Real world incidence, severity and timing of adverse events (AEs) among patients with metastatic non-small cell lung cancer (NSCLC) receiving second-line (2L) immuno-oncology (IO) therapy vs chemotherapy (C)

Article

Author: Kaur, S ; Korytowsky, B ; Gutierrez, M E ; Lane, D C ; Nwokeji, E D ; Canavan, B F ; Norden, A D ; Tuell, K ; Siegartel, L ; Noh, L ; Xu, Y ; Whittington, J ; Goldberg, S L

01 Mar 2000·HypertensionQ1 · MEDICINE

High-Fat Diet Elevates Blood Pressure and Cerebrovascular Muscle Ca ²⁺ Current

Q1 · MEDICINE

Article

Author: Walker, Glenn K. ; Vollmer, Alan ; Massey, Kenneth D. ; Wilde, Dixon W. ; Grekin, Roger J.

Abstract —Dietary fat contributes to the elevation of blood pressure and increases the risk of stroke and coronary artery disease. Previous observations have shown that voltage-gated Ca 2+ current density is significantly increased in hypertension and can be affected by free fatty acids (FAs). We hypothesized that a diet of elevated fat level would lead to an increase in blood pressure, an elevation of L-type Ca 2+ current, and an increase in saturated FA content in vascular smooth muscle cell membranes. Male Osborne-Mendel rats were fed normal rat chow or a high-fat diet (Ob/HT group) for 8 weeks. Blood pressures in the Ob/HT group increased moderately from 122.5±0.7 to 134.4±0.8 mm Hg ( P <0.05, n=26). Voltage-clamp examination of cerebral arterial cells revealed significantly elevated L-type Ca 2+ current density in the Ob/HT group. Voltage-dependent inactivation of the Ob/HT L-type channels was significantly delayed. Total serum FA contents were significantly elevated in the Ob/HT group, and HPLC analyses of fractional pools of FAs from segments of abdominal aorta revealed that arachidonic acid levels were elevated in the phospholipid fraction in Ob/HT. No differences in vascular membrane cholesterol contents were noted. Plasma cholesterol was significantly elevated in portal venous and cardiac blood samples from Ob/HT rats. These findings suggest that an elevation of plasma FAs may contribute to the development of hypertension via a process involving the elevation of Ca 2+ current density and an alteration of channel kinetics in the vascular smooth muscle membrane.

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