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Kinins and nitric oxide in patients with chronic chagas disease and systemic arterial hypertension

Renata Dellalibera-Joviliano1, Reinaldo B Bestetti1, Gabriel S Lopes2

  • 1Department of Medicine, UNAERP Medical School, University of Ribeirão Preto, Campus Ribeirão Preto, Brazil.

Cardiovascular Pathology : the Official Journal of the Society for Cardiovascular Pathology
|July 17, 2020
PubMed

Insights

This study reveals increased kinin and nitric oxide (NO) activity in patients with chronic Chagas disease (CCHD) and systemic arterial hypertension (SAH). These findings enhance understanding of the CCHD-SAH condition.

Area of Science:

  • Cardiovascular Research
  • Immunology
  • Pathogenesis Studies

Background:

  • Chronic Chagas disease (CCHD) and Systemic Arterial Hypertension (SAH) frequently coexist in endemic areas.
  • The underlying pathogenesis of co-occurring CCHD and SAH (CCHD-SAH) remains unclear.
  • Nitric Oxide (NO) and kinins are implicated in myocardial inflammation in experimental CCHD.

Purpose of the Study:

  • To investigate the roles of kinin-kallikrein system components and nitric oxide (NO) in patients with CCHD-SAH.
  • To elucidate the pathogenesis of CCHD-SAH by examining specific molecular markers.

Main Methods:

  • Thirty-seven CCHD patients (15 CCHD alone, 22 CCHD-SAH) and 11 SAH patients were studied, alongside 30 healthy controls.
  • Measurements included plasma levels of high- and low-molecular weight kininogens (HKg, LKg), plasma kallikrein (Pkal, Tcal), Kininase II, and plasma NO.
  • CCHD-SAH was defined by ECG/Doppler abnormalities and elevated blood pressure.

Main Results:

  • CCHD-SAH patients exhibited lower HKg and LKg levels compared to other groups (P < .0001).
  • Pkal and Tcal levels were significantly higher in CCHD-SAH patients (P < .0001).
  • Kininase II was lower in patients versus controls (P < .0001), while NO levels were elevated in CCHD-SAH patients compared to SAH patients and controls (P > .0001).

Conclusions:

  • Findings suggest heightened kinin and NO activity in patients with CCHD-SAH.
  • This indicates an activated kinin-kallikrein system and increased NO bioavailability in CCHD-SAH.
  • These pathways likely contribute to the complex pathogenesis of CCHD-SAH.
Abstract

Keywords:
Chagas cardiomyopathyChagas diseaseKininKininogensNitric oxideSystemic arterial hypertension

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