Lipid bilayer in genetic hypertension.

Abstract

Membrane microviscosity, phospholipid composition, and turnover were measured in cultured vascular smooth muscle cells isolated from mesenteric arteries of stroke-prone spontaneously hypertensive and age-matched, normotensive Wistar-Kyoto rats. Membrane microviscosity, measured with fluorescence polarization, revealed greater microviscosity (lower fluidity) of the membranes isolated from smooth muscle cells from hypertensive as compared with those isolated from normotensive rats (p<0.01). Preincubation of membranes from hypertensive rats with 5 mM calcium reduced membrane microviscosity in "core" and in "surface" regions of the bilayer toward values observed in Wistar-Kyoto rats. Phospholipid composition did not differ between intact aortas and cultured mesenteric cells or between those tissues obtained from normotensive and from hypertensive rats. The total lipid-associated radioactivity was significantly lower in cells from stroke-prone spontaneously hypertensive rats than in those from Wistar-Kyoto controls (/?<0.01). Phosphatidylcholine incorporated 70% and phosphatidylinositol 16% of total lipid-associated radioactivity, with no difference between cells from hypertensive and normotensive animals. Turnover of phosphatidylethanolamine was greater in cells from Wistar-Kyoto rats (p=0.02), whereas turnover of phosphatidylserine was greater in cells from stroke-prone spontaneously hypertensive rats (p=0.04). The greater microviscosity of the lipid bilayer in hypertension is a generalized defect of the matrix in which the transport proteins function. We hypothesize that this defect is responsible for the multiple abnormalities of membrane transport systems that have been described in genetic hypertension. (Hypertension 1991;18:748-757)

2-Hydroxyoleic Acid

“…22 Indeed, alterations of membrane cholesterol or phospholipid content, phospholipid distribution, the molecular species of particular phospholipid classes, and the degree of FA saturation have all been reported in both hypertensive humans 1,4,23 and in experimental animal models of hypertension. 2,24 Interestingly, we recently demonstrated that in elderly hypertensive patients, alterations in cell membrane lipid levels are also associated with a reduction in the density of signaling proteins involved in the control of BP, such as G proteins and PKC. 22 Therefore, changes in lipid composition of the plasma membrane might alter signaling pathways involved in the control of BP.…”

“…Changes in the plasma or membrane lipid composition have been reported in both hypertensive humans 1 and in animal models of hypertension. 2,3 These changes have been associated with abnormalities in cation transport systems, 4 cytosolic Ca 2ϩ regulation, 5 and impaired signal transduction. 6 As a result, it has been proposed that modifications of the membrane lipid composition can affect the physical and functional properties of membranes and in consequence, might account for the alterations in signaling implicated in the physiological control of blood pressure (BP).…”

Dietary calcium and blood pressure in experimental models of hypertension. A review.

“…Based on numerous reports of abnormalities in cell membrane transport systems associated with hypertension, Bohr and colleagues 204 have hypothesized that there is a defect in the lipid bilayer of vascular smooth muscle membrane in hypertensive individuals. This defect results in decreased membrane fluidity and enhanced excitability as a consequence of increased Ca 2+ flux across the cell membrane.…”

Lipid composition and fluidity in the jejunal brush-border membrane of spontaneously hypertensive rats. Effects on activities of membrane-bound proteins

“…It has been suggested that a generalized physico-chemical alteration of the lipid bilayer, the matrix in which all the membrane proteins function, may be responsible for these multiple membrane abnormalities (6,7,8). Thus, previous reports have found consistent differences in the lipid composition of erythrocyte and platelet membranes and other tissues in hypertension (9,10,11).…”