Increased cardiac sympathetic activity: Cause or compensation in vasovagal syncope?

Excerpt

Vasovagal syncope is relatively common, often occurring during orthostatic stress [1]. Hypotension and loss of consciousness are attributed to inhibition of sympathetic vasoconstrictor tone and/or parasympathetic-mediated bradycardia [1]. While a variety of factors may lead to vasovagal syncope, an initial compensatory increase in sympathetic activity to the heart may paradoxically activate cardiac sensory nerves traveling in the vagus nerve, thereby causing reflex inhibition of sympathetic activity to blood vessels, vasodilation, parasympathetic activation and bradycardia. Chemical factors, either produced endogenously or injected intravascularly, can also activate this reflex, referred to as the Bezold–Jarisch reflex [2]. Chemical factors used experimentally to trigger the reflex include veratrum alkaloids such as veratridine, capsaicin, nicotine, prostanoids, and the serotonin 5-HT₃ receptor agonist phenylbiguanide [2]. …