptor
Drugs: Isoprenaline and salbutamol
Effect: vasodilation and bronchial dilation
Tissue: vascular and bronchial smooth muscle
How they work: Gs protein-coupled - activates cAMP and protein kinase pathway
Dopaminergic 1 receptor
Drugs: Fenoldopam, dopexamine, dopaminergic
Effect: vasodilation in kidneys and splanchnic circulation
Tissue: renal and mesenteric vessels
How they act: Gs protein-coupled - activates cAMP and protein kinase pathway
Vasopressin 1
Drug: vasopressin
Effect: vasoconstriction
Tissue: vascular smooth muscle, liver, platelets
How they act: Gq protein-coupled - activating phospholipase enzymes
Vasopressin 2 receptor
Drug: vasopressin
Effect: Synthetic ADH – mediates water reabsorption in collecting ducts in response to osmoreceptors
Tissue: renal collecting ducts
How they act: Gs protein-coupled - activates cAMP and protein kinase pathway
Non-adrenoceptor mediated vasodilation or nitric oxide donors.
cGMP is activated when NO binds to guanylyl cyclase (GC) enzyme. GC concerts CTP into cGMP.
This activated protein kinase G which causes calcium levels to decrease = smooth muscle relaxation.
cGMP decreased both preload and afterload by causing vasodilation of veins and arteries. cGMP-mediated smooth muscle dilators reduce myocardial work and O2 consumption while also increasing oxygenation by vasodilation of the coronary arteries.
e.g. nitrates cause vasodilation and reduce preload. Reduce diastolic wall stress to improve sub endocardial blood flow. This improves the oxygen supply and demand ratio which reduces anginal pain