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The cardiovascular amplifiers in human primary hypertension and their role in a strategy for detecting the underlying
P I Korner1, G L Jennings, M D Esler
1Baker Medical Research Institute, Prahran, Victoria, Australia.
Insights
In chronic hypertension, muscle hypertrophy in blood vessels and the left ventricle (LV) acts as amplifiers. Reversing this hypertrophy may help identify hypertension
Area of Science:
- Cardiovascular Physiology
- Hypertension Research
- Medical Science
Background:
- Chronic hypertension involves muscle hypertrophy in resistance vessels and the left ventricle (LV), contributing to hemodynamic amplification.
- In spontaneously hypertensive rats (SHR), early vessel and LV hypertrophy suggests a potential initiating role in hypertension.
- Left ventricular (LV) hypertrophy is prevalent in human hypertension, even in mild cases.
Purpose of the Study:
- To review evidence on the role of cardiac and vascular hypertrophy as hemodynamic amplifiers in chronic hypertension.
- To explore the potential of reversing hypertrophy to facilitate the identification of hypertension's initiating mechanisms.
- To postulate underlying disturbances in muscle performance contributing to primary hypertension.
Main Methods:
- Review of existing evidence on muscle hypertrophy in various hypertension models (SHR, Goldblatt).
- Analysis of the contribution of angiotensin II and hypertrophied cardiovascular structures to blood pressure elevation.
- Examination of studies investigating the effects of drug therapy on reversing hypertrophy and hypertension progression.
Main Results:
- Hypertrophy of resistance vessels and the left ventricle (LV) functions as a key hemodynamic amplifier in chronic hypertension.
- In Goldblatt hypertension, hypertrophied heart and vessels contribute significantly to sustained blood pressure elevation.
- Drug therapy can reverse cardiac and vascular hypertrophy, markedly slowing the redevelopment of hypertension.
Conclusions:
- Cardiovascular amplifiers, specifically hypertrophied heart and vessels, play a crucial role in maintaining chronic hypertension.
- Reversing hypertrophy is a potential therapeutic strategy that aids in diagnosing the root cause of hypertension.
- Primary hypertension may stem from intrinsic muscle performance disturbances, possibly triggered by the sympathetic nervous system or altered cation transport.
Abstract:
The present review considers evidence that in chronic hypertension, hypertrophy of the muscles of the resistance vessels and left ventricle (LV) accounts for their intrinsic properties as haemodynamic amplifiers. In spontaneously hypertensive rats (SHR) there is early hypertrophy of both vessels and LV, suggesting that they may initiate hypertension; slow development of alpha-adrenoceptors may contribute to the early preponderance of the LV amplifier. In human hypertension LV hypertrophy occurs in most patients, including a high proportion of mild hypertensives. In Goldblatt one-kidney hypertension the stenosis resistance, which is the initiating cause, accounts for 25% of the rise in blood pressure throughout, with 75% initially due to systemic constrictor action of angiotensin II and later due to the amplifier properties of the hypertrophied heart and vessels. The cardiovascular amplifiers must be important in all chronic hypertension, so that if hypertrophy can be reversed, detection of the initiating mechanism should be easier. Studies in patients indicate that drug therapy can reverse hypertrophy and that subsequent redevelopment of hypertension is markedly slowed. We postulate an intrinsic disturbance of muscle performance in all primary hypertension, which may be triggered through the sympathetic nervous system in some patients and through altered cation transport in others.