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Experiments on myocardial strips isolated from the right auricular myocardium of patients with heart failure showed that tyrosine, histidine, and tryptophan increased the amplitude of electrically stimulated contractions. The nature of this effect and clinical implications are discussed.

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Histidine (3x10(-5) g/ml) had no effect on contractility and chronoinotropic relationships in frog myocardium, but rapidly and reversibly increased myocardial beta-adrenoreactivity (increased myocardial response to 7x10(-8), 3x10(-7), and 4x10(-6) g/ml epinephrine) and potentiated the positive effect of epinephrine (7x10(-8), 3x10(-7) g/ml) on chronoinotropic relationships in the myocardium. Histidine is considered to be a component of endogenous sensitizer of beta-adrenoceptors in human blood modulating the function of cardiomyocytes.

Experiments were performed with 62 longitudinal strips of the uterine horns from 10 nonpregnant rats. The ability of continuously infused epinephrine in high concentration (10(-6) g/ml, 30 min) to suppress spontaneous contractions due to activation of beta-adrenoceptors progressively decreased, which was associated with receptor desensitization. Histidine in a concentration of 3 x 10(-11) g/ml had no effect, while in concentrations of 3 x 10(-8), 3 x 10(-7), and 3 x 10(-6) g/ml decreased the degree of desensitization. Our results indicate that histidine not only potentiates beta-adrenoceptor activation, but also prevents the development of desensitization. These data should be taken into account during therapy with beta-adrenoceptor agonists.

Human blood serum exhibiting β-adrenoceptor-sensitizing activity does not prevent manifestation of similar activity of histidine, tryptophan, tyrosine, mildronat, and preductal. This opens prospects for the use of analogues of endogenous β-adrenoceptor-sensitizing agent in clinical practice.