Evidence of Altered Structure of the Erythrocyte Membrane in Spontaneously Hypertensive Rats

Orlov, S.N.; Gulak, Pavel V.; Litvinov, I. S.; Postnov, Yu. V.

doi:10.1042/cs0630043

Cited by 51 publications

(29 citation statements)

References 7 publications

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“…However, unlike genetically determined hypertension, secondary hypertension models, such as deoxycorticosterone-salt hypertension, two kidney-one clip Goldblatt hypertension and portal hypertension in rats, are not associated with demonstrable alterations in membrane fluidity (7) or lipid composition (8). This is consistent with the assumption that patients and animals with genetically determined hypertension have a predetermined generalized defect of the cell membrane matrix, in which the transport systems operate, that leads to an increase of bilayer microviscosity.…”

supporting

confidence: 75%

Structural properties of lipid reconstructs and lipid composition of normotensive and hypertensive rat vascular smooth muscle cell membranes

Oliveira

Lamy

Paula

et al. 2009

Braz J Med Biol Res

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Multiple cell membrane alterations have been reported to be the cause of various forms of hypertension. The present study focuses on the lipid portion of the membranes, characterizing the microviscosity of membranes reconstituted with lipids extracted from the aorta and mesenteric arteries of spontaneously hypertensive (SHR) and normotensive control rat strains (WKY and NWR). Membrane-incorporated phospholipid spin labels were used to monitor the bilayer structure at different depths. The packing of lipids extracted from both aorta and mesenteric arteries of normotensive and hypertensive rats was similar. Lipid extract analysis showed similar phospholipid composition for all membranes. However, cholesterol content was lower in SHR arteries than in normotensive animal arteries. These findings contrast with the fact that the SHR aorta is hyporeactive while the SHR mesenteric artery is hyperreactive to vasopressor agents when compared to the vessels of normotensive animal strains. Hence, factors other than microviscosity of bulk lipids contribute to the vascular smooth muscle reactivity and hypertension of SHR. The excess cholesterol in the arteries of normotensive animal strains apparently is not dissolved in bulk lipids and is not directly related to vascular reactivity since it is present in both the aorta and mesenteric arteries. The lower cholesterol concentrations in SHR arteries may in fact result from metabolic differences due to the hypertensive state or to genes that cosegregate with those that determine hypertension during the process of strain selection.

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supporting

confidence: 75%

Structural properties of lipid reconstructs and lipid composition of normotensive and hypertensive rat vascular smooth muscle cell membranes

Oliveira

Lamy

Paula

et al. 2009

Braz J Med Biol Res

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“…Standard deviations of systolic blood pressure from several different studies vary between I to 16 mmHg (Franklin et al, 1982;Yen et al, 1974, Orlov et al, 1982Ten Berg, 1980;Rupp & Jakob, 1981) independently of the genetic status of the animals used. Generally the standard deviations of different strains within one study do not differ to the same extent as the standard deviations between different studies.…”

Section: Discussionmentioning

confidence: 99%

Blood pressure in rats: a comparison of a multifactorial experimental design to measurements in an outbred stock

Büttner¹,

Hackbarth

Wollnik³

et al. 1984

Lab Anim

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SummarySystolic blood pressure was measured in males of 8 inbred strains and 1 outbred stock of rats 5 times over a period of 20 min on 5 consecutive days. The strain means ranged between 107'9 mmHg and 149'3 mmHg. The estimated variance between strains (V = 248'7 mmHg) was about 5 times higher than the variance within strains (V = 54'3 mmHg). The intraindividual variance within strains was relatively constant (V = 24'0-37'6 mmHg), while the interindividual variance varied to a great extent (V = 4'5-44'5 mmHg) from strain to strain. The outbred stock showed values of blood pressure and components of variance similar to those of a single inbred strain. Thus, by investigation of a battery of 8 inbred strains in a multifactorial experimental design a greater phenotypic variability due to genetic strain differences is achieved than by measurements in a single outbred stock.

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“…The deficit in total lipid-associated 32 P observed in VSMC from SHRSP indicates that this tissue has a generalized defect in its mechanism for incorporating exogenous phosphate into lipids. To determine whether there were also differences among the phospholipids in their uptakes of 32 P, the results for individual phospholipid classes were expressed as percentages of total lipid-associated radioactivity after 2 hours of incubation ( Table 2).…”

Section: Phosphorus-32 Labeling Of Phospholipids In Vascularmentioning

confidence: 98%

Lipid bilayer in genetic hypertension.

et al. 1991

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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)

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Evidence of Altered Structure of the Erythrocyte Membrane in Spontaneously Hypertensive Rats

Cited by 51 publications

References 7 publications

Structural properties of lipid reconstructs and lipid composition of normotensive and hypertensive rat vascular smooth muscle cell membranes

Structural properties of lipid reconstructs and lipid composition of normotensive and hypertensive rat vascular smooth muscle cell membranes

Blood pressure in rats: a comparison of a multifactorial experimental design to measurements in an outbred stock

Lipid bilayer in genetic hypertension.

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