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Increased plasma norepinephrine accompanies persistent tachycardia after hydralazine
Hypertension (Dallas, Tex. : 1979)
|March 1, 1983
Summary
Hydralazine causes persistent tachycardia by activating the peripheral sympathetic nervous system. This leads to increased heart rate and norepinephrine levels, even as blood pressure normalizes.
Area of Science:
- Pharmacology
- Cardiovascular Physiology
- Neuropharmacology
Background:
- The antihypertensive drug hydralazine can cause persistent tachycardia.
- The role of the peripheral sympathetic nervous system in this side effect is not fully understood.
Purpose of the Study:
- To investigate the involvement of the peripheral sympathetic nervous system in hydralazine-induced persistent tachycardia.
- To examine the relationship between heart rate, plasma norepinephrine, and blood pressure changes after hydralazine administration.
Main Methods:
- Intravenous administration of various hydralazine doses to five hypertensive patients.
- Measurement of heart rate, plasma norepinephrine concentration, and blood pressure over time.
- Analysis of temporal correlations between these physiological parameters.
Main Results:
- Significant correlations were observed between increased heart rate, plasma norepinephrine, and reduced blood pressure at 15 and 30 minutes post-injection.
- At 240 minutes, heart rate and norepinephrine levels remained elevated and disproportionate to blood pressure reduction.
- A consistent correlation between heart rate and plasma norepinephrine was found at 15, 30, and 240 minutes.
Conclusions:
- Continued activation of the peripheral sympathetic nervous system contributes to hydralazine-induced persistent tachycardia.
- Temporal discordance between sympathetic activation and blood pressure suggests a specific mechanism.
- Findings highlight the importance of the sympathetic nervous system in mediating hydralazine's cardiovascular effects.