Cardiovascular reflexes from cardiac sensory receptors

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Abstract
The mammalian heart, especially its left ventricle, is densely innervated by sensory nerves. One set of these travels to the brainstem in the vagus nerves; the other to the spinal cord in sympathetic nerves. Excitation of vagal cardiac afferents, especially unmyelinated afferents from the left ventricle, cause a reflex bradycardia and fall in blood pressure and, under some conditions, a massive release of AVP. The sympathetic afferents convey the sensation of cardiac pain, but innocuous stimuli may cause a reflex tachycardia and rise in blood pressure. Both sympathetic and vagal cardiac afferents can be excited by mechanical distension of the heart (mechanoreceptors), and by a variety of foreign and endogenous chemical substances (chemosensitive receptors). It is not yet clear whether the effective natural stimulus to these receptors is mechanical, or through the chemical products of myocardial metabolism. Neither is it clear whether information from the heart exerts a minute-to-minute regulatory effect on the circulation, or whether it has a purely defensive role in the face of extreme disturbances of cardiac function. Cardiogenic reflexes are also thought to be the cause of haemodynamic and humoral disturbances that occur in clinical conditions such as myocardial ischaemia or infarction, left ventricular outflow obstruction, and acute reduction in central blood volume as well as during coronary angiography.