Angina pectoris often results from ischemic episodes that excite chemosensitive and mechanoreceptive receptors in the heart. Ischemic episodes release a collage of chemicals, including adenosine and bradykinin, that excites the receptors of the sympathetic and vagal afferent pathways. Sympathetic afferent fibers from the heart enter the upper thoracic spinal cord and synapse on cells of origin of ascending pathways.
This review focuses on the spinothalamic tract, but other pathways are excited as well. Excitation of spinothalamic tract cells in the upper thoracic and lower cervical segments, except C7 and C8 segments, contributes to the anginal pain experienced in the chest and arm. Cardiac vagal afferent fibers synapse in the nucleus tractus solitarius of the medulla and then descend to excite upper cervical spinothalamic tract cells.
The lack of VR1 receptors on the inner surface could explain why no pain is felt. VR1 could also be a target for drugs that reduce or prevent chest pain, Pan says.
Capsaicin, the pungent ingredient in chilli peppers, activates VR1. Previous studies had shown that, when applied to the heart surfaces of animals, capsaicin causes changes in blood pressure and heart rate similar to those seen in heart attacks. But the receptors involved in producing these changes were not known. Pan used immunofluorescence labelling to show that VR1 was located on the outer surface of the heart.
To determine whether the receptor was involved in the cardiac reflex response, he destroyed the nerves containing VR1 in one group of rats and compared their response with a group with intact VR1 receptors.
In the intact rats, both capsaicin and bradykinin — a chemical released during heart attacks — led to an increase in blood pressure and nerve activity. But in rats with no VR1, no increases were detected at all.
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