A method for determination of antiplasmin activity is presented. Plasmin and plasma are incubated, and the remaining plasmin activity is measured spectrophotometrically by means of the plasmin specific tripeptide substrate H-d-Val-l-Leu-l-Lys-p-nitroanilide. The method is simple, rapid and easily automatized. By the immunoadsorption technique, and with the aid of purified substances it is shown that the measured activity is mainly due to a new antiplasmin [2,4] and possibly to some extent to alpha1-antitrypsin and C1-esterase inhibitor have no antiplasmin activity in the method. Heparin and epsilonaminocaproic acid interfered with the assay.
alpha 2-Antiplasmin and alpha 2-macroglobulin have been studied during the menstrual cycle, pregnancy and parturition in healthy women, and during use of various types of contraception in both healthy and diabetic women, and compared with a reference group of healthy men and women. alpha 2-Antiplasmin showed a slight sex difference, with higher values in women. The luteal phase of the menstrual cycle showed slightly higher values than the other phases. alpha 2-Antiplasmin increased during pregnancy, decreased (probably due to consumption) during labor and increased again in the puerperium. Treatment with neither combined contraceptive pills nor low dose progestogen pills gave any changes in alpha 2-antiplasmin. alpha 2-Macroglobulin showed low values during menstruation. The increase during pregnancy and treatment with combined contraceptive pills is in accordance with earlier findings. It is concluded that synthesis and metabolism of alpha 2-antiplasmin are under hormonal influence. The role of alpha 2-antiplasmin in the decreased fibrinolysis in pregnancy is discussed.
To determine whether the urinary excretion of kallikrein is altered in patients with previously malignant hypertension.Twenty-two patients with malignant hypertension (fundus hypertonicus III or IV) in the Gothenburg area were studied over a 3-year period. After treatment had begun they were investigated for blood pressure control, family history of hypertension, renal function and urinary kallikrein and plasma prekallikrein concentrations. Twenty-two patients with treated non-malignant hypertension and 36 control subjects were investigated concomitantly. The two hypertensive groups were also separated into subgroups of essential and secondary hypertension.Prekallikrein was activated and kallikrein determined by a spectrophotometric assay using a synthetic chromogenic substrate. Renal function was estimated by serum creatinine and 51Cr-ethylenediaminetetraacetic acid clearance.Prekallikrein levels tended to be elevated in all groups of hypertensive patients compared with controls whilst urinary kallikrein was significantly decreased in malignant hypertensives. The most pronounced suppression of urinary kallikrein was seen in the group of patients with essential malignant hypertension. The differences persisted when urinary kallikrein was related to the degree of renal impairment or when urinary volume was taken into account. There was no relation between family history of hypertension and low levels of urinary kallikrein.Decreased urinary kallikrein could indicate depressed activity in the renal kallikrein-kinin system, which may be associated with the initiation of essential malignant hypertension.
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