Role of the renin-angiotensin system in the development of congestive heart failure in the dog as assessed by chronic converting-enzyme blockade
Autor: | Kurt Kochsiek, Gerhart Liebau, Hansgeorg Steilner, Dorothea Witkowski, Matthias Holzschuh, Günter A.J. Riegger |
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Rok vydání: | 1984 |
Předmět: |
medicine.medical_specialty
Vasopressin Sympathetic nervous system Captopril Proline Angiotensin-Converting Enzyme Inhibitors Renin-Angiotensin System chemistry.chemical_compound Norepinephrine Internal medicine Renin–angiotensin system Renin medicine Animals cardiovascular diseases Pulmonary Wedge Pressure Cardiac Output Heart Failure Aldosterone business.industry Cardiac Pacing Artificial medicine.disease Angiotensin II Arginine Vasopressin medicine.anatomical_structure Endocrinology chemistry Heart failure Cardiology Vascular resistance Vascular Resistance Cardiology and Cardiovascular Medicine business medicine.drug |
Zdroj: | The American journal of cardiology. 53(4) |
ISSN: | 0002-9149 |
Popis: | Hormonal factors may be important in the regulation of peripheral vascular resistance (PVR) in congestive heart failure (CHF). The role of the renin-angiotensin system in the development of CHF was studied in 16 unanesthetized dogs. CHF was induced by rapid right ventricular pacing, with and without chronic converting-enzyme inhibition (CEI) by captopril. The hemodynamic changes and the activity of renin, aldosterone, norepinephrine and vasopressin were studied. The control dogs showed a greater decrease in cardiac output and a greater increase of mean pulmonary artery pressure than the captopril-treated group. In the group with CEI, only a small, transient increase in PVR was observed during the development of CHF; in the control group, there was an increase of 94% of basal values. The control group showed a continual increase of renin, aldosterone and norepinephrine. Four control dogs showed an inappropriately high secretion of arginine vasopressin. The increase of sympathetic nervous activity was only insignificantly attenuated by angiotensin II inhibition and was without a considerable influence on PVR except for an early transient increase in vascular tone. In our animal model, the renin-angiotensin system plays an important role in the regulation of PVR in CHF. In this kind of CHF the sympathetic nervous system appears to be of minor importance for the long-term regulation of PVR. Plasma arginine vasopressin levels were increased in control dogs; this increase may contribute to the increased vascular tone. |
Databáze: | OpenAIRE |
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