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Abnormalities of autonomic nervous control in human hypertension
1Division of Hypertension, University of Michigan Medical School, Ann Arbor 48109-0356.
Insights
Hypertension pathophysiology evolves from early hyperkinetic stages to established essential hypertension, with sympathetic overactivity playing a key role in blood pressure and coronary risk. Understanding this progression aids in improving antihypertensive treatment efficacy.
Area of Science:
- Cardiovascular Physiology
- Hypertension Pathophysiology
- Autonomic Nervous System
Background:
- Hypertension pathophysiology varies across disease stages, from early hyperkinetic borderline hypertension to established essential hypertension.
- Early stages show increased sympathetic drive and decreased parasympathetic inhibition, leading to elevated cardiac output and blood pressure.
- Advanced hypertension features decreased beta-adrenergic responsiveness, decreased cardiac compliance, and resistance vessel hypertrophy, resulting in high vascular resistance.
Purpose of the Study:
- To elucidate the evolving pathophysiology of hypertension.
- To investigate the role of sympathetic overactivity in hypertension and associated coronary risk.
- To inform improvements in antihypertensive treatment strategies.
Main Methods:
- The study reviews the pathophysiological changes in different stages of hypertension.
- It examines the relationship between sympathetic overactivity and pressure-independent risk factors for atherosclerosis and coronary heart disease.
- The analysis considers the efficacy of current antihypertensive treatments in reducing coronary events.
Main Results:
- Early hypertension is characterized by hyperkinetic circulation, responsive to autonomic blockade.
- Established hypertension involves high vascular resistance and hyperreactive vessels, with sympathetic overactivity persisting as a key factor.
- Hypertension is linked to atherosclerosis risk factors (dyslipidemia, overweight, hyperinsulinemia) and poorer coronary heart disease outcomes, with sympathetic overactivity implicated in this added risk.
Conclusions:
- Sympathetic overactivity is a crucial pathophysiological factor throughout hypertension, contributing to both elevated blood pressure and increased coronary risk.
- Current antihypertensive treatments may be less effective than expected in reducing coronary events in hypertensive patients.
- Targeted antihypertensive drug selection is crucial for patients with hypertension and associated risk factors to improve clinical outcomes.
Abstract:
The pathophysiology of various stages of hypertension is different. In early hyperkinetic borderline hypertension, the sympathetic drive to the heart and blood vessels is increased while the parasympathetic cardiac inhibition is decreased. The elevated cardiac output, vascular resistance, and blood pressure at that stage can be fully normalized by autonomic blockade. As hypertension advances, a hyperkinetic circulation is less evident, since beta-adrenergic responsiveness and cardiac compliance tend to decrease. Simultaneously hypertrophy of the resistance vessels increases the baseline vascular resistance and the vessels' responsiveness to constrictive stimuli. Eventually a picture of a normal cardiac output/high vascular resistance typical for established essential hypertension emerges. As the blood vessels become hyperreactive, the same degree of vasoconstriction/blood pressure elevation can be achieved with less sympathetic tone. In that phase the sympathetic overactivity is less evident, as the brain resets itself to maintain the same blood pressure elevation with a small amount of sympathetic discharge. While sympathetic overactivity may be less evident in established hypertension, it remains an important pathophysiologic factor, not only for the maintenance of blood pressure, but also for a number of other abnormalities in hypertension. Hypertension is intimately associated with higher levels of pressure-unrelated risk for development of atherosclerosis: dyslipidemia, overweight, and hyperinsulinemia. Furthermore, a number of factors in hypertension favor a poorer outcome from coronary heart disease. These pressure-independent factors increase the risk of coronary thrombosis, arrhythmic deaths, and coronary spasms. Sympathetic overreactivity appears to be crucially implicated in the evolution of this added coronary risk in hypertension. Understanding the pathophysiology of coronary risk and its relationship to sympathetic overreactivity in hypertension is helpful in seeking further improvements in clinical practice. At present antihypertensive treatment is less efficacious in reducing coronary events in hypertension than would be expected. Judicious use of appropriate drugs promises to further improve the efficacy of antihypertensive treatment in those patients who, in addition to high blood pressure, also have other associated risk factors.