Abstract
1. Mental disorders associated with chronic stressors are established risk factors for cardiac morbidity and mortality, but there is no satisfactory explanation of the mechanistic link between mental and cardiac disorders. 2. The present article presents the hypothesis suggesting that abnormal functioning of serotonin 5-HT(1A) receptors in the lower brain stem may represent this missing link. Currently available data suggest that there may be a global downregulation of 5-HT(1A) receptors in depressive and panic patients. 3. Recent animal results indicate that 5-HT(1A) receptors, located in the medullary raphe, possibly on the raphe-spinal presympathetic cardiomotor neurons, reduce stress-elicited activation of these neurons. 4. Decreased density/function of 5-H(1A) receptors in the raphe area (possibly occurring during chronic stress/depression) may lead to increased sympathetic outflow to the heart and, consequently, to the increase in noradrenalin release from the cardiac sympathetic nerve terminals.
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