In connection with the problem of the possible role played by the sympathomimetic neurohormones (nor-epinephrine and epinephrine) in the pathogenesis of essential hypertension, interest has been focused lately on substances which are capable of abnormally intensifying the vasoconstrictor power of epinephrine in the mesentery of the rat and the perfused rabbit's ear, such as the chemically undefined agent which originates in the kidney (1) and protein fractions, extracted from the kidneys and other tissues, as well as hypertensin and tyrosin (2). A participation of adrenal cortical steroids in such sensitizing mechanisms is suggested by the restoration of the impaired VEM formation in the
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Raab et al. (1950) studied this question.
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