Abstract
Altitude hypoxia induces an increase in adrenergic activity in humans. However, a
decrease in maximal heart rate is observed after a few days of exposure to altitudes
above 3500 m, as well as a decrease in chronotropic response to isoproterenol infusion.
This phenomenon has been linked to a desensitization of β-adrenoceptors (βAR), and/or
an increase in parasympathetic activity. A decrease in the density of βAR in chronic
hypoxia has been found in rat left ventricle and in human lymphocytes, without modification
of the affinity of βAR for an agonist or antagonist, and a decreased adenylate cyclase
activity in the right ventricle. In the same conditions, the density of adenosine
A1 receptors is decreased by 46% in rat myocardium, without alteration in the coupling
between hormone, receptor and Gi protein. The density of muscarinic receptors is increased
by 40%, with an increase in the affinity for an agonist, suggesting an augmented parasympathetic
effect. Hypoxia probably acts on all the receptors involved in the modulation of cardiac
chronotropic activity; the combined effects of chronic hypoxia on these receptors
tend to a beneficial limitation of myocardial oxygen consumption, especially during
heavy exercise.
Key words
Hypobaric hypoxia - adrenergic receptors - muscarinic receptors - adenosinergic receptors
- heart
