[CHANGES OF THE OXIDATIVE STATUS, MITOCHONDRIAL FUNCTION, BLOOD PRESSURE AND INDICATORS OF HEMOSTASIS IN STRESSED...

Area of Science:

• Biochemistry
• Physiology
• Pharmacology

Background:

• Stress impacts physiological and metabolic processes.
• Nitric oxide (NO) plays a role in stress responses.
• Lipid peroxidation and mitochondrial dysfunction are indicators of cellular stress.

Purpose of the Study:

• To examine metabolic changes in female rats under acute stress.
• To investigate the role of nitric oxide synthase (NOS) in stress-induced alterations.
• To evaluate the effects of NOS inhibitors on stress markers.

Main Methods:

• Acute stress induced by cervical dorsal skin fold suspension in female rats.
• Measurement of nitric oxide metabolites in blood serum and tissue homogenates (heart, brain).
• Assessment of lipid peroxidation, mitochondrial function, blood pressure, and hemostasis parameters.
• Administration of neuronal NOS inhibitor (7-nitroindazole) and inducible NOS inhibitor (aminoguanidine).

Main Results:

• Stress increased nitric oxide metabolites, lipid peroxidation, and mitochondrial dysfunction in the heart and brain.
• Mean arterial blood pressure rose by 18.9%, and hemostasis was impaired.
• Neuronal NOS inhibition worsened stress-induced changes.
• Inducible NOS inhibition attenuated the detrimental effects of stress.

Conclusions:

• Acute stress significantly alters metabolism, cardiovascular function, and hemostasis in female rats.
• Nitric oxide, particularly from inducible NOS, is implicated in mediating stress-induced damage.
• Targeting inducible NOS may offer a therapeutic strategy to mitigate stress-related physiological disturbances.