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Sympathetic alterations after sodium restriction and short-term captopril administration
P J Mills1, J E Dimsdale, M G Ziegler
1Department of Medicine, University of California, San Diego Medical Center 92103-0804.
Journal of the American College of Cardiology
|January 1, 1993
Summary
Short-term captopril therapy impacts the sympathetic nervous system by decreasing neuropeptide Y and increasing plasma norepinephrine and cortisol. These effects suggest captopril influences sympathetic markers, potentially contributing to its therapeutic benefits.
Area of Science:
- Cardiovascular Pharmacology
- Neuroendocrinology
- Hypertension Research
Background:
- Angiotensin-converting enzyme (ACE) inhibitors' therapeutic effects extend beyond the renin-angiotensin system.
- Emerging evidence implicates the sympathetic nervous system in ACE inhibitor efficacy.
Purpose of the Study:
- To investigate short-term captopril's effects on sympathetic nervous system markers.
- To assess changes in plasma norepinephrine, neuropeptide Y, beta-adrenergic receptors, and cortisol.
Main Methods:
- Double-blind, placebo-controlled crossover study in 12 hypertensive and 20 normotensive men.
- Participants received captopril (25 mg twice daily) or placebo during 5-day sodium-restricted diets (10 mEq).
Main Results:
- Captopril significantly decreased neuropeptide Y and angiotensin II.
- Plasma norepinephrine, cortisol, and renin levels increased with captopril treatment.
- Isoproterenol-stimulated cyclic adenosine monophosphate (AMP) in lymphocytes also increased.
Conclusions:
- Short-term captopril therapy modulates key sympathetic nervous system components.
- Observed changes (decreased neuropeptide Y, increased norepinephrine and beta-adrenergic receptors) align with improved cardiac output and reduced peripheral resistance.