Relationship between hepatic angiotensinogen mRNA expression and plasma angiotensinogen in patients with chronic hepatitis

Takahashi, D. Y.; Tamura, Kouichi; Ushikubo, Toshiaki; Moriya, Akihiko; Yokoyama, Nobuyuki; Nyui, Nobuo; Chiba, Eiko; Hibi, Kiyoshi; Ishigami, Tomoaki; Yabana, Machiko; Tomiyama, Masakazu; Umemura, Satoshi; Ishii, Masao

doi:10.1016/s0024-3205(97)00129-x

Cited by 12 publications

(6 citation statements)

References 29 publications

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“…Angiotensionogen (AGT), the first substrate of the RAAS, is an α 2 -glycoprotein and present at nanomolar concentrations in serum [25, 41]. Cleavage by renin yields the decapeptide Ang I, which is then converted by angiotensin converting enzyme (ACE; EC 3.4.15.1) to the active octapeptide Ang II (Figure 1).…”

Section: Pparα and Pparγ Regulate Angiotensinogen Gene Expressionmentioning

confidence: 99%

PPARs in the Renal Regulation of Systemic Blood Pressure

Röszer

Ricote

2010

PPAR Research

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Recent research has revealed roles for the peroxisome proliferator activated receptor (PPAR) family of transcription factors in blood pressure regulation, expanding the possible therapeutic use of PPAR ligands. PPARα and PPARγ modulate the renin-angiotensin-aldosterone system (RAAS), a major regulator of systemic blood pressure and interstitial fluid volume by transcriptional control of renin, angiotensinogen, angiotensin converting enzyme (ACE) and angiotensin II receptor 1 (AT-R1). Blockade of RAAS is an important therapeutic target in hypertension management and attenuates microvascular damage, glomerular inflammation and left ventricular hypertrophy in hypertensive patients and also show antidiabetic effects. The mechanisms underlying the benefits of RAAS inhibition appear to involve PPARγ-regulated pathways. This review summarizes current knowledge on the role of PPARs in the transcriptional control of the RAAS and the possible use of PPAR ligands in the treatment of RAAS dependent hypertension.

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Section: Pparα and Pparγ Regulate Angiotensinogen Gene Expressionmentioning

confidence: 99%

PPARs in the Renal Regulation of Systemic Blood Pressure

Röszer

Ricote

2010

PPAR Research

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“…The blood was centrifuged immediately and the plasma separated and kept frozen at −80°C until the time of assay. P-NE was measured by a high-performance liquid chromatographic method, as described previously (20). Plasma renin activity and plasma aldosterone were measured by radioimmunoassay, also as described previously (20,21).…”

Section: Laboratory Measurementsmentioning

confidence: 99%

“…P-NE was measured by a high-performance liquid chromatographic method, as described previously (20). Plasma renin activity and plasma aldosterone were measured by radioimmunoassay, also as described previously (20,21). Hematocrit, plasma fibrinogen, serum total protein, serum creatinine, serum uric acid, blood glucose, serum total cholesterol, and serum C-reactive protein were measured by routine methods in the Department of Clinical Chemistry, Yokohama City University School Hospital.…”

Section: Laboratory Measurementsmentioning

confidence: 99%

Ambulatory Blood Pressure Variability Is Increased in Diabetic Hypertensives

Ozawa

Tamura

Iwatsubo

et al. 2008

Clinical and Experimental Hypertension

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The purpose of this study was to examine the possible difference in the 24-hr BP profile--including short-term BP variability, assessed as the standard deviation--between diabetic and non-diabetic hypertensives. We measured 24-hr ambulatory BP in 11 diabetic hypertensives (diabetic HT) and 10 non-diabetic hypertensives (non-diabetic HT) who were hospitalized for the educational program in our hospital and were under stable salt intake. Renal function and sleep apnea were also estimated. There were no significant differences in 24-hr systolic BP (141 mmHg vs. 135 mmHg, ns), daytime systolic BP (143 mmHg vs. 138 mmHg, ns), and nighttime systolic BP (135 mmHg vs. 130 mmHg, ns) between diabetic HT and non-diabetic HT. The values of 24-hr HR (69.7 beats/min vs. 65.2 beats/min, ns) and 24-hr HR variability (9.9 beats/min vs. 10.1 beats/min, ns) were also similar between the groups. Interestingly, diabetic HT had a significantly greater 24-hr systolic and diastolic BP variability than non-diabetic HT (18.2 mmHg vs. 14.5 mmHg, p < 0.05; 11.5 mmHg vs. 9.6 mmHg, p < 0.05, respectively). The values for creatinine clearance, urinary protein excretion, and apnea-hypopnea index were similar between the groups. Bivariate linear regression analysis demonstrated that fasting blood glucose was the primary determinant of 24-hr diastolic BP variability (r = 0.661, p < 0.01). Multiple stepwise regression analysis revealed that fasting blood glucose was a significant and independent contributor to 24-hr systolic BP variability (r = 0.501, p < 0.05). Taken together, these results demonstrate that BP variability is increased in diabetic hypertensives. Furthermore, it is possible that an elevation of fasting blood glucose may contribute to the enhanced BP variability in hypertensives.

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“…Interestingly, the C allele of A-20C is consistently the less frequent allele in both Japanese (0.20 21 ) and whites (0.19 4 ). Ishigami et al 24 showed that the plasma angiotensinogen concentration in a Japanese population increased linearly according to the A-20C genotype (ie, AAϽACϽCC), partly reflecting increased AGT mRNA levels in the liver 26 due to the influence of A-20C genotype on the transcriptional regulation of AGT. We are currently in the process of examining these polymorphisms in our population.…”

Section: Discussionmentioning

confidence: 99%

Angiotensinogen Gene Polymorphisms M235T/T174M

Niu

Jiao²,

Zhang³

et al. 1999

Hypertension

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Abstract-The gene encoding angiotensinogen (AGT) has been widely studied as a candidate gene for hypertension. Most studies to date have relied on case-control analysis to test for an excess of AGT variants among hypertensive cases compared with normotensive controls. However, with this design, nothing guarantees that a positive finding is due to actual allelic association as opposed to an inappropriate control population. To avoid this difficulty in our study of essential hypertension in Anqing, China, we tested AGT variants using the transmission/disequilibrium test, a procedure that bypasses the need for a control sample by testing for excessive transmission of a genetic variant from parents heterozygous for that variant. We analyzed two AGT polymorphisms, M235T and T174M, which have been associated with essential hypertension in whites and Japanese, using data on 335 hypertensive subjects from 315 nuclear families and their parents. Except in the group of subjects younger than 25 years, M235 and T174 were the more frequently transmitted alleles. ypertension, a leading cause of cardiovascular and renal disease in the United States, results from a combination of genetic and environmental factors. Because of the public health significance of this disorder, many studies on the genetic basis of hypertension have been performed. 1-9 Several of these studies have tested genes with potential biological relevance to ascertain whether certain variants appear to influence the disease process. 3-9 One frequently studied gene has been angiotensinogen (AGT), a logical candidate, given the strong correlation of plasma angiotensinogen levels and blood pressure. 10 Located on 1q42 to 43, AGT comprises five exons and four introns spanning 13 kb. 11 Although several polymorphisms in the AGT region have been identified, 3 much interest has focused on two coding region polymorphisms, M235T and T174M, both in exon 2. More specifically, through case-control studies, many 3-5 but not all 6 -9 investigators have concluded that the threonine allele (T235) of M235T and the methionine allele (M174) of T174M are associated with elevated risk for hypertension. The validity of these case-control studies, however, depends on the ability of identifying a suitable control group, since different genetic backgrounds with varying polymorphism frequencies can potentially lead to spurious results.To eliminate the need for an external control group in our study of M235T and T174M in rural Chinese, we have collected nuclear families consisting of hypertensive individuals and their parents and have applied family-based association testing using the transmission/disequilibrium test (TDT). 12 With TDT, parental alleles transmitted to the affected hypertensive offspring are compared with those not transmitted. As a result, each family provides its own controls, and false-positives due to poorly matched controls are avoided.In addition to the sophistication of the TDT study design, the other defining feature of our investigation is the unique nature of ...

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Relationship between hepatic angiotensinogen mRNA expression and plasma angiotensinogen in patients with chronic hepatitis

Cited by 12 publications

References 29 publications

PPARs in the Renal Regulation of Systemic Blood Pressure

PPARs in the Renal Regulation of Systemic Blood Pressure

Ambulatory Blood Pressure Variability Is Increased in Diabetic Hypertensives

Angiotensinogen Gene Polymorphisms M235T/T174M

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