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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Molecular and cellular biochemistry 119 (1993), S. 3-9 
    ISSN: 1573-4919
    Keywords: cardiac hypertrophy ; neonatal heart ; ribosome formation ; protein synthesis ; α1-adrenergic agonist ; cardiac myocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The pig heart grows at a maximal rate in the first 2–3 days of life due to a volume overload imposed on the heart at birth. Rates of ribosome formation and protein synthesis cannot be further accelerated duringin vitro perfusion with agents that increase cyclic AMP, that bind to α1-adrenergic receptors or that bind to angiotensin II receptors. Growth of the heartin vivo can be restrained by treatment with an angiotensin-converting enzyme inhibitor, enalapril maleate, or an angiotensin receptor antagonist, DuP 753. In the enalapril-treated heart, norepinephrine plus propranolol, but not angiotensin II, accelerated ribosome formation. Rapid growth of the left ventricle of pig heart during the first 10 days of life is due largely to eccentric hypertrophy.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-4919
    Keywords: bradykinin ; HOE 140 ; enalapril maleate ; hypertrophy ; angiotensin 11 ; newborn heart
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Rapid growth of the left ventricle of the newborn pig heart can be restrained by treating piglets with the angiotensin converting enzyme inhibitor, enalapril maleate. This reduced rate of growth is reflected in vitro by reduced rates of ribosome formation and protein synthesis, and may be due to decreased availability of angiotensin II (All), a potentially hypertrophic agent; decreased numbers of All receptors; increased availability of bradykinin, a potentially antihypertrophic agent; or reduced hemodynamic load on the left ventricle. Because enalapril decreases degradation of bradykinin, the role of bradykinin as an inhibitor of cardiac growth in the newborn heart was investigated. Addition of 1 × 10−5 M bradykinin and 1 × 10−6 Menalapril to the perfusate of isolated hearts from 2 day old piglets did not significantly alter heart rate, contents of ATP or creatine phosphate or rates of ribosome formation or protein synthesis during 1 h of perfusion. Similarly, exposure of myocytes isolated from the left ventricular free wall of piglets to 5 × 10−6 M bradykinin for 72 h did not alter the rate of [3H]-phenylalanine incorporation into total protein. The reduced rate of left ventricular growth in vivo caused by enalapril administration was not reversed by simultaneous treatment with the specific bradykinin receptor antagonist, HOE 140. HOE 140 alone did not alter ventricular growth as compared to hearts from untreated piglets. In summary, these results demonstrate that the reduced rate of left ventricular growth in vivo and the reduced rate of ribosome formation and protein synthesis in the left ventricle in vitro after enalapril treatment of piglets is not the result of an inhibitory effect of bradykinin on cardiac growth.
    Type of Medium: Electronic Resource
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