1999
DOI: 10.1159/000022111
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Does the Plasma Endothelin-1 Concentration Reflect Atherosclerosis in the Elderly?

Abstract: Background and Objective: Recently, attention has been focused on endothelin-1 (ET-1) as an indicator of atherosclerosis. However, normal levels of ET-1 are frequently found in elderly patients. We investigated the relationships between echocardiographic findings and ET-1 in 117 inpatients for rehabilitation. Methods: The patients were 34 men and 83 women, 83.4 ± 0.8 years old (mean ± SE), with the following diseases: cerebrovascular diseases (n = 83), cardiovascular diseases of New York Heart Association Clas… Show more

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Cited by 11 publications
(8 citation statements)
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“…Studies from several laboratories have reported that (i) circulating levels of ET-1 are elevated in insulin resistance associated with aging [Sayama et al, 1999], metabolic syndrome X [Ferri et al, 1997], obesity [Ferri et al, 1995[Ferri et al, , 1997, polycystic ovary syndrome [DiamantiKandarakis et al, 2001], and type 2 diabetes [Takahashi et al, 1990;Ferri et al, 1997]; (ii) ET-1 administration in vivo leads to insulin resistance in rats [Juan et al, 1996;Wilkes et al, 2003], and humans [Teuscher et al, 1998]; (iii) blockade of the endothelin type-A (ET-A) receptor prevents ET-1-induced reduction in insulin sensitivity in humans [Ottosson-Seeberger et al, 1997], as well as in vitro [Chou et al, 1994;Jiang et al, 1999;Idris et al, 2001;Ishibashi et al, 2001] and in vivo [Teuscher et al, 1998;Wilkes et al, 2003] models of ET-1-induced insulin resistance; and (iv) key signal transduction mechanisms of insulin action in skeletal muscle [Idris et al, 2001;Wilkes et al, 2003], smooth muscle [Jiang et al, 1999], and fat [Chou et al, 1994;Idris et al, 2001;Ishibashi et al, 2001] cells are impaired following chronic ET-1 treatment. The results of our studies are in full agreement with these observations and further demonstrate ET-1-induced defects in lipid membrane, actin cytoskeletal, and signaling events regulating GLUT4 trafficking.…”
Section: Discussionmentioning
confidence: 99%
“…Studies from several laboratories have reported that (i) circulating levels of ET-1 are elevated in insulin resistance associated with aging [Sayama et al, 1999], metabolic syndrome X [Ferri et al, 1997], obesity [Ferri et al, 1995[Ferri et al, , 1997, polycystic ovary syndrome [DiamantiKandarakis et al, 2001], and type 2 diabetes [Takahashi et al, 1990;Ferri et al, 1997]; (ii) ET-1 administration in vivo leads to insulin resistance in rats [Juan et al, 1996;Wilkes et al, 2003], and humans [Teuscher et al, 1998]; (iii) blockade of the endothelin type-A (ET-A) receptor prevents ET-1-induced reduction in insulin sensitivity in humans [Ottosson-Seeberger et al, 1997], as well as in vitro [Chou et al, 1994;Jiang et al, 1999;Idris et al, 2001;Ishibashi et al, 2001] and in vivo [Teuscher et al, 1998;Wilkes et al, 2003] models of ET-1-induced insulin resistance; and (iv) key signal transduction mechanisms of insulin action in skeletal muscle [Idris et al, 2001;Wilkes et al, 2003], smooth muscle [Jiang et al, 1999], and fat [Chou et al, 1994;Idris et al, 2001;Ishibashi et al, 2001] cells are impaired following chronic ET-1 treatment. The results of our studies are in full agreement with these observations and further demonstrate ET-1-induced defects in lipid membrane, actin cytoskeletal, and signaling events regulating GLUT4 trafficking.…”
Section: Discussionmentioning
confidence: 99%
“…Such heterogeneity of the endothelium is also detected by electron microscopy [22] with activated endothelial cells close to arteriosclerotic plaques. Clinical evidence of endothelial dysfunction is difficult to obtain because neither NO nor ET-1 from venous blood can be determined reliably [14,15,23].…”
Section: Endothelial Dysfunctionmentioning
confidence: 99%
“…Aging, an inevitable situation for all living organisms, is also associated with inflammatory processes. The aging process causes many problems, such as deregulation of normal bodily functions, which leads to many chronic disorders, such as damage to the vascular endothelium or atherosclerosis, and will often produce hypertension (16,17). Old age combined with hypertension may increase the risk of hypertension-related complications (18).…”
Section: Introductionmentioning
confidence: 99%