300-POS

Abstract

Objectives Compared to the diets on which humans evolved, modern diets have increased membrane-stiffening components such as long-chain saturated and trans-fatty acids. Increased vascular stiffness, as measured by pulse wave velocity, is associated with increased incidence and severity of preeclampsia (Hausvater, 2012). As one of the determinants of arterial stiffness, vascular smooth muscle tone is regulated by many factors including endocrine signals as well as nitric oxide, salt, oxidant stress, and mechanical stimulation through cell stretch and calcium signaling. It is generally believed that mechanotransduction in endothelial cell membranes is initiated at the local force-membrane interface by inducing local conformational changes or unfolding of membrane-bound proteins, followed by a cascade of diffusion-based signaling in the cytoplasm (Hoffman, 2011). The objective of this study is to develop a model of how diet-induced endothelial membrane stiffness might impact membrane-based mechanotransduction and cause hypertension. Methods Literature review. Results Because the arterial intima functions as a sensor, blood pressure homeostatic response might be modulated by the flexibility of endothelial membranes. Factors that stiffen cell membranes (such as salt, trans-fatty acids, and sympathetic neurohormones) might restrict protein conformational shift and invoke an inappropriately high contraction response and increased blood pressure. Factors that increase membrane flexibility (such as polyunsaturated fatty acids) might heighten the sensitivity of endothelial membranes to stretch. Similarly to a diaphragm pressure transducer in a barometer, if the diaphragm material is stiff, the signal is attenuated; conversely, a flexible diaphragm makes the instrument more sensitive to pressure. Conclusions Pulse wave velocity might provide a noninvasive method of measuring the success of dietary interventions in reducing endothelial stiffness and risk of preeclampsia. Disclosures N.R. Hart: None.