Obesity, Hypoxemia, and Hypertension
Mechanistic Insights and Therapeutic Implications
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See related article, pp 227–235
Four decades ago, Trzebski et al in Warsaw reported an astonishing discovery, namely that hypersensitivity and augmented tonic activity of arterial chemoreceptors contribute to increased arterial pressure in young hypertensive men.1 This discovery has stood the test of time. In addition to increasing ventilation, activation of carotid chemoreceptors increases sympathetic nerve activity and arterial pressure. Young borderline hypertensive humans have a striking augmentation of the sympathetic nerve responses to chemoreceptor activation by hypoxemia.2 Conversely, suppression of arterial chemoreceptors by breathing 100% oxygen decreases sympathetic nerve activity and arterial pressure in hypertensive but not normotensive humans.3
Studies in spontaneously hypertensive rats and normotensive (Wistar) rats have paralleled and advanced these concepts.4,5 Spontaneously hypertensive rats display augmented increases in carotid sinus afferent activity during hypoxemia. In addition, carotid body denervation reduces the development and maintenance of increased sympathetic activity and arterial pressure in spontaneously hypertensive rats but not normotensive Wistar rats.4 The augmented sympathetic nerve response to hypoxemia is manifest in young prehypertensive spontaneously hypertensive rats and seems to result from a membrane abnormality that underlies the increased chemoreceptor sensitivity and activity.5 This suggests a primary genetic molecular mechanism for increased chemoreceptor sensitivity and tonic activity in spontaneous hypertension.
These and other studies in humans and rats have prompted interest in carotid body denervation as treatment for resistant, sympathetically mediated essential hypertension in humans.6
To this story of carotid chemoreceptors in spontaneous hypertension, Tom …