Stimulation of sensory nerve endings in the heart can induce potent reflex hemodynamic effects, primarily vasodilation and bradycardia. The afferent limb of the reflex consists of cardiac sensory nerve endings that originate in the atria and ventricles and travel through the vagus to the central nervous system. Mechanical stimulation of the ventricle, either by acute increases in left ventricular pressures and inotropism or by ventricular distortion, may also elicit the reflex. The cardiac inhibitory reflex should be suspected whenever hypotension is associated with paradoxical bradycardia, such as during the inferoposterior myocardial infarction. Afferents for the reflex are distributed preferentially in the inferoposterior wall of the left ventricle. Thus, in animal studies, occlusion of the circumflex coronary artery results in hypotension and bradycardia, and no reflex skeletal muscle vasoconstriction in response to the hypotension. These reflex responses are less pronounced with occlusion of the left anterior descending artery.
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