Beta-1 adrenergic inhibition of kallikrein release from rat kidney cortical slices.

Renal storage; release, and biosynthesis of kallikrein were studied using rat cortical slices. This model permitted the study of the direct effect of norepinephrine on the renal kallikrein system in the absence of changes in perfusion pressure. Kallikrein was measured by its kininogenase activity and its direct immunoreactive concentration.

Renal kallikrein excretion as a distal nephrotoxicity marker during cadmium exposure in rats.

Cadmium exposure is known to induce hypertension, but development of hypertension is not universal in exposed animals. However, the cellular uptake of cadmium could also exert renal cytotoxic effects which have been, until now, essentially only studied at the proximal tubule level. Kallikrein is an enzyme synthetized in renal cortex and excreted in the urine in the distal tubule.

B2-kinin receptor like binding in rat glomerular membranes.

Incubation of a radiolabeled bradykinin analog, [125I]-Tyr8-BK with a crude membrane preparation obtained from isolated rat glomeruli revealed a time dependent binding. The binding was saturable, reversible and was a linear function of protein membrane concentration. The radiolabeled Tyr8-BK bound to a single class of binding sites with an equilibrium dissociation constant (KD) of 3.

Urinary kallikrein excretion following chronic sinoaortic denervation in conscious dogs.

Urinary kallikrein excretion (UKE) was investigated in neurogenic hypertensive dogs for a period of 8 months. The animals were made hypertensive by sinoaortic denervation (SAD). Plasma catecholamine levels (PC), plasma renin activity (PRA), plasma aldosterone concentration (PAC) and urinary sodium excretion (UNa) were also measured.

Purification of human active urinary kallikrein: comparative inhibition studies of kininogenase and amidolytic activities.

Large scale purification of human active urinary kallikrein is described. The final preparation was found homogeneous by means of SDS Page electrophoresis, amino acid composition and N-terminal analysis. The apparent molecular weight, determined on SDS Page electrophoresis, was 4.

Short lasting increase in urinary specific kallikrein activity during long term administration of furosemide.

Furosemide was administered for seven days to normal rats. Urinary kallikrein excretion showed a biphasic response during the seven consecutive days of study. During the initial three days only the kininogenase activity showed a significant increase without any variation in the excretion of the immunoreactive kallikrein.