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Cardiac contractile and coronary flow reserves in deoxycorticosterone acetate-salt hypertensive rats
Insights
Deoxycorticosterone acetate-salt hypertension in rats preserves cardiac contractility and coronary flow despite left ventricular hypertrophy and increased vascular resistance. This suggests a maintained cardiac reserve despite structural changes.
Area of Science:
- Cardiovascular Physiology
- Hypertension Research
- Cardiac Function
Background:
- Deoxycorticosterone acetate-salt (DOCA-salt) hypertension is a model for studying cardiovascular adaptations.
- Understanding the impact of hypertension on cardiac contractility and coronary circulation is crucial for clinical management.
Purpose of the Study:
- To investigate the effects of established DOCA-salt hypertension on cardiac contractility and coronary blood flow in conscious rats.
- To assess cardiac and coronary functional reserves during the progression of hypertension and left ventricular hypertrophy.
Main Methods:
- Comparison of cardiac contractility (peak rate of pressure change) and coronary flow (microsphere method) in DOCA-salt hypertensive rats and sham-treated controls.
- Assessment of contractile reserve using beta-adrenergic stimulation (isoproterenol) and blockade (propranolol).
- Evaluation of coronary flow reserve with dipyridamole-induced maximal vasodilation.
Main Results:
- Hypertensive rats exhibited increased left ventricular mass and preserved resting and stimulated peak contractility (dp/dt) at 18 weeks.
- Reduced beta-adrenergic contractile reserve but increased mobilization of contractile capacity observed.
- No significant differences in basal or maximally dilated coronary flow or coronary flow reserves.
- Increased minimal coronary vascular resistance indicated structural vascular alterations.
Conclusions:
- Cardiac contractility and coronary flow reserves are maintained in established DOCA-salt hypertension despite left ventricular hypertrophy.
- Structural coronary vascular changes occur, increasing resistance but not compromising basal flow or reserve.
- The heart adapts to hypertension by mobilizing a greater portion of its contractile capacity.
Abstract:
Cardiac contractility and coronary flow were compared in conscious rats with established deoxycorticosterone acetate-salt hypertension and in those with sham treatment. The hypertensive rats showed a 32% increase in left ventricular/body weight ratio at 9 weeks of treatment and 42% at 18 weeks of treatment. Resting peak rate of change of pressure (dp/dt) was unchanged at 9 weeks and increased at 18 weeks in hypertensive rats, while isoproterenol-stimulated maximal, propranolol-induced minimal, and Ca2+-stimulated maximal peak dp/dt were greater at 18 weeks. These data indicate the preservation of contractile function. At 18 weeks, the beta-adrenergic receptor-mediated contractile reserve, estimated from isoproterenol-stimulated maximal and resting peak dp/dt, was reduced but the propranolol-induced decrease in peak dp/dt was increased in hypertensive rats compared with sham-treated rats. Thus, at this stage, a greater portion of the total contractile capacity appeared to be mobilized with prolongation of hypertension and progression of left ventricular hypertrophy. No differences were observed in left ventricular and right ventricular coronary flow (microspheres) and left ventricular inner/outer flow ratio at rest and with dipyridamole-induced maximal coronary dilatation, at 9 and 18 weeks. There were no alterations in left or right ventricular coronary flow reserves, as estimated from resting and dipyridamole-induced values. The minimal coronary vascular resistance (normalized for gram of tissue) of both the left and right ventricles was increased at either stage, which suggests the occurrence of structural coronary vascular changes. Thus, basal coronary flow and a coronary flow reserve were uncompromised despite evidence of structural coronary vascular alterations in these hypertensive rats.