Reflex bradycardia is abradycardia (decrease inheart rate) in response to thebaroreceptor reflex, one of the body's homeostatic mechanisms for preventing abnormal increases inblood pressure. In the presence of highmean arterial pressure, the baroreceptor reflex produces a reflex bradycardia as a method of decreasing blood pressure by decreasingcardiac output.[citation needed]
Blood pressure (BP) is determined by cardiac output (CO) andtotal peripheral resistance (TPR), as represented by the formulaBP = CO × TPR. Cardiac output (CO) is affected by two factors, the heart rate (HR) and thestroke volume (SV), the volume of blood pumped from oneventricle of the heart with each beat (CO = HR × SV, thereforeBP = HR × SV × TPR). In reflex bradycardia, blood pressure is reduced by decreasing cardiac output (CO) via a decrease in heart rate (HR).[citation needed]
An increase in blood pressure can be caused by increased cardiac output, increased total peripheral resistance, or both.Thebaroreceptors in thecarotid sinus sense this increase in blood pressure and relay the information to thecardiovascular centres in themedulla oblongata. In order to maintainhomeostasis, the cardiovascular centres activate theparasympathetic nervous system. Via thevagus nerve, the parasympathetic nervous system stimulates neurons that release the neurotransmitteracetylcholine (ACh) at synapses withcardiac muscle cells. Acetylcholine then binds toM2 muscarinic receptors, causing the decrease in heart rate that is referred to as reflex bradycardia.[citation needed]
The M2 muscarinic receptors decrease the heart rate by inhibitingdepolarization of thesinoatrial node viaGi protein-coupled receptors and through modulation ofmuscarinic potassium channels. Additionally, M2 receptors reduce the contractile forces of the atrial cardiac muscle and reduce the conduction velocity of theatrioventricular node (AV node). However, M2 receptors have no effect on the contractile forces of the ventricular muscle.[1]
Stimuli causing reflex bradycardia include: