Low doses of noncatecholamines like metanephrine potentiate vascular contractile responses to other stimulating agents, likely by releasing storage norepinephrine.
Animal data indicate norepinephrine-dependent vascular potentiation by noncatecholamines; leaves open translation to human physiology or therapy.
Contractile responses of vascular smooth muscle strips (rabbit aorta) to angiotensin, vasopressin and serotonin are potentiated by amounts of metanephrine, ephedrine or tyramine that produce no contractions by themselves. Epinephrine and norepinephrine contractions of aortic strips are not potentiated. Phentolamine and bretylium prevent this potentiating effect of meta-nephrine and ephedrine; the effect of tyramine is blocked by bretylium but only partially by high doses of phentolamine. Contractions of strips pretreated with reserpine are not potentiated except when repleted with norepinephrine. It is suggested as a working hypothesis that low doses of metanephrine release storage norepinephrine which acts on the contractile machinery to potentiate its response to other stimulating agents.
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Khairallah et al. (1966) studied this question.
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