Plasma endothelin-1 levels in obese hypertensive and normotensive men

Ferri, C.; Bellini, C.; Desideri, G.; Francesco, L. Di; Baldoncini, R.; Santucci, A.; Mattia, G. De

doi:10.2337/diabetes.44.4.431

Cited by 61 publications

(80 citation statements)

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“…Finally, it should be noted that the dose of endothelin-1 used for these studies greatly exceeds reported plasma levels, which rarely exceed 25 pmol/l under pathological conditions [2,3]. The secretion of endothelin-1 in the body is abluminal and not directly into the blood stream.…”

Section: Discussionmentioning

confidence: 82%

“…Many studies have reported elevated plasma endothelin-1 concentrations associated with hyperinsulinaemia, hypertension and insulin resistance [2,3,5,20], but the cause(s) of the elevated plasma levels of endothelin-1 in these disease states are yet to be determined. It is also unclear whether endothelin-1 blockers (in particular endothelin-1 A blockers) are a beneficial therapy for patients suffering from cardiovascular disease and type 2 diabetes.…”

Section: Discussionmentioning

confidence: 99%

“…Endothelin-1 is a locally produced vasoactive peptide released from vascular endothelial cells, plasma levels of which are often elevated in patients with hypertension, obesity, type 2 diabetes, peripheral vascular resistance as well as other disease states associated with cardiovascular disease [1][2][3][4][5][6]. In addition, endothelin-1 release may be stimulated by insulin, and may be involved in maintaining vasomotor tone at rest and during insulin stimulation [4,7].…”

Section: Introductionmentioning

confidence: 99%

“…Since plasma levels of endothelin-1 are elevated in various states of insulin resistance [1][2][3][4][5][6], the aim of this study was to test the hypothesis that elevated plasma levels of endothelin-1 may prevent full perfusion of muscle, thereby limiting delivery of insulin and glucose and contributing to insulin resistance. Our approach was to examine the effect of endothelin-1 infusion (both alone and in conjunction with insulin infusion) in vivo on femoral blood flow (FBF) and muscle capillary perfusion, muscle glucose uptake, and whole-body glucose infusion rate (GIR).…”

Section: Introductionmentioning

confidence: 99%

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Acute blockade by endothelin-1 of haemodynamic insulin action in rats

et al. 2006

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Aims/hypothesis Plasma levels of endothelin-1 are frequently elevated in patients with hypertension, obesity and type 2 diabetes. We hypothesise that this vasoconstrictor may prevent full perfusion of muscle, thereby limiting delivery of insulin and glucose and contributing to insulin resistance. Materials and methods The acute effects of endothelin-1 on insulin-mediated haemodynamic and metabolic effects were examined in rats in vivo. Endothelin-1 (50 pmol min −1 kg −1 for 2.5 h) was infused alone, or 30 min prior to a hyperinsulinaemic-euglycaemic insulin clamp (10 mU min −1 kg −1 for 2 h). Insulin clamps (10 or 15 mU min −1 kg −1 ) were performed after 30 min of saline infusion. Results Endothelin-1 infusion alone increased plasma endothelin-1 11-fold (p<0.05) and blood pressure by 20% (p<0.05). Endothelin-1 alone had no effect on femoral blood flow, capillary recruitment or glucose uptake, but endothelin-1 with 10 mU min −1 kg −1 insulin caused a decrease in insulin clearance from 0.35±0.6 to 0.19± 0.02 ml/min (p=0.02), resulting in significantly higher plasma insulin levels (10 mU min −1 kg −1 insulin: 2,120± 190 pmol/l; endothelin-1+10 mU min −1 kg −1 insulin: 4,740± 910 pmol/l), equivalent to 15 mU min −1 kg −1 insulin alone (4,920±190 pmol/l). The stimulatory effects of equivalent doses of insulin on femoral blood flow, capillary recruitment and glucose uptake were blocked by endothelin-1.Conclusions/interpretation Endothelin-1 blocks insulin's haemodynamic effects, particularly capillary recruitment, and is associated with decreased muscle glucose uptake and glucose infusion rate. These findings suggest that elevated endothelin-1 levels may contribute to insulin resistance of muscle by increasing vascular resistance and limiting insulin and glucose delivery.

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Section: Discussionmentioning

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Acute blockade by endothelin-1 of haemodynamic insulin action in rats

et al. 2006

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“…Participation of insulin in the modulation of plasma ET-1 levels was suspected. 28,29 It is also known that a higher concentration of serum insulin is observed in obese subjects. 30,31 Thus, FBS was included in the analysis to adjust for the confounding factor of insulin resistance of subjects.…”

Section: Various Measurements and Survey Of Life Habitsmentioning

confidence: 99%

The Lack of Relationship between an Endothelin-1 Gene Polymorphism (Ala288Ser) and Incidence of Hypertension: A Retrospective Cohort Study among Japanese Workers

Kaetsu

Kishimoto

Osaki

et al. 2004

Journal of Epidemiology

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BACKGROUND: Some case-control association studies revealed the relationship between some endothelin-1 (ET-1) gene polymorphisms and blood pressure. Because no report was available about the relationship between any ET-1 gene polymorphism and incidence of hypertension, we examined the relationship between novel ET-1 gene polymorphism (G862T / Ala288Ser in exon 5) and incidence of hypertension by a retrospective cohort study. METHODS: The subjects were Japanese workers at a company in Shimane Prefecture in Japan. The polymorphism with genome DNA extracted from the blood of the workers was analyzed using the polymerase chain reaction confronting two pair primers method. According to the results of two regular health checkups with a 6-year interval, the study population was divided into two groups by blood pressure and antihypertensive treatment in 1998, after excluding people who had hypertension in 1992. RESULTS: There were 133 (93 males and 40 females) incidences of hypertension observed among the study population of 922 (540 males and 382 females). In the univariate analysis, odds ratios o Ala/Ser and Ser/Ser against Ala/Ala were 0.98 (95% confidence interval [CI]): 0.7-1.4) and 0.79 (95% CI: 0.4-1.6), respectively. In the multivariate analysis adjusted for sex, age, body mass index, serum total cholesterol, fasting blood sugar, and smoking and drinking habits, odds ratios for Ala/Ser and Ser/Ser against Ala/Ala were 0.97 (95% CI: 0.7-1.4) and 0.75 (95% CI: 0.4-1.5), respectively. CONCLUSIONS: The ET-1 gene polymorphism in this study did not seem to be associated with the incidence of hypertension among the Japanese workers.

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