Abstract
Tyrosine, the amino acid precursor of catecholamines, increases blood pressure (BP) in hemorrhaged hypotensive rats. Since tyrosine may also be decarboxylated to form tyramine ∞, which releases norepinephrine from sympathetic terminals, we tested the hypothesis that tyramine formation might mediate tyrosine's ability to increase BP. Three lines of evidence indicate that tyrosine does not act via this mechanism: pretreatment with reserpine blocked tyramine's but not tyrosine's pressor activity; pretreatment with hexamethonium left tyramine's effect intact but blocked the pressor response to tyrosine; and plasma tyramine did not increase after an hemodynamically-active dose of tyrosine (100 mg/kg).
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