Low Density Lipoprotein Receptors Mediate Intracellular Calcium Signals in Microalbuminuric Hypertensives

• Published in: American journal of hypertension 1998, Vol.11 (1), p.113-116
• Main Authors: Fong, Ronald L., Vadgama, Jay V., Laguer, Miriam R., Ward, Harry J.
• Format: Article
• Language: English
• Subjects: Adult; Albuminuria - complications; Albuminuria - metabolism; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Blood and lymphatic vessels; Blood Platelets - metabolism; Calcium - metabolism; Cardiology. Vascular system; Clinical manifestations. Epidemiology. Investigative techniques. Etiology; Humans; Hyperlipidemia; Hyperlipidemias - complications; Hypertension - complications; Hypertension - metabolism; intracellular calcium; LDL cholesterol; Medical sciences; microalbuminuria; Middle Aged; platelet; Proteinuria - complications; Receptors, LDL - metabolism; Signal Transduction
• ISSN: 0895-7061; 1879-1905; 1941-7225
• DOI: 10.1016/S0895-7061(97)00370-1

Hyperlipidemia is an established risk factor for progressive renal damage and proteinuria. Platelets and vascular smooth muscle cells (VSMC) are known to possess low density lipoprotein (LDL) cholesterol receptors. We used platelet LDL receptors to investigate the hypothesis that elevated lipids could activate intracellular calcium [Ca 2+] i signals, leading to altered vascular tone and permeability. We divided essential hypertensives into microalbuminuric positive (MA+) and negative (MA−) groups and measured baseline and LDL stimulated levels of [Ca 2+] i. The MA+ group demonstrated a significantly higher mean baseline [Ca 2+] i level (119.0 ± 24.5 v 86.2 ± 25.4 μmol/mL, P = .001). The MA+ group also displayed greater elevations in [Ca 2+] i levels after stimulation with LDL in concentrations of 10 and 25 μg/mL (100.9 ± 54.8 v 40.9 ± 20.2, P = .04 and 111.6 ± 51.0 v 52.9 ± 39.9 μmol/mL, P = .03, respectively). Our data indicate that hypertensive patients with early glomerular capillary injury display exaggerated influx of [Ca 2+] i after LDL receptor stimulation. Heightened LDL receptor sensitivity may facilitate LDL mediated [Ca 2+] i signals, leading to increased VSMC tone and proliferation and progressive renal disease.