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Nitric Oxide in Systemic and Pulmonary Hypertension
1Department of Physiology, Tzu Chi College of Medicine, Hualien, Taiwan.
Journal of Biomedical Science
|January 1, 1997
Summary
In hypertension, nitric oxide (NO) production may be enhanced, acting as a compensatory mechanism to lower blood pressure and peripheral resistance. This contrasts with the traditional view of impaired NO function in hypertensive states.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
- Pharmacology
Background:
- Endothelium-derived nitric oxide (NO) is crucial for regulating vascular tone and arterial pressure.
- Endothelial dysfunction and impaired NO production are traditionally linked to hypertension.
- Existing research presents conflicting findings on NO's role in long-term hypertension.
Purpose of the Study:
- To investigate the role of nitric oxide (NO) in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY).
- To determine the impact of NO synthase inhibition on arterial pressure and hemodynamics in hypertensive and normotensive models.
- To explore the compensatory role of NO production in pulmonary hypertension during hypoxia.
Main Methods:
- Administration of N(G)-nitro-L-arginine monomethyl ester (L-NAME), an NO synthase inhibitor, to SHR and WKY rats.
- Measurement of arterial pressure (AP) and total peripheral resistance (TPR) following L-NAME administration.
- Utilized arterial impedance analysis to assess pulsatile hemodynamics.
- Measured NO release in pulmonary veins during ventilatory hypoxia.
Main Results:
- L-NAME caused a significantly greater increase in AP and TPR in SHR compared to WKY, despite higher baseline values in SHR.
- Pulsatile hemodynamics, including characteristic impedance and wave reflection, were minimally affected by L-NAME and showed no significant differences between SHR and WKY.
- Ventilatory hypoxia induced pulmonary hypertension with a concurrent increase in NO production in the pulmonary circulation, which was attenuated by NO inhibition.
Conclusions:
- Basal NO release in SHR is not impaired but enhanced, serving as a compensatory mechanism to maintain lower arterial pressure and peripheral resistance.
- The role of NO in hypertension may be heterogeneous, involving impairment, no change, or enhancement depending on the species, model, and vascular bed.
- Increased NO production in the pulmonary circulation during hypoxia acts as a compensatory mechanism against pulmonary vasoconstriction.