Journals / The Anatolian Journal of Cardiology / 2015 / Cilt: 15 - Sayı: 7

The relationship of plasma catestatin concentrations with metabolic and vascular parameters in untreated hypertensive patients: Influence on high-density lipoprotein cholesterol

Pages
577–585
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Coexistence of low catestatin levels with low HDL-C may provide a probable mechanism for the predictive value of low HDL-C for increased hypertension and cardiovascular events.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objective: Catestatin has several cardiovascular actions, in addition to diminished sympatho-adrenal flow.
📊
Key Findings & Data:Decreased plasma catestatin levels may reflect a predisposition for the development of hypertension and metabolic disorders.
💡
Conclusion & Impact:Coexistence of low catestatin levels with low HDL-C may provide a probable mechanism for the predictive value of low HDL-C for increased hypertension and cardiovascular events.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Objective: Catestatin has several cardiovascular actions, in addition to diminished sympatho-adrenal flow. Decreased plasma catestatin levels may reflect a predisposition for the development of hypertension and metabolic disorders. We planned to investigate the possible roles of catestatin in untreated hypertensive patients. As a secondary objective, we compared catestatin concentrations of healthy subjects with those of hypertensive patients in order to understand whether catestatin is increased reactively or diminished at onset. Methods: Our study was cross-sectional and observational. The patient group, comprising 109 consecutive untreated hypertensive patients without additional systemic or coronary heart disease, underwent evaluations of plasma catestatin, waist circumference, lipid parameters, left ventricular mass, carotid intima-media thickness, and flow-mediated dilation of the brachial artery. Additionally, we measured catestatin con- centrations of 38 apparently healthy subjects without any disease using a commercial enzyme-linked immunosorbent assay kit. Results: We documented increased catestatin concentrations in previously untreated hypertensive patients compared to healthy controls (2.27±0.83 vs. 1.92±0.49 ng/mL, p=0.004). However, this association became insignificant after adjustments for age, gender, height, and weight. Within the patient group, catestatin levels were significantly higher in females. Among all study parameters, age, high-density lipoprotein cholesterol (HDL-C) corre- lated positively to plasma catestatin, whereas triglycerides, hemoglobin, and left ventricular mass correlated negatively to plasma catestatin. We could not detect an association between vascular parameters and catestatin. Catestatin levels were significantly elevated with increasing HDL-C (1.91±0.37, 2.26±0.79, and 3.1±1.23 ng/mL in patients with HDL-C <40, 40-60, and >60 mg/dL, respectively). Multiple linear regression analysis revealed age (beta: 0.201, p=0.041) and HDL-C (beta: 0.390, p<0.001) as independent correlates of plasma catestatin concentration. Additionally, male gender (beta:-0.330, p=0.001) and plasma catestatin (beta: 0.299, p=0.002) were significantly associated with HDL-C concentrations. Conclusion: We documented that plasma catestatin is an independent predictor of high-density lipoprotein cholesterol. In addition to antihy- pertensive effects, catestatin appears to be related to improved lipid and metabolic profiles. Coexistence of low catestatin levels with low HDL-C may provide a probable mechanism for the predictive value of low HDL-C for increased hypertension and cardiovascular events.

🔖

Cite This Article

DURAKOĞLUGİL, M. E., AYAZ, T., KOCAMAN, S. A., KIRBAŞ, A., DURAKOĞLUGİL, T., ERDOĞAN, T., ÇETİN, M., ŞAHİN, O. Z., ÇİÇEK, Y. (2015). The relationship of plasma catestatin concentrations with metabolic and vascular parameters in untreated hypertensive patients: Influence on high-density lipoprotein cholesterol. The Anatolian Journal of Cardiology, Cilt: 15 - Sayı: 7, 577–585. https://ajindex.com/articles/365573

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (12)

  1. Helle KB. The chromogranin A-derived peptides vasostatin-I and catestatin as regulatory peptides for cardiovascular functions. Cardiovasc Res 2010
  2. [CrossRef] 2. Mahata SK, Mahata M, Fung MM, O’Connor DT. Catestatin: a mul- tifunctional peptide from chromogranin A. Regul Pept 2010
  3. [CrossRef] 3. Mahata SK, O’Connor DT, Mahata M, Yoo SH, Taupenot L, Wu H, et al. Novel autocrine feedback control of catecholamine release. A discrete chromogranin a fragment is a noncompetitive nicotinic cholinergic antagonist. J Clin Invest 1997
  4. [CrossRef] 4. Mahata SK, Mahata M, Parmer RJ, O’Connor DT. Desensitization of catecholamine release. The novel catecholamine release-inhibito- ry peptide catestatin (chromogranin a344-364) acts at the receptor to prevent nicotinic cholinergic tolerance. J Biol Chem 1999
  5. [CrossRef] 5. Rao F, Wen G, Gayen JR, Das M, Vaingankar SM, Rana BK, et al. Catecholamine release-inhibitory peptide catestatin (chromo- granin A(352-372)): naturally occurring amino acid variant Gly364Ser causes profound changes in human autonomic activity and alters risk for hypertension. Circulation 2007
  6. [CrossRef] 6. Mahata SK, Mahata M, Wen G, Wong WB, Mahapatra NR, Hamilton BA, et al. The catecholamine release-inhibitory “cates- tatin” fragment of chromogranin a: naturally occurring human variants with different potencies for multiple chromaffin cell nico- tinic cholinergic responses. Mol Pharmacol 2004
  7. [CrossRef] 7. O’Connor DT, Kailasam MT, Kennedy BP, Ziegler MG, Yanaihara N, Parmer RJ. Early decline in the catecholamine release-inhibitory peptide catestatin in humans at genetic risk of hypertension. J Hypertens 2002
  8. [CrossRef] 8. Delles C, Padmanabhan S. Genetics and hypertension: is it time to change my practice? Can J Cardiol 2012
  9. [CrossRef] 9. Cheung BM, Li C. Diabetes and hypertension: is there a common metabolic pathway? Curr Atheroscler Rep 2012
  10. [CrossRef] 10. Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA, et al. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation 2005
  11. [CrossRef] 11. Devereux RB, Reichek N. Echocardiographic determination of left ventricular mass in man. Anatomic validation of the method. Circulation 1977
  12. [CrossRef] 12. Corretti MC, Anderson TJ, Benjamin EJ, Celerm