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Biochemical Mechanisms of Cardiac Hypertrophy (1987)

Morgan, H E ; Gordon, E E ; Kira, Y ; [et al.]

Palo Alto, Calif. : Annual Reviews

Annual Review of Physiology 49 (1987), S. 533-543

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ISSN: 0066-4278

Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff

Topics: Medicine , Biology

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1146/annurev.ph.49.030187.002533

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The effect of culture and membrane potential on Goα expression in neonatal rat cardiac myocytes (1991)

Foster, K. A. ; McDermott, P. J. ; Robishaw, J. D.

Springer

Molecular and cellular biochemistry 104 (1991), S. 63-72

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ISSN: 1573-4919

Keywords: immunoblotting ; inositol phosphate ; muscarinic receptors

Source: Springer Online Journal Archives 1860-2000

Topics: Biology , Chemistry and Pharmacology , Medicine

Notes: Abstract The effects of culture and membrane potential on Goα39 expression were examined in neonatal rat cardiac myocytes. During six days of culture, the amount of Goα39 in myocytes increased six-fold. The increase in Goα39 appeared to be programmed, since Goα39 of rat hearts also increased in vivo within three days after birth before declining by six days after birth. Furthermore, the age of the rat from which cardiac myocytes were isolated determined the amount of Goα39 that accumulated in cultured cells with myocytes from two day-old rats producing more Goα39 than myocytes from six day-old rats. In addition, agents which alter membrane potential (KCl and bupivacaine) inhibited the accumulation of Goα39 in cultured myocytes. In an attempt to identify the signaling pathway in which cardiac Goα39 is involved, muscarinic receptor-stimulated inositol phosphate production was examined, but was found to be comparable in myocytes that had six-fold differences in Goα39 content. Thus Goα39 does not appear to couple muscarinic receptors to phospholipase C in rat cardiac myocytes.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF00229805

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Mechanisms of cardiac hypertrophy in canine volume overload (1998)

Matsuo, T. ; Nagatomo, Y. ; McDermott, P. J. ; [et al.]

In: Other Sources

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Publication Date: 2019-07-13

Description: This study tested whether the modest hypertrophy that develops in dogs in response to mitral regurgitation is due to a relatively small change in the rate of protein synthesis or, alternatively, is due to a decreased rate of protein degradation. After 3 mo of severe experimental mitral regurgitation, the left ventricular (LV) mass-to-body weight ratio increased by 23% compared with baseline values. This increase in LV mass occurred with a small, but not statistically significant, increase in the fractional rate of myosin heavy chain (MHC) synthesis (Ks), as measured using continuous infusion with [3H]leucine in dogs at 2 wk, 4 wk, and 3 mo after creation of severe mitral regurgitation. Translational efficiency was unaffected by mitral regurgitation as measured by the distribution of MHC mRNA in polysome gradients. Furthermore, there was no detectable increase in translational capacity as measured by either total RNA content or the rate of ribosome formation. These data indicate that translational mechanisms that accelerate the rate of cardiac protein synthesis are not responsive to the stimulus of mitral regurgitation. Most of the growth after mitral regurgitation was accounted for by a decrease in the fractional rate of protein degradation, calculated by subtracting fractional rates of protein accumulation at each time point from the corresponding Ks values. We conclude that 1) volume overload produced by severe mitral regurgitation does not trigger substantial increases in the rate of protein synthesis and 2) the modest increase in LV mass results primarily from a decrease in the rate of protein degradation.

Keywords: Life Sciences (General)

Type: The American journal of physiology (ISSN 0002-9513); 275; 1 Pt 2; H65-74

Format: text

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Comparative effects of contraction and angiotensin II on growth of adult feline cardiocytes in primary culture (1996)

Cooper, G. 4th ; McDermott, P. J. ; Zile, M. R. ; [et al.]

In: Other Sources

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Publication Date: 2019-07-13

Description: The purposes of this study were 1) to determine whether angiotensin II causes growth of adult feline cardiocytes in long-term culture, 2) to compare the growth effects of angiotensin II with those resulting from electrically stimulated contraction, and 3) to determine whether the anabolic effects of contraction are exerted via the angiotensin type 1 receptor. Adult feline cardiocytes were cultured on laminin-coated trays in a serum-free medium. Cardiocytes were either electrically stimulated to contract (1 Hz, 5-ms pulse duration, alternating polarity) or were nonstimulated and quiescent. Quiescent cells were studied as controls and after treatment with angiotensin II (10(-8) M), losartan (10(-6) M; an angiotensin type 1-receptor antagonist), or angiotensin II plus losartan. Contracting cells were studied in the presence and absence of angiotensin II or losartan. In quiescent cardiocytes, angiotensin II treatment on day 7 significantly increased protein synthesis rates by 22% and protein content per cell by 17%. The effects of angiotensin II were completely blocked by losartan. Electrically stimulated contraction on days 4 and 7 in culture significantly increased protein synthesis rate by 18 and 38% and protein content per cell by 19 and 46%, respectively. Angiotensin II treatment did not further increase protein synthesis rate or protein content in contracting cardiocytes. Furthermore, losartan did not block the anabolic effects of contraction on protein synthesis rates or protein content. In conclusion, angiotensin II can exert a modest anabolic effect on adult feline cardiocytes in culture. In contracting feline cardiocytes, angiotensin II has no effect on growth. Growth caused by electrically stimulated contraction occurs more rapidly and is greater in magnitude than that caused by angiotensin II. Growth of contracting adult feline cardiocytes is not dependent on activation of the angiotensin receptor.

Keywords: Life Sciences (General)

Type: The American journal of physiology (ISSN 0002-9513); 271; 1 Pt 2; H29-37

Format: text

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