Alterations in rat myocardial mechanics under Goldblatt hypertension and experimental aortic stenosis

Kämmereit, A; Jacob, R.

doi:10.1007/bf01908392

Cited by 18 publications

(7 citation statements)

References 35 publications

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“…In the case of the rat, the myosin isoenzymes are shifted towards myosin V3 during the transition from the neonatal to the adult state, most probably due to a decrease in the thyroid hormone level during postnatal development. This age-dependent change in the isoenzyme pattern provides a rational basis for the gradual decrease of actomyosin ATPase activity (24)(25)(26) and velocity of shortening (24,25,27) during aging. It follows that increasing age will narrow the range of adaptation, i.e., the adaptational reserve, towards pressure overload.…”

Section: The Range Of Adaptation Of Myofibrillar Atpase From Rat Heartmentioning

confidence: 99%

Polymorphic myosin as the common determinant of myofibrillar ATPase in different haemodynamic and thyroid states

Rupp

1982

Basic Res Cardiol

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SummaryChronic alterations in haemodynamic load or thyroid state affect the ATPase activity of myofibrils from the rat heart. In order to determine the limits of such an adaptational reaction, the Ca2+-dependent activation of myofibrils containing only myosin V1 or V 3 was investigated. These limiting states were achieved by changes in the thyroid state, i.e., myosin V 1 myofibrils were obtained from 5-week-old rats, and myosin V 3 myofibrils from hypothyroid rats. Analysis of the activation of myofibrillar ATPase by Ca 2+ using the model-independent Hill equation showed that transition of the myosin isoenzymes neither affected Ca 2+ sensitivity (pCas0 % = 6.52) nor positive co-operativity (n = 2.4). The ATPase activity at saturating Ca 2+ concentrations was 192 nMole Pmg -1 rain -1 in myosin Vl-myofibrils and was reduced to 131 nMole Pmg -~ min -1 in the case of myosin V3-myofibrils. Beside changes in the thyroid hormone state, polymorphic myosin is also influenced by chronic pressure overload and endurance training of a swimming routine. Such haemodynamically induced changes in myofibrillar ATPase were accounted for on the basis of the altered myosin isoenzyme pattern and the ATPase activities of isoenzymatically homogeneous myofibrils obtained by changes in the thyroid state. It can therefore be concluded that both haemodynamic load and thyroid state affect myofibrillar ATPase by a common mechanism, namely, by inducing a change in the isoenzyme pattern of myosin due to a redirected expression of myosin genes. Myosins from other mammals were compared with rat myosin on pyrophosphate gels. The Ca 2+-dependent activation of myofibrillar ATPase from euthyroid and hypothyroid adult mice suggested the existence of a polymorphic myosin which was verified by the pyrophosphate gel technique. The mouse myosin isoenzymes were, however, less separated on pyrophosphate gels when compared with the rat myosins. It therefore seems advisable to consider both the activation properties of myofibrillar ATPase, as well as electrophoretie properties, for defining the adaptational state of myocardium of higher mammalian species.

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Section: The Range Of Adaptation Of Myofibrillar Atpase From Rat Heartmentioning

confidence: 99%

Polymorphic myosin as the common determinant of myofibrillar ATPase in different haemodynamic and thyroid states

Rupp

1982

Basic Res Cardiol

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“…Whereas left ventricular contractility, microcirculation, and fibrosis are not decreased in hypertrophy due to swimming training or experimental hyperthyroidism, considerable change in these parameters has been described in hypertrophy secondary to chronic pressure (15)(16)(17)(18) or volume overload (19,20).…”

Section: Introductionmentioning

confidence: 99%

Morphometric analysis of collagen network and plasma perfused capillary bed in the myocardium of rats during evolution of cardiac hypertrophy

et al. 1986

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In order to investigate the consequences of different types of cardiac hypertrophy on myocardial capillary and fibrosis density in rats we describe here, in the same hearts, the pattern of capillary bed density visualized by fluorescein isothiocyanate dextran (FITC-dextran) and the pattern of fibrosis density as determined by automated image analysis. Pressure overload was induced by clipping one renal artery in rats (one-clip, two-kidney Goldblatt hypertension, RHV). Volume overload was induced by creation of an arteriovenous shunt between the abdominal aorta and the vena cava (aorto-caval fistula model ACF). Animals were sacrified at 1, 3 and 6 months following surgical procedure. Immediately prior to sacrifice, FITC-dextran (MW 150,000) was injected with the animal under ether anesthesia. Five minutes later, cardiac diastolic arrest was induced by the i.v. injection of potassium chloride. The heart was rapidly excised and placed in a formaldehyde solution. The degree of cardiac hypertrophy was calculated after measurement of cardiac weight. Left ventricular wall thickness and cavity area were measured by microscopic methods. Capillary density and geometry were determined by morphometric methods, under ultraviolet light microscopy, using a graphic tablet connected to a microcomputer. The degree of myocardial fibrosis, visualized with Sirius Red, was estimated by the use of automated image analysis using light microscopy. In renovascular hypertension, cardiac hypertrophy was maximum at one month (36%) and persisted through the six months of the study. This increase in cardiac mass was concentric, due to a significant increase in ventricular wall thickness and was associated with a marked increase in fibrosis and a significant decrease in subendocardial capillary density. These effects existed already one month and did not change with time. In the aorto-caval fistula model, cardiac hypertrophy was also maximum at one month (+56%), but this eccentric increase in cardiac mass was associated with no significant change in left ventricular wall thickness, but rather with a significant increase in the surface area of the left ventricular cavity. This volume overload hypertrophy was associated with a decrease in subendocardial capillary density which was negatively correlated with time. In contrast to concentric hypertrophy there was no increase in the fibrosis density compared to the sham-operated groups. Despite the identical degrees of hypertrophy, pressure and volume cardiac overload differed in a significant manner in both left ventricular wall thickness and cavity surface area.(ABSTRACT TRUNCATED AT 400 WORDS)

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“…Endocardial action potentials in general, and HBP action potentials in particular, have a distinctive steep relation between duration and stimulation frequency which may be due to a difference in the rate dependence of a membrane conductance ( RENOVASCULAR hypertension in rats produced by unilateral clipping of one renal artery imposes a gradual and chronic pressure overload on the heart. Left ventricular hypertrophy resulting from such a chronic pressure overload is associated with characteristic contractile Kammereit and Jacob, 1979; Capasso et al, 1980), ultrastructural (Wendt-Gallitelli andLoud et al, 1978;Anversa et al, 1978;Wendt-Gallitelli et al, 1979), and electrophysiological alterations (Gulch et al, 1979; Aronson, 1980).…”

mentioning

confidence: 99%

“…Left ventricular hypertrophy resulting from such a chronic pressure overload is associated with characteristic contractile Kammereit and Jacob, 1979;Capasso et al, 1980), ultrastructural (Wendt-Gallitelli andLoud et al, 1978;Anversa et al, 1978;Wendt-Gallitelli et al, 1979), and electrophysiological alterations (Gulch et al, 1979;Aronson, 1980).…”

mentioning

confidence: 99%

Non-uniform electrophysiological properties and electrotonic interaction in hypertrophied rat myocardium.

Keung¹,

Aronson²

1981

Circulation Research

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SUMMARY We studied the distribution and nature of the electrical changes associated with myocardial hypertrophy induced by renal hypertension in rats. Standard microelectrode techniqueB were used to study transmembrane action potentials recorded from endocardial, papillary muscle, and epicardial fibers from hypertrophied (HBP) and normal (SHAM) hearts. We also determined the effects of stimulation frequency on the action potentials recorded from these preparations. To assess whether altered intercellular electrical connections contribute to the electrophygiological changes associated with hypertrophy, we analyzed the spatial steady state voltage decrement produced by passing intracellular constant current pulses and determined the effective input resistance (R^,) of endocardial HBP and SHAM preparations. Our results show that the action potential prolongation that accompanies hypertrophy is not uniform. Thus, the entire course of repolarization is prolonged in endocardial and papillary muscle fibers, but only the latter half of repolarization is prolonged in epicardial fibers. Endocardial action potentials in general, and HBP action potentials in particular, have a distinctive steep relation between duration and stimulation frequency which may be due to a difference in the rate dependence of a membrane conductance ( RENOVASCULAR hypertension in rats produced by unilateral clipping of one renal artery imposes a gradual and chronic pressure overload on the heart. Left ventricular hypertrophy resulting from such a chronic pressure overload is associated with characteristic contractile Kammereit and Jacob, 1979; Capasso et al., 1980), ultrastructural (Wendt-Gallitelli andLoud et al., 1978;Anversa et al., 1978;Wendt-Gallitelli et al., 1979), and electrophysiological alterations (Gulch et al., 1979; Aronson, 1980).The most consistent alterations in the myocardium of rats with renal hypertension are enlargement of the myocytes and prolongation of the action potential. However, the degree of alteration in these properties appears to vary according to the region of the left ventricle studied. For example, in a morphometric study of hypertrophied left ventricles from rats with renal hypertension, Loud et al. (1978) and Anversa et al. (1978) reported a greater enlargement of epicardial cells than endocardial cells after 1-4 weeks of hypertension. In the same model, Aronson (1980) recently reported a 50% prolongation of action potential duration in hypertrophied rat papillary muscle driven at a cycle length of 1000 msec (35°C), and Gulch et al. (1979) reported a 180% increase in action potential duration in left ventricular trabeculae driven at a cycle length of 5000 msec (25°C). These results suggest that hypertrophy induced by renal hypertension may be a non-uniform process that affects endocardial, papillary muscle, and epicardial fibers to a different degree.The purpose of the present study was to characterize further the distribution and nature of the electrical changes associated with myocardial hypertrophy. This was...

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Alterations in rat myocardial mechanics under Goldblatt hypertension and experimental aortic stenosis

Cited by 18 publications

References 35 publications

Polymorphic myosin as the common determinant of myofibrillar ATPase in different haemodynamic and thyroid states

Polymorphic myosin as the common determinant of myofibrillar ATPase in different haemodynamic and thyroid states

Morphometric analysis of collagen network and plasma perfused capillary bed in the myocardium of rats during evolution of cardiac hypertrophy

Non-uniform electrophysiological properties and electrotonic interaction in hypertrophied rat myocardium.

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