[Revascularization of the myocardium and kidneys in patients with combined atherosclerotic lesions of coronary and renal arteries].

The study included a total of 109 patients presenting with combined atherosclerotic lesions of coronary and renal arteries. Depending on severity of angina pectoris, the patients were subdivided into two groups. Group One consisted of patients subjected to revascularization of the myocardium and kidneys, and Group Two comprised those with a dominating clinical picture of vasorenal hypertension syndrome and undergoing surgery on renal arteries alone.

[Atypical binding sites of low density lipoproteins in human vascular smooth muscle cells].

Lipoprotein-binding sites on cultured human omental vascular smooth muscle cells have been investigated. Two sites specifically binding low density lipoprotein (Kd1 = 1 microgram/ml and Kd2 = 50 micrograms/ml) were found. The properties of the high affinity site are similar to those of the previously described "classical" apo B,E-receptor.

["Classical" apo B,E-receptor does not mediate the activating effect of low density lipoproteins on the second messenger system in human platelets and vascular smooth muscle cells].

The possible role of the "classical" LDL receptor (apo B,E-receptor) in activation of second messenger systems in human platelets and vascular smooth muscle cells (VSMC) has been investigated. The LDL-induced elevation of free cytoplasmic Ca2+ in platelets and VSMC was not inhibited by EGTA, which is known to block the LDL interaction with the apo B,E-receptor. Heparin abolished the binding of LDL to the apo B,E-receptor but did not influence the LDL-induced accumulation of inositol phosphates in VSMC.

[Hormone-like action of blood plasma lipoproteins on human platelets and smooth vascular muscle cells].

It has been found that blood lipoproteins are capable of inducing rapid and reversible elevations of [Ca2+]i in human blood platelets and vascular smooth muscle cells (VSMC) loaded with Ca(2+)-sensitive fluorescent probes. The effects of LDL and HDL3 were dose-dependent and reached saturation at physiological concentrations of these lipoproteins. Both lipoproteins activated the phosphoinositide turnover, producing elevated levels of diacylglycerol and inositol mono-, bis- and triphosphates.