Evidence map›Paper›PMID 39585243›Full record

ArticleBioscience reports2024

The physiological anti-hypertensive peptide catestatin and its common human variant Gly364Ser: differential cardiovascular effects in a rat model of hypertension.

Jitesh Singh Rathee, Dhanya R Iyer, Malapaka Kiranmayi, Samarasimha Reddy, V V Sureshbabu, Nitish R Mahapatra

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Article in Bioscience reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1 citing paper in PubMed.

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5 · Who and what money

Authors and funding

6 authors.

Jitesh Singh RatheeBio-Organic Division, Bhabha Atomic Research Centre, Mumbai 400085, India.
Dhanya R IyerDepartment of Biotechnology, Bhupat and Jyoti Mehta School of Biosciences, Indian Institute of Technology Madras, Chennai 600036, India.
Malapaka KiranmayiDepartment of Biotechnology, Bhupat and Jyoti Mehta School of Biosciences, Indian Institute of Technology Madras, Chennai 600036, India.
Samarasimha ReddyDepartment of Studies in Chemistry, Central College Campus, Bangalore University, Dr. B. R. Ambedkar Veedhi, Bangalore 560001, India.
V V SureshbabuDepartment of Studies in Chemistry, Central College Campus, Bangalore University, Dr. B. R. Ambedkar Veedhi, Bangalore 560001, India.
Nitish R MahapatraDepartment of Biotechnology, Bhupat and Jyoti Mehta School of Biosciences, Indian Institute of Technology Madras, Chennai 600036, India.ORCID 0000-0002-0695-3510

Funding

Department of Atomic Energy, Government of India (DAE)Department of Biotechnology, Ministry of Science and Technology, India (DBT) BT/PR12820/BRB/10/726/2009Department of Biotechnology, Ministry of Science and Technology, India (DBT) BT/PR23017/MED/30/1838/2017, BT/PR25796/GET/119/98/2017
6 · The paper itself

Abstract

Catestatin (CST), a 21-amino acids physiological peptide, has emerged as a key modulator of cardiovascular functions due to its anti-hypertensive and cardioprotective properties. However, the ramifications of the most common human variant of CST (viz., Gly364Ser) on cardiovascular pathophysiology remain partially understood. In this study, hypertension was induced in uninephrectomized rats by treatment with deoxycorticosterone-acetate and sodium chloride (DOCA-salt). The DOCA-salt-induced hypertensive (DSHR) animals were then intraperitoneally administered with either CST wild-type (CST-WT) or 364Ser variant (CST-Ser) peptide. CST-Ser was profoundly less effective than CST-WT in rescuing the elevated systolic blood pressure [from ∼211 mmHg to ∼176 mmHg, p < 0.0001 (CST-Ser) versus ∼116 mmHg, p < 0.0001 (CST-WT)] and heart rate [from ∼356 bpm to ∼314 bpm, p = 0.66 (CST-Ser) versus ∼276 bpm, p = 0.02 (CST-WT)]. CST-Ser also showed diminished effects in lowering diastolic blood pressure and mean arterial pressure in the DSHR animals. Furthermore, CST-Ser was inefficient/markedly less potent in rescuing the impaired contractile and diastolic function in DSHR animals [improvements in the contractility index by ∼22 s-1 (CST-Ser), p = 0.15 versus by ∼84 s-1 (CST-WT), p < 0.0001 and decrease in end-diastolic pressure by ∼4 mmHg (CST-Ser), p = 0.015 versus by ∼14 mmHg (CST-WT), p < 0.0001]. Moreover, CST-Ser exerted less potent anti-inflammatory effects on the DSHR hearts than CST-WT. These findings are in concordance with the elevated systolic/diastolic blood pressure observed in Ser variant carriers from various human populations. This study provides compelling evidence for the diminished anti-hypertensive and cardioprotective effects of the CST-Gly364Ser variant.

Indexed as

Antihypertensive AgentsBlood PressureChromogranin ADisease Models, AnimalHeart RateHypertensionPeptide FragmentsAnimalsDesoxycorticosterone AcetateHumansMaleRatsRats, Sprague-DawleyAntihypertensive AgentsChromogranin Achromogranin A (344-364)Desoxycorticosterone AcetatePeptide Fragmentsblood pressurecardioprotectioncatestatinhuman genetic variantinflammation

Identifiers

PMID39585243
PMCPMC11667095

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.