Release of Plasminogen Activator by the Isolated Perfused Dog Kidney

Plasminogen activator activity in cultures from human tissues. An immunological and histochemical study

“…Such activity may be identical with that of a labile activator, plasma type activator, which differs immunologically from UK (8) and is elicited in blood in vivo (4)(5)(6)(7)(8) and in the isolated kidney in vitro (32) after stimuli similar to those of our experiments. Stimulatory response was no longer demonstrated after tissue was cultured, although it was not apparent whether cells in culture failed to produce appropriate activator or lacked mechanism for its release.…”

“…3. The specimens were cut, washed, and then incubated for 10-30 min in HBSS and in HBSS containing nicotinic acid (0.1 mg/ml) or acetylcholine (20 ug/ml) which have been shown to stimulate the release of plasminogen activator in vivo (6,8) and in isolated organs in vitro (32). All fragments yielded activator activity in supernatant HBSS, but those stimulated with nicotinic acid or acetylcholine released 3-to 5-fold greater activity, particularly when fragments were derived from the medulla.…”

Regulation of the Synthesis and Secretion of Plasminogen Activators by Endothelial Cells

“…An immediate release of t-PA can also be observed after stimulation of perfused vascu lar beds, such as in the dog kidney [127], the pig ear [128], the dog coronary circulation [129], and the rat hindleg [130]. This release is triggered by many compounds, including thrombin, histamine, bradykinin, epineph rine and calcium ionophore A23187 [re viewed by Emeis,13].…”

Effect of Heparin on Renal Function in Patients with Oliguria

“…In the case of glomerulonephritis circulating immune complexes, when concentrated in the renal filters, damage platelets (Cochrane and Dixon, 1968) so that intraglomerular coagulation follows. The natural renal protective mechanisms are its endothelial cell fibrinolytic potential (Holemans et al, 1965;Holemans et al, 1967), resulting in the production of small fibrin degradation products which themselves protect platelets from aggregation (Larrieu et al, 1967) and immune damage (Salmon and Lambert, 1971), and the phagocytic capacity for fibrin and immune complexes of the mesangial and endothelial cells (Vassalli and McCluskey, 1965 Similar platelet deposition and coagulation is a feature of certain types of transplant rejection (Porter, 1967;Burrows et al, 1970). In malignant hypertension it is likely that the high intravascular tension, leading to fibrin insudation through arteriolar walls, also damages endothelial cells (Wardle, 1971), which even in arteries do have some fibrinolytic activity (Onoyama and Tanaka, 1969).…”