Artículos de revistas
Structural properties of lipid reconstructs and lipid composition of normotensive and hypertensive rat vascular smooth muscle cell membranes
Fecha
2009-09-01Registro en:
Brazilian Journal of Medical and Biological Research. Associação Brasileira de Divulgação Científica, v. 42, n. 9, p. 844-853, 2009.
0100-879X
S0100-879X2009000900012.pdf
S0100-879X2009000900012
10.1590/S0100-879X2009005000012
WOS:000270233200012
Autor
Oliveira, Tiago.Ribeiro de
Lamy, Maria Teresa
De Paula, Urdiel Macedo
Guimarães, Luciana Lopes
Toledo, Marcos Sergio de
Takahashi, Helio Kiyoshi
Straus, Anita Hilda
Lindsey, Charles Julian
Paiva, Therezinha Bandiera
Institución
Resumen
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 co-segregate with those that determine hypertension during the process of strain selection.