Abstract

Carotid bodies are monitors of oxygen and glucose delivery to the brain. Faced with the threat of hypoxia or hypoglycemia carotid bodies initiate responses to counter the threat. General corrective action is to improve the perfusion by increasing the arterial blood pressure. Specific corrective actions are to stimulate ventilation to improve oxygen availability or to induce insulin resistance to raise blood glucose levels. Inappropriateness of response caused by misreading of hypoxia as hypoglycemia and hypoglycemia as hypoxia is observed experimentally and clinically. The response to all four types of hypoxia, namely, hypoxic, anemic, histotoxic and ischemic (or stagnant) hypoxia, is stimulation of ventilation and elevation of blood pressure. Ischemia produced by narrowing of the artery to the carotid body activates the carotid bodies. The activation produces hypertension, stimulation of ventilation and insulin resistance that manifests as non-insulin dependent diabetes mellitus. There is epidemiologic and necropsy evidence for the onset of atherosclerotic changes in childhood. Early atherosclerotic changes occurring in the region of carotid arteries and their bifurcation narrows the lumen of the arteries to the carotid bodies and produce hypo-perfusion of the carotid bodies. This ischemic hypoxia is a causative, or at least a permissive factor for hypertension and/or non-insulin dependent diabetes mellitus. It is suggested that neither non-insulin dependent diabetes mellitus causes hypertension nor hypertension causes diabetes mellitus, but both are caused by dysfunctional carotid bodies.

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