PubMed · 5738869
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P Deffrenne, R Verney. 1968. [Cervical aorta].. https://pubmed.ncbi.nlm.nih.gov/5738869/
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Lipoprotein lipase (LPL), bound to the luminal surface of vascular endothelium catalyzes lipoprotein triglyceride hydrolysis. Studies were performed to identify human aortic endothelial (HAEC) cell-surface proteins having high affinity for LPL. LPL-sepharose affinity chromatography of [35S]O4 labeled HAEC proteins identified a 220-kDa proteoglycan. Ligand blotting of HAEC plasma membrane proteins with LPL revealed two specific binding proteins of MW 116 kDa and 85 kDa, respectively, which were not released from the cell-surface by heparin treatment. Since the 220-kDa and 116-kDa proteins have been reported previously in bovine endothelial cells, we focused on the 85-kDa protein. The 85-kDa protein was not labelled by incubation of the cells with [35S]O4, suggesting that it is not a sulfated proteoglycan. Treatment of HAEC with tunicamycin markedly decreased detection of the 85-kDa protein, suggesting that it is likely a glycoprotein synthesized by HAEC. We conclude that HAEC cell surface has three specific LPL binding proteins, a 220-kDa proteoglycan, a 116-kDa protein and a novel 85-kDa protein.
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A decrease in the vascular compliance of the large elastic vessels (reduction of their "Windkessel" function) is of decisive importance for the pathogenesis and prognosis of cardiovascular complications such as arteriosclerosis, left ventricular hypertrophy and heart failure. The effect of the antihypertensive calcium antagonist isradipine on the "Windkessel" function of the aorta was measured in terms of the central haemodynamics in ten patients (eight men, two women; mean age 58 +/- 3 years) with essential hypertension (WHO stage I-II) before and 3 months after treatment. The mean arterial blood pressure was obtained invasively from the aortic arch, cardiac output or stroke volume being obtained by the indicator dilution method. The ratio stroke volume/blood pressure amplitude was calculated as a measure of vascular compliance. After 3 months of treatment with isradipine the mean arterial blood pressure fell from 114 +/- 4 to 97 +/- 3 mm Hg (P < 0.01), and total peripheral resistance from 22 +/- 1 to 18 +/- 1 U, P < 0.05), while vascular compliance rose from 1.07 +/- 0.10 to 1.58 +/- 0.10 ml/mm Hg, P < 0.05. The increase in compliance resulted from both the fall in blood pressure per se and the pressure-independent increase in the distensibility of the vessel wall (87 +/- 8% as against 107 +/- 13%, P < 0.05). As the fall in afterload favoured regression in left ventricular hypertrophy and heart failure, this pressure-independent structural and (or) functional change in the great elastic arteries could be decisive for the cardiovascular prognosis of hypertensives.