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Carbon monoxide and hypertension.

Joseph F Ndisang1, Hortense E Nsoh Tabien, Rui Wang

  • 1Departments of Physiology and Anatomy and Cell Biology, University of Saskatchewan, Saskatoon, Canada.

Journal of Hypertension
|May 29, 2004
PubMed
Summary

The heme oxygenase/carbon monoxide system plays a critical role in hypertension. While boosting heme oxygenase-1 lowers blood pressure in young hypertensive rats, this effect is lost in adults, suggesting a complex compensatory mechanism.

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Area of Science:

  • Cardiovascular Physiology
  • Biochemistry
  • Pharmacology

Background:

  • Heme oxygenase (HO) produces carbon monoxide (CO), a gasotransmitter involved in vascular tone and apoptosis.
  • Dysfunctional HO/CO system is linked to hypertension pathogenesis and maintenance.
  • The role of HO-2 in vascular hypertension requires further investigation.

Purpose of the Study:

  • To investigate the role of the heme oxygenase/carbon monoxide system in hypertension.
  • To explore the therapeutic potential of modulating HO-1 expression in hypertension.

Main Methods:

  • Studies in spontaneously hypertensive rats (SHRs) at different ages.
  • Pharmacological induction and gene delivery to modulate heme oxygenase-1 expression.
  • Assessment of blood pressure, vascular contractility, apoptosis, and oxidative stress.

Main Results:

  • Upregulating heme oxygenase-1 (HO-1) reduced blood pressure in young SHRs, an effect blocked by metalloporphyrins.
  • In adult SHRs, the HO/CO system appears normalized, with HO-1 manipulation failing to lower blood pressure.
  • HO/CO system dysfunction contributes to vascular issues in hypertension, including altered contractility, apoptosis, and oxidative stress.

Conclusions:

  • Abnormalities in the heme oxygenase/carbon monoxide system are critical in hypertension development.
  • Targeting the HO/CO system offers potential for novel hypertension therapeutics.
  • Therapeutic strategies must consider age-dependent compensatory mechanisms in hypertension.

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