The correlation of DNA synthesis and DNA polymerase activity in the developing chick heart

Doyle, Catherine M.; Zak, Radovan; Fischman, Donald A.

doi:10.1016/0012-1606(74)90174-2

Cited by 38 publications

(12 citation statements)

References 37 publications

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“…However, because of hypertrophy, the amount of protein per chick ventricle doubles by 7 days after hatching when compared to the value observed on the 18th incubation day. By contrast, the DNA content per ventricle changes slightly (~10%) and therefore the number of cells per milligram wet weight changes very little during this time (Doyle et al, 1974). In our experiments, the ratio of protein to wet weight increased significantly (P < 0.01) from 0.10 ± 0.003 on the 18th incubation day to 0.14 ± 0.003 at 1 week after hatching.…”

Section: Effects Of Ach On Cardiac Cyclic Amprelationship To "Indirecmentioning

confidence: 48%

Dual mechanism for inhibition of calcium-dependent action potentials by acetylcholine in avian ventricular muscle. Relationship to cyclic AMP.

Biegon¹,

Pappano²

1980

Circulation Research

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SUMMARY Acetylcholine (ACh) and carbamylcholine (Carb) inhibited Ca-dependent action potentials and contractions in ventricular muscle from the avian heart. The inhibition by choUnergic drugs was antagonized by atropine (muscarinic) and occurred by two pathways, "indirect" and "direct." Before hatching, ACh had no effect per se, but it inhibited Ca-dependent action potentials that had been augmented by isoproterenol (ISO). This "indirect" pathway for inhibition was detected as early as the 7th incubation day. Acetylcholine had no effect on basal cyclic AMP content, but it reduced cyclic AMP when the nucleotide had been increased by ISO. After hatching, ACh inhibited Ca-dependent action potentials and contractions not only "indirectly" but also "directly." "Direct" inhibition by ACh occurred in preparations treated with 6-hydroxydopamine (or reserpine) and propranolol, so that endogenous cardiac catecholamines probably were not involved. Further, basal levels of cyclic AMP increased after hatching and "direct" inhibition by ACh was associated with a reduction of cyclic AMP. These results are interpreted in a model in which cyclic AMP modulates the permeability of the membrane to Ca 2+ and in which GTP regulates the /J-adrenergic receptor and adenylate cyclase. It is speculated that "indirect" muscarinic inhibition results from interference with GTP-dependent regulation of /?-adrenergic receptor/adenylate cyclase interaction and "direct" muscarinic inhibition results from interference with GTP-dependent regulation of adenylate cyclase.

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Section: Effects Of Ach On Cardiac Cyclic Amprelationship To "Indirecmentioning

confidence: 48%

Dual mechanism for inhibition of calcium-dependent action potentials by acetylcholine in avian ventricular muscle. Relationship to cyclic AMP.

Biegon¹,

Pappano²

1980

Circulation Research

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“…DNA synthesis in these cells has been reported to cease completely sometime between 2 and 6 weeks after birth (Zak, 1974;Claycomb, 1975;Dowell and McManus, 1978). Various mechanisms have been suggested for this effect including the decline of nuclear phosphokinase activities (Limas, 1978), loss of DNA polymerase (Claycomb, 1973;Doyle et al, 1974), reduced DNA accessibility for gene transcription and, from in vitro studies, contact inhibition of myocyte proliferation (Fishman et al, 1975). In addition, it has been suggested that adrenergic innervation of the heart may be the physiological signal that changes the growth pattern of the muscle cells (Claycomb, 1977).…”

Section: Discussionmentioning

confidence: 99%

Morphometric study of early postnatal development in the left and right ventricular myocardium of the rat. I. Hypertrophy, hyperplasia, and binucleation of myocytes.

Anversa¹,

Olivetti²,

Loud³

1980

Circulation Research

185

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SUMMARY We reviewed the absolute amd differential growths of the myocyte populations in the left (L) and right (R) ventricular myocardium morphometrically from 1 to 5 days and from 5 to 11 days after birth. From 1 to 11 days hypertrophy of the average myocyte in the ventricles was (L) 2.7-and (R) 2.4-fold, and myocyte proliferation was (L) 2.0-and (R) 1.2-fold. Mean cell volume, cell length, and percent binucleation of cardiac myocytes were similar in both ventricles at 1, 5, and 11 days of age. During this period, average myocyte length increased 2-fold (12 sarcomere lengths), and the percentage of binucleate myocytes increased approximately from 2.7 to 17 to 48%. Myocyte hypertrophy from 1 to 5 days resulted mainly from an increase in the volume of cytoplasm per nucleus and from 5 to 11 days from the accumulation of binucleate cells. No differences were observed in the characteristics of epicardial and endocardial myocytes in either ventricle up to 11 days of age. The 61% greater proliferation of myocytes in the left ventricle was the principal basis for the development of a 2-fold difference in ventricular weight gains: (L) 6.2-and (R) 3.4-fold. No increase in right ventricular midwall thickness was observed, in contrast to a 2.7-fold increase of the left ventricle. It was concluded that, as a result of the circulatory changes occurring shortly after birth, right ventricular growth is analogous to eccentric hypertrophy, whereas left ventricular growth represents a combination of eccentric and concentric hypertrophy. Circ Res 46: 495-502, 1980 GROWTH of the myocardium during the early postnatal period must accommodate not only the increasing demands of the rapidly growing animal but also the relatively abrupt changes in the patterns of blood flow and circulatory resistance occuring shortly after birth. Work required of the left and right ventricles is approximately equal as they pump in parallel during fetal life (Heymann and Rudolph, 1973;Rudolph, 1974). With closure of the foramen ovale and ductus arteriosus after birth, blood flow is henceforth in series through the right and left ventricles, resulting in a greater volume work load on each ventricle. In the same period, pulmonary resistance is lowered by expansion of the collapsed lungs (Klopfenstein and Rudolph, 1978;Rudolph, 1979), peripheral resistance increases with loss of the placental circulation (Rudolph, 1970), and the pressure load on the left ventricle becomes significantly greater than that on the right ventricle (Assali et al., 1965). The combi-

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“…During embryonic and fetal stages of development, the myocardium enlarges by cell proliferation (Manasek, 1968;Weinstein and Hay, 1970;Jeter and Cameron, 1971;Hay and Low, 1972;Chacko, 1973;Goldstein et al, 1974;Mikawa et al, 1992;Mima et al, 1995), whereas shortly after hatching or birth, proliferation ceases and tissue enlargement is produced by cellular hypertrophy (Peterson and Baserga, 1965;Doyle et al, 1974;Anversa et al, 1980;Zak, 1984;Klug et al, 1995). Hypertrophic myocardial cells become polyploid and multinucleated (Klug et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

Regulation of proliferation of the fetal myocardium

2000

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One site fits all: Yi Lu and co‐workers have reported the conversion of sperm‐whale myoglobin into a functional nitric oxide reductase. For this purpose, they designed a second metal binding site in the wild‐type holo‐protein and demonstrated NO reduction with the structurally characterized model, making thereby a significant contribution to the rapidly developing field of artificial metalloenzymes.

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The correlation of DNA synthesis and DNA polymerase activity in the developing chick heart

Cited by 38 publications

References 37 publications

Dual mechanism for inhibition of calcium-dependent action potentials by acetylcholine in avian ventricular muscle. Relationship to cyclic AMP.

Dual mechanism for inhibition of calcium-dependent action potentials by acetylcholine in avian ventricular muscle. Relationship to cyclic AMP.

Morphometric study of early postnatal development in the left and right ventricular myocardium of the rat. I. Hypertrophy, hyperplasia, and binucleation of myocytes.

Regulation of proliferation of the fetal myocardium

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