Ca2+ Binding and Membrane Fluidity in Essential and Renal Hypertension

Orlov, Sergei N.; Postnov, Yu. V.

doi:10.1042/cs0630281

Cited by 82 publications

(28 citation statements)

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“…26 Based on this, it is possible that the vasorelaxant effect of polyunsaturated fatty acids may be mediated in part by changes in fluidity. Reduced fluidity and lowered linoleic acid and cis-unsaturated fatty acid content were found in platelet membranes of hypertensive patients, 7 erythrocyte membranes of patients with essential hypertension 27 and SHR, 28 and SHR VSMC. 28 It has also been shown that concentrations of saturated fatty acids such as palmitic and stearic acid are increased while unsaturated fatty acids such as linoleic and arachidonic acid are decreased in the plasma phospholipid fraction of hypertensive patients compared with normal individuals.…”

Section: Discussionmentioning

confidence: 99%

Linoleic Acid Induces Relaxation and Hyperpolarization of the Pig Coronary Artery

et al. 1998

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Abstract-Linoleic acid, a polyunsaturated C 18 fatty acid, is one of the major fatty acids in the coronary arterial wall. Although diets rich in linoleic acid reduce blood pressure and prevent coronary artery disease in both humans and animals, very little is known about its mechanism of action. We believed that its beneficial effects might be mediated by changes in vascular tone. We investigated whether linoleic acid induces relaxation of porcine coronary artery rings and the mechanism involved in this process. Linoleic acid and two of its metabolites, 13-hydroxyoctadecadienoic acid (13-HODE) and 13-hydroperoxyoctadecadienoic acid (13-HPODE), induced dose-dependent relaxation of prostaglandin (PG) F 2␣ -precontracted rings that was not affected by indomethacin (10 Ϫ5 mol/L), a cyclooxygenase inhibitor, or cinnamyl-3,4-dihydroxy-␣-cyanocinnamate (CDC; 10 Ϫ5 mol/L), a lipoxygenase inhibitor. Removal of endothelial cells had no effect on vasorelaxation, suggesting a direct effect on the vascular smooth muscle cells (VSMC). When rings were contracted with KCl, linoleic acid failed to induce relaxation. Although tetrabutylammonium (5ϫ10 Ϫ3 mol/L), a nonselective K ϩ channel blocker, slightly inhibited the relaxation caused by linoleic acid, glibenclamide (10 Ϫ6 mol/L), an ATP-sensitive K ϩ channel blocker, and charybdotoxin (7.5ϫ10-activated K ϩ channel blockers, had no effect. However, relaxation was completely blocked by ouabain (5ϫ10 Ϫ7 mol/L), a NaIn addition, linoleic acid (10 Ϫ6 mol/L) caused sustained hyperpolarization of porcine coronary VSMC (from -49.5Ϯ2.0 to -60.7Ϯ4.2 mV), which was also abolished by ouabain. We concluded that linoleic acid induces relaxation and hyperpolarization of porcine coronary VSMC via a mechanism that involves activation of the Na Key Words: linoleic acid Ⅲ nitric oxide Ⅲ prostaglandins Ⅲ endothelium-derived hyperpolarizing factorinoleic acid, a polyunsaturated C 18 fatty acid (18:2n-6), is one of the main essential fatty acids, and is one of the major fatty acids in the arterial wall, 1 which can be liberated by phospholipase activity.2,3 Linoleic acid is the principal precursor of arachidonic acid (20:4n-6), which is the substrate for synthesis of prostaglandins and thromboxane A 2 . Structurally related derivatives of arachidonic acid and linoleic acid have been demonstrated in blood vessels and related tissues. Linoleic acid can be enzymatically or nonenzymatically 4 converted to 13-HPODE, which can be further reduced to 13-HODE. Production of these hydro(per)oxy metabolites has been reported in aortas from rats, rabbits, and cows, 1 and unlike the fetal calf aorta 5 their formation is independent of cyclooxygenase activity. Lipoxygenation of linoleic acid resulted in 13-HODE formation in endothelial cells.6 Linoleic acid metabolites are formed in larger quantities than the corresponding arachidonic acid metabolites, 1 suggesting that they may be of biological significance.Several studies have suggested that hypertension and cardiovascular disease are caused in part by a relat...

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Section: Discussionmentioning

confidence: 99%

Linoleic Acid Induces Relaxation and Hyperpolarization of the Pig Coronary Artery

et al. 1998

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“…28 Many experiments have revealed that the reduction of blood pressure after dietary linoleic acid intake is mediated by the changes in the prostaglandin metabolism, 8 ' 29 a reduced sympathetic nervous activity, 5 and the changes of the fluidity in cell membrane. 30 - 31 We demonstrated that sodium-potassium pump activity was elevated greatly in the HLA group. Sodium handling abnormalities have been reported in patients and rats with hereditary forms of arterial hypertension.…”

Section: Supplement I Hypertensionmentioning

confidence: 94%

Dietary linoleic acid prevents the development of deoxycorticosterone acetate-salt hypertension.

Kawahara

Sano²,

Kubota³

et al. 1990

Hypertension

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The aim of this study was to elucidate the effect of dietary variations of linoleic acid on the development of deoxycorticosterone acetate (DOCA)-salt hypertension in rats. All rats were divided into three groups and fed one of the following isocaloric diets with 8% NaCl: a high linoleic acid (HLA) (20% sunflower oil), a moderate linoleic acid (5% lard oil+15% sunflower oil), or a low linoleic acid (DLA) (20% lard oil). After 4 weeks of feeding, we determined intraerythrocyte sodium, potassium, and magnesium concentrations, intra-aortic and lymphocyte magnesium content, and erythrocyte ouabain-sensitive "Na efflux rate constant. Cytoplasmic free calcium concentration of lymphocytes from thymus was also determined with quin-2 as a fluorescent indicator. In the HLA group, the elevation of systolic blood pressure was significantly attenuated, and intraerythrocyte sodium concentration was significantly lower than in the DLA group. There were greater intraerythrocyte potassium and magnesium concentrations, intra-aortic and lymphocyte magnesium contents, and erythrocyte ouabainsensitive u Na efflux rate constant in the HLA group as compared with other groups. Cytoplasmic free calcium concentration in the HLA group was significantly lower than in other groups. Systolic blood pressure significantly correlated negatively with intraerythrocyte and intra-aortic magnesium concentrations and intraerythrocyte potassium concentration, and correlated positively with cytoplasmic free calcium concentration. Erythrocyte ouabainsensitive a Na efflux rate constant significantly correlated positively with intraerythrocyte magnesium concentration. These findings suggest that dietary linoleic acid can attenuate the development of DOCA-salt hypertension. It is assumed that the mechanism of its hypotensive effect might be because of a decrease in intracellular sodium and calcium concentration and an increase in intracellular magnesium content, resulting in the elevation of sodium-potassium pump activity. (Hypertension 1990;15(suppl I):I-81-I-87)

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“…Such parameters may be relevant the erythrocyte membrane in hypertensives. 41 However, the fluidity of the cell membrane, on which the to an increased risk of vascular complications which are associated with low flow conditions including deformability of the erythrocyte depends, may be influenced by other factors such as the lipids which atherogenesis, thrombogenesis and ischaemia. 3 form part of the membrane bilayer.…”

Section: Red Cell Rigidity (Lack Of Deformability)mentioning

confidence: 99%

The role of rheological and haemostatic factors in hypertension

Lee

1997

J Hum Hypertens

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Research into the pathogenesis of hypertension has, in tors are known to be involved in thrombogenesis, their potential role in the pathogenesis of patients with hyperthe past, tended to concentrate on changes in vascular geometry, cardiac output and blood volume. However, tension has received increasing attention. The purposes of this review are to update previous reviews and to patients with hypertension are known to be at an increased risk of both coronary heart disease and ceresummarise the relationship between hypertension, its complications and treatment and a range of haemorheobrovascular disease; complications which are thrombotic in origin. Since rheological and haemostatic faclogical factors.

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Ca2+ Binding and Membrane Fluidity in Essential and Renal Hypertension

Cited by 82 publications

References 0 publications

Linoleic Acid Induces Relaxation and Hyperpolarization of the Pig Coronary Artery

Linoleic Acid Induces Relaxation and Hyperpolarization of the Pig Coronary Artery

Dietary linoleic acid prevents the development of deoxycorticosterone acetate-salt hypertension.

The role of rheological and haemostatic factors in hypertension

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