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Published on: July 7, 2016

The Influence of Basic Therapy and New Drugs on NO-Dependent Mechanisms of Cardiac Destruction in Chronic Heart

Igor Belenichev1, Olena Popazova2, Olexiy Goncharov1

  • 1Department of Pharmacology and Medical Formulation with Course of Normal Physiology, Zaporizhzhia State Medical and Pharmaceutical University, 69000 Zaporizhzhia, Ukraine.

Biomedicines
|May 27, 2026
PubMed

Insights

Novel therapies targeting nitric oxide (NO) dysfunction in chronic heart failure (CHF) show promise. The compound Hypertril demonstrates significant cardioprotective effects by enhancing NO bioavailability, offering a new approach to managing this condition.

Area of Science:

  • Cardiovascular Medicine
  • Pharmacology
  • Biochemistry

Background:

  • Chronic heart failure (CHF) is a major cause of mortality, linked to nitric oxide (NO) system dysfunction, mitochondrial issues, and oxidative stress.
  • Current treatments like ACE inhibitors, SGLT2 inhibitors, and beta-blockers manage symptoms but often fail to address underlying biochemical mechanisms of cardiomyopathy.
  • Impaired NO production and reactive oxygen species (ROS) accumulation worsen myocardial function and disease progression in CHF.

Purpose of the Study:

  • To review the pathophysiological role of NO system dysfunction and ROS in CHF.
  • To explore next-generation beta-blockers with multifunctional properties, including antioxidant and NO-mimetic effects.
  • To evaluate the cardioprotective potential of the novel compound Hypertril.

Main Methods:

  • Review of existing literature on NO pathways, oxidative stress, and cardiomyopathy.
  • Examination of experimental data on the novel compound Hypertril (1-(β-phenylethyl)-4-amino-1,2,4-triazolium bromide).
  • Analysis of Hypertril's effects on endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) expression and NO bioavailability.

Main Results:

  • Hypertril demonstrated significant cardioprotective potential in experimental models.
  • The compound improved eNOS/iNOS expression and enhanced NO bioavailability more effectively than conventional beta-blockers.
  • Hypertril led to stabilized electrocardiogram (ECG) parameters and restored cardiac energy metabolism.

Conclusions:

  • NO-mimetic agents like Hypertril offer a promising therapeutic strategy for CHF.
  • Targeting NO bioavailability can optimize the pharmacological management of chronic heart failure.
  • Next-generation beta-blockers with enhanced NO-mimetic and antioxidant properties are crucial for future CHF treatment.

Keywords:
ACE inhibitorsapoptosischronic heart failuremitochondrial dysfunctionnitric oxideoxidative stressreactive oxygen speciesβ-blockers

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