[The influence of calcium ion antagonists on the effects of bradykinin].

On the isolated segments of the ileum of the guinea-pig, anesthetized and nonanesthetized rats and mice it was established that calcium ion antagonists from different chemical series exert the nonspecific antibradykinin action, reducing the main biological effects of bradykinin--myotropic, depressor, nociceptive and microcirculatory. To a greater extent the mentioned properties show up in the derivatives of 1,4-dihydropyridine (phoridon, etc.) that may play the certain role in the therapeutic action of the drugs in the diseases associated with the activation of the kinin system of the organism.

[The effect of fenigidin (nifedipine) and verapamil on renin activity, the levels of ionized calcium and aldosterone in the blood plasma and on the hemodynamic indices of rats with spontaneous hypertension].

Nifedipine and verapamil (10 mg/kg orally) were found to induce a significant increase of renin activity, a decrease of aldosterone and ionized calcium levels in blood plasma in spontaneously hypertensive rats. A preliminary administration of a hypertonic solution of sodium chloride decreased renin activity, ionized calcium and aldosterone levels that contributed to the enhancement of the hypotensive effect of calcium antagonists. It was established that nifedipine by its effect on the parameters of hemodynamics and the condition of renin-angiotensin system as well as the blood plasma ionized calcium level is superior to verapamil.

[Influence of captopril on the in vitro and in vivo effects of leu- and met-enkephalins].

Captopril (10(-6) g/ml) enhanced and prolonged the inhibitory effect of leu- and met-enkephalins on the contractions of the isolated guinea-pig ileum section induced by electrical stimulation. In mice, the drug (25 mg/kg, subcutaneously) increased the degree and duration of the analgetic effect of enkephalins. It is concluded that the analgetic effect of captopril is related to the influence on the activity of the endogenous antinociceptive system.

[Induction of blood plasma carboxycathepsin (angiotensin I-converting enzyme) in normo- and hypertensive rats in response to a single administration of captopril].

The experiments were carried out to elucidate the effect of carboxycathepsin (CC) activity inhibition by a specific inhibitor--captopril--on plasma enzyme concentration in normotensive rats and rats with renovascular hypertension. A single oral administration of captopril (10 mg/kg body weight) produced an increase in CC concentration in both hypertensive and sodium-depleted normotensive rats with a parallel decrease in arterial pressure, but had no effect on sodium-repleted normotensive rats. It is suggested that the increase in plasma CC concentration is a compensatory response to the inhibition of CC activity by captopril; it is also possible that the increase observed reflects the state of renin-angiotensin system.

[Experimental study of the effect of captopril on pain reactions].

The experiments on the electrical stimulation of the isolated guinea-pig ileum have shown that captopril (10(-6)-10(-4) g/ml) caused dose-dependent inhibition of the organ contractions, abrogated by naloxone. In mice, the drug in the doses of 0.1 to 0.

[Antagonism of parmidin to kinin effects].

Parmidin in 10(-9)-10(-5) g/ml concentrations displays specific and competitive antagonism to spasmogenic effects of bradykinin and methionyl-lysil-bradykinin on isolated segments of the guinea pig ileum, rat uteral cornua, cat jejunum and spiral strips of the rabbit aorta. Its antagonism to the spasmogenic effect of lysil-bradykinin is of both competitive and non-competitive character. In rats parmidin in 100 mg/kg dose decreased the paw edema, induced by kinins but it did not influence the similar effect of histamine and that of prostaglandin F2.