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Search: (WFRF:(Bergström Göran 1964)) srt2:(2005-2009) > (2008)

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1.
  • Bernberg, Evelina, 1981, et al. (author)
  • Effects of social isolation and environmental enrichment on atherosclerosis in ApoE-/- mice
  • 2008
  • In: Stress. - 1607-8888 .- 1025-3890. ; 11:5, s. 381-9
  • Journal article (peer-reviewed)abstract
    • Social support and a stimulating environment have been suggested to reduce stress reactions and cardiovascular risk. The aim of this study was to assess the role of environmental enrichment and social interaction for development of atherosclerosis in atherosclerosis prone mice. Male ApoE-/- mice were divided into four groups and followed during 20 weeks: (i) enriched environment (E, n=12), (ii) deprived environment (ED, n=12), (iii) enriched environment with exercise (E-Ex, n=12) and (iv) socially deprived by individual housing (SD, n=10). Plasma lipid and cytokine concentrations were measured. Atherosclerosis was quantified in cross-sections of innominate artery and en face in thoracic aorta. Plaque area was significantly increased in SD mice in the innominate artery (P<0.05 vs. all other groups), but not in the thoracic aorta. Plasma lipids were increased in SD mice (P<0.001 vs. all for total cholesterol, P<0.05 vs. E and P<0.01 vs. ED for triglycerides). Plasma concentration of granulocyte-colony stimulating factor (G-CSF) was decreased in SD mice compared to E mice (P<0.05). Thus, social isolation increased atherosclerosis and plasma lipids in ApoE-/- mice. Reduction in plasma G-CSF levels may hamper endothelial regeneration in the atherosclerotic process. While environmental enrichment did not affect atherosclerosis, social isolation accelerated atherosclerosis.
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2.
  • Johansson, Maria E., et al. (author)
  • Angiotensin type 2 receptor is expressed in human atherosclerotic lesions.
  • 2008
  • In: Journal of the renin-angiotensin-aldosterone system : JRAAS. - : Hindawi Limited. - 1470-3203 .- 1752-8976. ; 9:1, s. 17-21
  • Journal article (peer-reviewed)abstract
    • OBJECTIVE: Expression of the angiotensin type 2 receptor (AT2-receptor) occurs in many animal models of atherosclerosis. However, its expression in human plaques and its functional role remains undetermined. This study examined AT2-receptor expression in human atherosclerotic plaque and also explored its potentially important functional role in atherosclerosis. MATERIAL AND METHODS: We analysed carotid atherosclerotic plaques obtained from 14 Caucasian patients who had previously undergone endarterectomy for symptomatic carotid artery stenosis. Half of all subjects received treatment with an angiotensin receptor blocker (ARB) (n=7); the remaining subjects received no intervention in the renin-angiotensin system (n=7). Immunohistochemistry measured tissue expression of smooth muscle cells (a-actin), macrophages (CD68 antibody), collagen (picro-sirius), and AT2-receptor (AT2-receptor antibody). RESULTS: AT2-receptor expression occurred consistently in all specimens. Although cellular localisation varied, AT2-receptor expression levels correlated with macrophage levels (p<0.01). Compared to conventional treatment, ongoing ARB treatment affected neither AT2-receptor levels nor plaque composition. CONCLUSIONS: AT2-receptor is expressed in human atherosclerotic plaque. Furthermore, we detected no functionally important role of AT2-receptor expression and found no evidence that ARB treatment regulates AT2-receptor expression.
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3.
  • Johansson, Maria E, 1977, et al. (author)
  • Hyperinsulinemic rats are normotensive but sensitized to angiotensin II.
  • 2008
  • In: American Journal of Physiology. Regulatory Integrative and Comparative Physiology (USA). - : American Physiological Society. - 0363-6119 .- 0363-6119 .- 1522-1490. ; 294:4
  • Journal article (peer-reviewed)abstract
    • The effect of insulin on blood pressure (BP) is debated, and an involvement of an activated renin-angiotensin aldosterone system (RAAS) has been suggested. We studied the effect of chronic insulin infusion on telemetry BP and assessed sympathetic activity and dependence of the RAAS. Female Sprague-Dawley rats received insulin (2 units/day, INS group, n = 12) or insulin combined with losartan (30 mg.kg(-1).day(-1), INS+LOS group, n = 10), the angiotensin II receptor antagonist, for 6 wk. Losartan-treated (LOS group, n = 10) and untreated rats served as controls (n = 11). We used telemetry to measure BP and heart rate (HR), and acute ganglion blockade and air-jet stress to investigate possible control of BP by the sympathetic nervous system. In addition, we used myograph technique to study vascular function ex vivo. The INS and INS+LOS groups developed euglycemic hyperinsulinemia. Insulin did not affect BP but increased HR (27 beats/min on average). Ganglion blockade reduced mean arterial pressure (MAP) similarly in all groups. Air-jet stress did not increase sympathetic reactivity but rather revealed possible blunting of the stress response in hyperinsulinemia. Chronic losartan markedly reduced 24-h-MAP in the INS+LOS group (-38 +/- 1 mmHg P < 0.001) compared with the LOS group (-18 +/- 1 mmHg, P
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  • Result 1-3 of 3

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