Human adipose tissue expresses angiotensinogen and the enzymes required for its conversion to angiotensin II

Carlsson, Lena; Karlsson, Cecilia; Lindell, Kajsa; Ottosson, Malin; Sjöström, Lars; Carlsson, Björn

doi:10.1016/s1096-6374(99)80058-6

Cited by 35 publications

(48 citation statements)

References 31 publications

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“…This result emphasized the link between PAI-1 and the renin-angiotensin system. Interestingly, two studies showed that both human adipocytes and preadipocytes expressed angiotensinogen and the enzymes of the reninangiotensin system and were then able to synthesize and secrete angiotensin II [65,66]. Thus it could be hypothesized that adipose tissue and renin-angiotesin system, might be the link between elevated plasma PAI-1 and hypertension, particularly in obesity [53,67].…”

Section: Discussionmentioning

confidence: 99%

Prothrombotic markers in asymptomatic dyslipidemic subjects

Karásek

Vaverková

Halenka

et al. 2010

J Thromb Thrombolysis

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The aim of this study was to evaluate the plasma levels of prothrombotic markers--von Willebrand factor (vWF), plasminogen activator inhibitor-1 (PAI-1), tissue plasminogen activator (t-PA)--in asymptomatic subjects with dyslipidemia. Asymptomatic subjects with dyslipidemia and their relatives (n = 234) were assessed for lipids and prothrombotic markers. Individuals were divided into four dyslipidemic phenotypes (DLP) according to apolipoprotein B (apoB) and triglycerides (TG): DLP1 (n = 58, apoB < 1.2 g/l and TG < 1.5 mmol/l), DLP2 (n = 47, apoB < 1.2 g/l and TG ≥ 1.5 mmol/l), DLP3 (n = 31, apoB ≥ 1.2 g/l and TG < 1.5 mmol/l) and DLP4 (n = 98, apoB ≥ 1.2 g/l and TG ≥ 1.5 mmol/l). Associations between prothrombotic markers and risk factors for atherosclerosis, markers of insulin resistance, and the intima-media thickness of the common carotid artery (IMT) were assessed too. Significant differences in PAI-1 between normolipidemic phenotype--DLP1 (62.5 (35.9-82.9) ng/ml) and hypertriglyceridemic phenotypes--DLP2 (82.2 (61.1-122.1) ng/ml, p < 0.01) and DLP4 (91.4 (63.5-111.8) ng/ml, p < 0.001) after adjustment for age, sex and body mass index, were found. Levels of t-PA were different only between DLP1 and DLP4 (1.9 (0.9-3.3) ng/ml vs. 5.3 (2.5-8.6) ng/ml, p < 0.05). There were no significant differences of vWF between DLPs. PAI-1 and t-PA correlated with lipid parameters, markers of insulin resistance, blood pressure and obesity. VWF was independently associated with IMT, which was increased in DLP4. Individuals with hypertriglyceridemic phenotypes showed increased levels of PAI-1 in comparison with normolipidemic subjects. The elevation of t-PA was presented only in patients with simultaneously elevated TG and apoB. The significant increase of IMT confirmed in the patients with DLP4 reveals individuals with the highest risk for atherosclerosis manifestation.

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Section: Discussionmentioning

confidence: 99%

Prothrombotic markers in asymptomatic dyslipidemic subjects

Karásek

Vaverková

Halenka

et al. 2010

J Thromb Thrombolysis

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“…Adipocytes are known to secrete angiotensinogen and angiotensin II (Ang II) as adipocytokines [7,8]. Ang II induces insulin resistance via suppression of intracellular signal transduction of insulin and dysregulation of adipocytokines, including TNF-a and adiponectin [9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Down-regulation of hepatic stearoyl-CoA desaturase 1 expression by angiotensin II receptor blocker in the obese fa/fa Zucker rat: possible role in amelioration of insulin resistance and hepatic steatosis

et al. 2009

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“…In more recent years, however, as a plethora of enzymes have been uncovered that catalyze the activation of prorenin to renin, the transformation of angiotensinogen to ANG I, the transformation of ANG I to ANG II, and the direct generation of ANG II from angiotensinogen, it has become apparent that a nonreninangiotensin system (NRAS) also exists [18,19]. In addition, several angiotensinases readily degrade ANG II [5-7, 20, 21].…”

Section: Discussionmentioning

confidence: 99%

Effect of Acetaldehyde Upon Cathepsin G and Chymase. NRAS Implications

Brecher

Dubord

2007

Dig Dis Sci

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Hypertension is commonly observed in alcoholics. Both the renin-angiotensin system (RAS) and the non-renin-angiotensin system (NRAS) have been implicated in the dynamics of blood pressure maintenance. In bilaterally nephrectomized rats, acetaldehyde has been reported to enhance the generation of the rate-limiting angiotensin I (ANG I) in the plasma, and in humans it inhibits the activity of several angiotensinases (A, B, and M) in the serum, thereby promoting a hypertensive set of reactions. We report here the results of a study on the effect of acetaldehyde upon cathepsin G and mast cell chymase. Acetaldehyde enhanced cathepsin G activity at all of the concentrations tested between 11.2 and 223.5 mM in a statistically significant manner. Since cathepsin G is one of several enzymes transforming ANG I into ANG II and is also capable of cleaving ANG II directly from angiotensinogen, we suggest that alcoholism, which will generate exogenous acetaldehyde from ingested alcohol, may be a contributory factor for an elevated cathepsin G activity and, consequently, hypertension via the NRAS. Chymase activity also is elevated in the presence of 440 mM acetaldehyde and diminished in the presence of 27 mM acetaldehyde. Since both enzymes also degrade ANG II, the degradative effects of each enzyme on ANG II may neutralize one another.

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Human adipose tissue expresses angiotensinogen and the enzymes required for its conversion to angiotensin II

Cited by 35 publications

References 31 publications

Prothrombotic markers in asymptomatic dyslipidemic subjects

Prothrombotic markers in asymptomatic dyslipidemic subjects

Down-regulation of hepatic stearoyl-CoA desaturase 1 expression by angiotensin II receptor blocker in the obese fa/fa Zucker rat: possible role in amelioration of insulin resistance and hepatic steatosis

Effect of Acetaldehyde Upon Cathepsin G and Chymase. NRAS Implications

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