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Myocardial and vascular structural adaptation to chronic pressure overload
M Nordlander1, H Wåhlander, P Friberg
1Department of Physiology, University of Göteborg, Sweden.
Journal of Cardiovascular Pharmacology
|January 1, 1987
Summary
Spontaneously hypertensive rats exhibit eccentric left ventricular hypertrophy, improving cardiac function. Antihypertensive therapy reverses coronary flow reduction and preserves cardiac performance in these hypertensive rats.
Area of Science:
- Cardiology
- Pharmacology
- Physiology
Background:
- Spontaneously hypertensive rats (SHRs) often develop cardiac abnormalities.
- Understanding left ventricular (LV) adaptations in hypertension is crucial for cardiovascular health.
Purpose of the Study:
- To investigate the effects of different antihypertensive therapies on LV function and structure in SHRs.
- To determine the impact of hypertension type (spontaneous vs. renal) on cardiac mechanics.
Main Methods:
- Isolated heart preparations from SHRs and renal hypertensive rats were used.
- Cardiac function and LV end-diastolic dimensions were measured under various perfusion conditions.
- Hearts were treated with calcium antagonists (felodipine, nifedipine), alpha-methyldopa, or a combination therapy.
Main Results:
- SHRs showed eccentric LV hypertrophy with elevated maximal cardiac function, unlike renal hypertensive rats.
- Calcium antagonists reduced LV wall thickness and increased LV end-diastolic volume (EDV).
- Coronary flow was reduced in SHRs, limiting cardiac function at low aortic pressures; this was reversible with therapy.
Conclusions:
- Eccentric hypertrophy in SHRs enhances stroke volume and maximal stroke work.
- Antihypertensive therapy, particularly calcium antagonists, can improve cardiac performance by reversing coronary vascular changes and increasing EDV.
- Therapeutic interventions are vital for managing cardiac dysfunction in hypertensive states.