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Do most antihypertensive agents have a sympatholytic action?
1Departments of Physiology and Medicine, Faculty of Medicine, Université de Montréal, PO Box 6128, Station Centre-Ville, Montreal, Quebec H3C 3J7, Canada. dechampj@physio.umontreal.ca
Current Hypertension Reports
|July 27, 2001
Summary
Essential hypertension involves sympathetic nervous system dysfunction, leading to increased sympathetic tone and altered adrenergic receptor balance. Antihypertensive therapies aim to reduce this sympathetic activity, particularly alpha1-adrenergic functions.
Area of Science:
- Cardiovascular Physiology
- Neuroendocrinology
- Pharmacology
Background:
- The sympathetic nervous system significantly influences cardiovascular functions.
- Essential hypertension is characterized by pre- and postsynaptic sympathetic dysfunctions.
- These dysfunctions often enhance sympathetic neurotransmission, increasing sympathetic tone and reactivity.
Purpose of the Study:
- To review the role of sympathetic nervous system dysfunction in essential hypertension.
- To examine the alterations in postsynaptic adrenergic receptor balance in hypertension.
- To discuss the implications of chronic sympathetic activation for cardiovascular complications and antihypertensive therapy.
Main Methods:
- Review of studies over the past three decades.
- Analysis of methodologies investigating sympathetic functions.
- Examination of human cardiovascular tissues for adrenergic receptor function.
Main Results:
- Hypertension is associated with enhanced sympathetic neurotransmission and increased sympathetic tone.
- A shift towards alpha1-adrenergic dominance and reduced beta-adrenergic function is observed in cardiovascular tissues.
- Chronic sympathetic activation contributes to cardiovascular complications.
Conclusions:
- Sympathetic nervous system dysfunction, particularly alpha1-adrenergic dominance, is a key feature of hypertension.
- Attenuating sympathetic tone is a critical goal of antihypertensive therapy.
- Current antihypertensive drugs effectively reduce sympathetic activity, especially postsynaptic alpha1-adrenergic functions.