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The sympathetic nervous system in essential hypertension
American Heart Journal
|October 1, 1986
Summary
Sympathetic nervous system (SNS) overactivity contributes to essential hypertension (EH). While not all patients show elevated norepinephrine, studies reveal increased SNS outflow, exaggerated responses to stimuli, and impaired baroreceptor function in EH.
Area of Science:
- Cardiovascular Physiology
- Nephrology
- Endocrinology
Background:
- Enhanced sympathetic nervous system (SNS) activity is implicated in essential hypertension (EH).
- Previous research indicates varied findings regarding norepinephrine (NE) levels in EH patients.
- Understanding SNS contributions is crucial for managing hypertension.
Purpose of the Study:
- To investigate the role of sympathetic nervous system activity in essential hypertension.
- To analyze markers of SNS function, including catecholamine levels and baroreceptor responses.
- To elucidate the mechanisms linking SNS to hypertension development and maintenance.
Main Methods:
- Measurement of plasma norepinephrine (NE) and epinephrine (E) levels.
- Assessment of renal NE spillover and 24-hour NE levels.
- Evaluation of depressor responses to SNS blocking agents like clonidine.
- Analysis of baroreflex sensitivity and vascular reactivity to NE.
- Examination of dopamine (DA) excretion patterns.
Main Results:
- A subset of younger EH patients exhibits elevated plasma NE, increased renal NE spillover, and higher 24-hour NE levels.
- EH patients show exaggerated NE responses to stress, exercise, and tilt table tests.
- Diminished baroreceptor control is observed early in EH development.
- Elevated plasma E during stress is linked to sodium retention and enhanced vascular reactivity.
- Reduced urinary-free DA responses suggest impaired natriuretic mechanisms in EH.
Conclusions:
- SNS overactivity, characterized by increased NE outflow and impaired baroreceptor function, contributes significantly to EH.
- Epinephrine may act as a cotransmitter, facilitating NE release and vasoconstriction.
- Deficiencies in dopamine-modulated natriuretic mechanisms may play a role in EH pathogenesis.