RAYNAUDS-PHENOMENON

Much has been learned about the complexity of the local, humoral and nervous factors regulating the normal behavior of the skin blood vessels, and many studies have addressed how this knowledge might relate to the causation of primary Raynaud's disease. Despite this, the mechanism(s) responsible for the attacks of digital vasospasm remain an enigma. A key question is whether these attacks represent an exaggeration of the normal mechanisms causing constriction of the digital vessels with local cooling, or are due to a specific abnormality. In this article it is suggested that multiple factors are responsible, including the possibility of co-transmitters released with norepinephrine from the sympathetic nerves, increased activation of beta-2-adrenoceptors on the nerve endings, a shift in the balance of alpha-1 and alpha-2 adrenoceptors on the vascular smooth muscle and in endothelium-derived relaxing and contracting factors, and altered interactions of the endothelium with the blood elements including the effects of increased platelet serotonin.