Serum Markers of Collagen Type I Metabolism in Spontaneously Hypertensive Rats

Dı́ez, Javier; Panizo, Ángel; Gil, Marı́a J.; Monreal, Ignacío; Hernández, Marta; Mindán, Javier Pardo

doi:10.1161/01.cir.93.5.1026

Cited by 106 publications

(64 citation statements)

References 29 publications

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“…PICP is considered to be a marker of cardiovascular collagen I-mediated fibrosis. 34 In our study, PICP release by renal arterioles was increased in hypertensive rats, which implies that at least a part of the increased extracellular matrix and collagen formation observed by histology was due specifically to collagen I deposition. This activation of collagen I expression was also reflected in the increased urinary excretion rate of PICP in L-NAME-treated animals.…”

Section: Discussionsupporting

confidence: 54%

Vascular Endothelin-1 Gene Expression and Synthesis and Effect on Renal Type I Collagen Synthesis and Nephroangiosclerosis During Nitric Oxide Synthase Inhibition in Rats

et al. 1999

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Background-The progression of hypertension during NO deficiency is associated with renal vascular fibrosis due to increased extracellular matrix (mainly collagen I) formation. The purpose of the present study was to investigate whether endothelin-1 (ET-1) is involved in this pathophysiological process. Methods and Results-Treatment of rats for 4 weeks with the NO synthase inhibitor N -nitro-L-arginine methyl ester (L-NAME) 50 mg ⅐ kg Ϫ1 ⅐ d Ϫ1 increased systolic blood pressure to 159Ϯ12 mm Hg. In animals treated with L-NAME, histological evaluation of renal sections revealed an increased formation of extracellular matrix (Masson's trichrome), and specifically of collagens (Sirius red). A part of this fibrosis was attributed to abnormal collagen I presence, because mRNA expression of the collagen I ␣1 chain (reverse transcription-polymerase chain reaction) and procollagen I formation (radioimmunoassay) were increased 3-and 2.5-fold, respectively, in the renal resistance vessels of hypertensive animals. In subsequent experiments, we examined whether ET-1 was involved in activation of collagen I formation. mRNA expression (RNase protection assay) of preproET-1 and ET-1 content (radioimmunoassay) were 10-fold and 3-fold increased, respectively, in renal microvessels of rats treated with L-NAME. Interestingly, in these vessels, ET-1 (immunostaining) was colocalized with sudanophilic lesions. Bosentan, an ET receptor antagonist (20 mg, coadministered with L-NAME canceled the increased mRNA expression and synthesis of collagen I and attenuated the severity of renal vascular lesions without affecting L-NAME-induced high blood pressure. Conclusions-These data demonstrate that ET-1 synthesis is increased in renal microvessels when NO production is suppressed. In this model of hypertension, ET-1 is a major activator of collagen I formation in renal resistance vessels and participates in the development of renal fibrosis without affecting systolic blood pressure. (Circulation. 1999;99:2185-2191.)

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Section: Discussionsupporting

confidence: 54%

Vascular Endothelin-1 Gene Expression and Synthesis and Effect on Renal Type I Collagen Synthesis and Nephroangiosclerosis During Nitric Oxide Synthase Inhibition in Rats

et al. 1999

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“…It means that CRF have worst systolic function among 3 disease groups. The serum PIP which was known to reflect the state of myocardial fibrosis well [9][10][11] was much higher in CRF group in spite of optimal anti-hypertensive agents compared with other three groups. It suggests that myocardial fibrosis may be related to LV dysfunction as well as the mechanism of LVH in CRF in some degree.…”

mentioning

confidence: 78%

“…On the other hand, it has been known that the plasma level of carboxy-terminal propeptide of procollagen type I (PIP) reflecting the synthesis of type I collagen is well correlated with fibrosis in myocardial interstitium. [9][10][11] So the degree of myocardial fibrosis can be estimated by the measurement of the serum PIP level.…”

Section: )6)mentioning

confidence: 99%

Comparison of Left Ventricular Hypertrophy, Fibrosis and Dysfunction According to Various Disease Mechanisms such as Hypertension, Diabetes Mellitus and Chronic Renal Failure

Koh

Jung

Park

et al. 2009

J Cardiovasc Ultrasound

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“…23 PICP/ ICTP is thought to reflect net synthesis of type I collagen. 24 Serum concentrations of PICP, PINP, ICTP and PIIINP were measured with radioimmunoassays purchased from Orion, Finland. All samples were measured according to instructions from the manufacturer and in duplicate.…”

Section: Assaysmentioning

confidence: 99%

Markers of collagen synthesis is related to blood pressure and vascular hypertrophy: a LIFE substudy

et al. 2005

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Cardiac fibrosis and high levels of circulating collagen markers has been associated with left ventricular (LV) hypertrophy. However, the relationship to vascular hypertrophy and blood pressure (BP) load is unclear. In 204 patients with essential hypertension and electrocardiographic LV hypertrophy, we measured sitting BP, serum collagen type I carboxy-terminal telopeptide (ICTP) reflecting degradation, procollagen type I carboxy-terminal propeptide (PICP) reflecting synthesis and LV mass by echocardiography after 2 weeks of placebo treatment and after 1 year of antihypertensive treatment with a losartan-or an atenolol-based regimen. Furthermore, we measured intima-media thickness of the common carotid arteries (IMT), minimal forearm vascular resistance (MFVR) by plethysmography and ambulatory 24-h BP in around half of the patients. At baseline, PICP/ICTP was positively related to IMT (r ¼ 0.24, Po0.05), MFVR men (r ¼ 0.35, Po0.01), 24-h systolic BP (r ¼ 0.24, Po0.05) and 24-h diastolic BP (r ¼ 0.22, Po0.05), but not to LV mass. After 1 year of treatment with reduction in systolic BP (175715 vs 151717 mmHg, Po0.001) and diastolic BP (9978 vs 8879 mmHg, Po0.001), ICTP was unchanged (3.771.4 vs 3.871.4 lg/l, NS) while PICP (121739 vs 102729 lg/l, Po0.001) decreased. The reduction in PICP/ICTP was related to the reduction in sitting diastolic BP (r ¼ 0.31, Po0.01) and regression of IMT (r ¼ 0.37, Po0.05) in patients receiving atenolol and to reduction in heart rate in patients receiving losartan (r ¼ 0.30, Po0.01). In conclusion, collagen markers reflecting net synthesis of type I collagen were positively related to vascular hypertrophy and BP load, suggesting that collagen synthesis in the vascular wall is increased in relation to high haemodynamic load in a reversible manner.

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Serum Markers of Collagen Type I Metabolism in Spontaneously Hypertensive Rats

Abstract: These results suggest that tissue metabolism of collagen type I is abnormal in SHR and can be normalized by treatment with quinapril. On the basis of our findings, we propose that serum PIP may be a marker of collagen type I-dependent myocardial fibrosis in rats with genetic hypertension.

Cited by 106 publications

References 29 publications

Vascular Endothelin-1 Gene Expression and Synthesis and Effect on Renal Type I Collagen Synthesis and Nephroangiosclerosis During Nitric Oxide Synthase Inhibition in Rats

Vascular Endothelin-1 Gene Expression and Synthesis and Effect on Renal Type I Collagen Synthesis and Nephroangiosclerosis During Nitric Oxide Synthase Inhibition in Rats

Comparison of Left Ventricular Hypertrophy, Fibrosis and Dysfunction According to Various Disease Mechanisms such as Hypertension, Diabetes Mellitus and Chronic Renal Failure

Markers of collagen synthesis is related to blood pressure and vascular hypertrophy: a LIFE substudy

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