Regulation of hepatic angiotensinogen synthesis and secretion by steroid hormones.

Klett, Christoph; Ganten, Detlev; Hellmann, W.; Kaling, Michael; Ryffel, Gerhart U.; Weimar-Ehl, T.; Hackenthal, E.

doi:10.1210/endo.130.6.1597163

Cited by 61 publications

(36 citation statements)

References 26 publications

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“…Previous studies have reported a higher plasma Agt concentration in women, especially in the homozygotes for the T allele at the AGT M235T locus (17). The promoter region of the AGT gene contains an estrogen responsive element (17) and estrogen has been shown to enhance Agt production both in humans (37,38) and animals (39). Thus, the gender differences observed in the present study may have a real physiological basis rather than being simply the result of spurious statistical observations.…”

Section: Discussionmentioning

confidence: 72%

Body Fat, Resting and Exercise Blood Pressure and the Angiotensinogen M235T Polymorphism: The Heritage Family Study

et al. 1999

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. Body fat, resting and exercise blood pressure and the angiotensinogen M235T polymorphism: the Heritage family study. Obes Res. 1999;7:423- 430.Objective: The association of resting and exercise blood pressure (BP) and fat mass with the angiotensinogen (AGT) M235T polymorphism was investigated in 522 sedentary Caucasian subjects from 99 families. Research Methods and Procedures:Resting BP was measured on two separate days, three times each day, and the mean of six valid measurements was used. Exercise BP was measured during a cycle ergometer test at a constant power output (50 W). Body composition was derived from underwater weighing and the AGT M235T polymorphism was typed with a polymerase chain reaction-based method. Results: Neither resting nor exercise BP was associated with the AGT genotypes. In mothers, the homozygotes for the T allele showed 8.8 kg and 7.1 kg greater (p=O.O17) age-adjusted body fat mass (FM) than the MM homozygotes and heterozygotes, respectively. Sixty-nine percent of all TT homozygotes were found in the highest FM tertile, whereas only 16% of the MM homozygotes fell in the same tertile (p = 0.008). Moreover, a significant interaction was seen between FM and T-allele carrier status in women with regard to resting diastolic BP (p = 0.002). Among women with a F M r 2 4 kg, carriers of the T allele showed a 6.3 mmHg higher diastolic blood pressure (DBP) than noncarriers whereas no difference was found in women with a FM less than 24 kg. A similar trend toward an interaction term was evident with resting systolic blood pressure (p = 0.01 1) and exercise DBP (p = 0.012). Body fat was not associated with the AGT polymorphism in fathers or in offspring. Discussion: These data suggest that the AGT M235T polymorphism is associated with body fatness in women, and that the relationship between DBP and AGT M235T polymorphism is dependent on FM in middle-aged sedentary normotensive women.

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Section: Discussionmentioning

confidence: 72%

Body Fat, Resting and Exercise Blood Pressure and the Angiotensinogen M235T Polymorphism: The Heritage Family Study

et al. 1999

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“…The synthesis of angiotensinogen in hepatocytes is regulated by estrogens (11). Plasma renin levels and angiotensin-converting enzyme (ACE) activity are significantly higher in estrogen-deficient compared with estrogen-replete rats and in postmenopausal women not receiving HRT compared with women on HRT (9,12).…”

mentioning

confidence: 99%

Menopause and Ovariectomy Cause a Low Grade of Systemic Inflammation that May Be Prevented by Chronic Treatment with Low Doses of Estrogen or Losartan

Abu-Taha¹,

Rius²,

Hermenegildo

et al. 2009

The Journal of Immunology

141

102

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The incidence of cardiovascular diseases in premenopausal women is lower than in men or postmenopausal women. This study reports the discovery of a low grade of systemic inflammation, including monocyte adhesion to arterial endothelium, elicited by menopause or estrogen depletion. Chronic treatment with low dose of 17-β-estradiol or inhibition of the renin-angiotensin system reduced this inflammation. Using an in vitro flow chamber system with human arterial and venous endothelial cells, we found that leukocytes from healthy postmenopausal women were more adhesive to the arterial endothelium than those from premenopausal women regardless of the stimulus used on endothelial cells. Increased circulating levels of IL-8, MCP-1, RANTES, and MIP-1α and monocyte CD11b expression were also encountered in postmenopausal vs premenopausal subjects. This translational data led us to investigate the mechanisms in Sprague-Dawley rats. Using intravital microscopy, we imaged mesenteric arterioles and found significant increases in arteriolar leukocyte adhesion, cell adhesion molecule expression, and plasma levels of cytokine-induced neutrophil chemoattractant (CINC/KC), MCP-1, and MIP-1α in 1-mo ovariectomized rats. Chronic treatment of ovariectomized rats with low dose of 17-β-estradiol, losartan, both, or benazepril inhibited ovariectomy-induced arteriolar mononuclear leukocyte adhesion by 77%, 58%, 92%, and 65% respectively, partly by inhibition of cell adhesion molecule up-regulation and the increase in circulating chemokines. These results demonstrate that menopause and ovariectomy generate a low grade of systemic inflammation. Therefore, administration of low doses of estrogens or inhibition of the renin-angiotensin system, at early stages of estrogen deficiency, might prevent the systemic inflammation associated with menopause and decrease the risk of suffering further cardiovascular diseases.

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“…Estrogens influence the rennin-angiotensin system by regulating the synthesis of angiotensinogen in hepatocytes (17). Plasma rennin levels and angiotensin-converting enzyme activity are significantly higher in estrogen-deficient versus estrogen-replete rats, and in postmenopausal women not receiving hormone replacement therapy (HRT) versus those receiving it (18,19).…”

mentioning

confidence: 99%

Trans- but Not Cis-Resveratrol Impairs Angiotensin-II–Mediated Vascular Inflammation through Inhibition of NF-κB Activation and Peroxisome Proliferator-Activated Receptor-γ Upregulation

Rius¹,

Abu-Taha²,

Hermenegildo

et al. 2010

The Journal of Immunology

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Angiotensin II (Ang-II) displays inflammatory activity and is implicated in several cardiovascular disorders. This study evaluates the effect of cis- and trans (t)-resveratrol (RESV) in two in vivo models of vascular inflammation and identifies the cardioprotective mechanisms that underlie them. In vivo, Ang-II–induced arteriolar leukocyte adhesion was inhibited by 71% by t-RESV (2.1 mg/kg, i.v.), but was not affected by cis-RESV. Because estrogens influence the rennin-angiotensin system, chronic treatment with t-RESV (15 mg/kg/day, orally) inhibited ovariectomy-induced arteriolar leukocyte adhesion by 81%, partly through a reduction of cell adhesion molecule (CAM) expression and circulating levels of cytokine-induced neutrophil chemoattractant, MCP-1, and MIP-1α. In an in vitro flow chamber system, t-RESV (1–10 μM) undermined the adhesion of human leukocytes under physiological flow to Ang-II–activated human endothelial cells. These effects were accompanied by reductions in monocyte and endothelial CAM expression, chemokine release, phosphorylation of p38 MAPK, and phosphorylation of the p65 subunit of NF-κB. Interestingly, t-RESV increased the expression of peroxisome proliferator-activated receptor-γ in human endothelial and mononuclear cells. These results demonstrate for the first time that the in vivo anti-inflammatory activity of RESV is produced by its t-RESV, which possibly interferes with signaling pathways that cause the upregulation of CAMs and chemokine release. Upregulation of proliferator-activated receptor-γ also appears to be involved in the cardioprotective effects of t-RESV. In this way, chronic administration of t-RESV may reduce the systemic inflammatory response associated with the activation of the rennin-angiotensin system, thereby decreasing the risk of further cardiovascular disease.

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Regulation of hepatic angiotensinogen synthesis and secretion by steroid hormones.

Cited by 61 publications

References 26 publications

Body Fat, Resting and Exercise Blood Pressure and the Angiotensinogen M235T Polymorphism: The Heritage Family Study

Body Fat, Resting and Exercise Blood Pressure and the Angiotensinogen M235T Polymorphism: The Heritage Family Study

Menopause and Ovariectomy Cause a Low Grade of Systemic Inflammation that May Be Prevented by Chronic Treatment with Low Doses of Estrogen or Losartan

Trans- but Not Cis-Resveratrol Impairs Angiotensin-II–Mediated Vascular Inflammation through Inhibition of NF-κB Activation and Peroxisome Proliferator-Activated Receptor-γ Upregulation

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