Android fat is also associated with a change in pressor response in circulation.
The displacement of norepinephrine ( noradrenaline ) from neuronal storage vesicles by acute tyramine ingestion is thought to cause the vasoconstriction and increased heart rate and blood pressure of the pressor response.
Specifically, in response to stress in a subject with central obesity the cardiac output dependent pressor response is shifted toward a generalised rise in peripheral resistance with an associated decrease in cardiac output.
When these vesicles are secreted upon tyramine ingestion, there is a decreased pressor response, as less norepinephrine is secreted into the synapse, and octopamine does not activate alpha or beta adrenergic receptors.
These can, however, induce a Jarisch Herxheimer reaction in over half those treated, producing anxiety, diaphoresis, fever, tachycardia and tachypnea with an initial pressor response followed rapidly by hypotension.
If one has had repeated exposure to tyramine, however, there is a decreased pressor response; tyramine is degraded to octopamine, which is subsequently packaged in synaptic vesicles with norepinephrine ( noradrenaline ).
A large dietary intake of tyramine ( or a dietary intake of tyramine while taking MAO inhibitors ) can cause the tyramine pressor response, which is defined as an increase in systolic blood pressure of 30 mmHg or more.
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