Effect of swimming training on cardiac function and myosin ATPase activity in SHR

Male spontaneously hypertensive rats (SHR) and Wistar-Kyoto normotensive rats (WKY) were subjected to swimming training 6 times/wk, commencing at 4 wk of age, to determine whether this type of endurance exercise might alter contractile proteins and cardiac function in young adult SHR. The total duration of exercise was 190 h. Myofibrillar adenosinetriphosphatase (ATPase) activity was assayed at various free [Ca2+] ranging from 10(-7) to 10(-5) M. Ca2+-stimulated ATPase activity of actomyosin and purified myosin was determined at various Ca2+ concentrations both in the low and high ionic strength buffers. Actin-activated myosin ATPase activity of purified myosin was assayed at several concentrations of actin purified from rabbit skeletal muscle. Under all these conditions the contractile protein ATPase activity was comparable between trained and untrained WKY and SHR. Analysis of myosin isoenzymes on pyrophosphate gels showed a single band corresponding to V1 isoenzyme, and there were no differences between swimming-trained and nontrained WKY and SHR. Ventricular performance was assessed by measuring cardiac output and stroke volume after rapid intravenous volume overloading. Both cardiac index and stroke index were comparable in nontrained WKY and SHR but were significantly increased in the trained groups compared with their respective nontrained controls. These results suggest that myosin ATPase activity and distribution of myosin isoenzymes are not altered in the moderately hypertrophied left ventricle whether the hypertrophy is due to genetic hypertension (SHR) or to exercise training (trained WKY). Moreover, the data indicate that SHR, despite the persistence of a pressure overload, undergo similar increases in left ventricular mass and peak cardiac index after training, as do normotensive WKY.     

Cardiac function in hypertrophied hearts from chronically exercised female rats

Physiological cardiac hypertrophy was produced in female rats by subjecting them to a swimming program for 8 wk. Conditioned rats (C) had body weights similar to sedentary control rats (S), but hearts from C weighed 33% more than hearts from S. Heart function was assessed in an isolated working-heart apparatus at similar heart rates and aortic diastolic pressures and over a range of 5-20 cmH2O left atrial filling pressure (LAP). At any given LAP, absolute values for cardiac output and coronary flow were greater (p less than 0.001) in C than S, but when these values were normalized for dry left ventricular (LV) weight, no differences were observed. Peak LV systolic pressure and ejection fraction were greater (p less than 0.01) in C than S at all LAP. Derived measures of contractility calculated at the midwall demonstrated greater (p less than 0.01) velocity and extent of circumferential fiber shortening in C compared with S. Therefore, chronic swimming in female rats leads to enhanced contractile performance of the left ventricle despite a marked degree of hypertrophy. These results contrast with our earlier observations in female rats trained by running where neither hypertrophy nor enhanced function were observed.     

Modulation of myosin isoenzyme populations and activities of monoamine oxidase and phenylethanolamine-N-methyltransferase in pressure loaded and normal rat heart by swimming exercise and stress arising from electrostimulation in pairs

The question of whether the effects of physical exercise on the heart of 15-weeks normotensive and hypertensive rats can be modulated by additional stressors was studied. Intermittent swimming (33-35 degrees C water, maximum 2 X 1.5 h/day, 2-6 weeks) was employed as a model of exercise. Electrostimulation of rats in pairs (maximum 2 X 1.5 h/day, 6 weeks) served as a model leading predominantly to stress. When the above procedures were combined, electrostimulation in pairs was performed in one session and was followed up by swimming. The myosin isoenzyme population was used as a marker of changes in contractile performance of myofibrils. Activities of the catecholamine-degrading enzyme monoamine oxidase (MAO) and the adrenaline-synthesizing enzyme phenylethanolamine-N-methyltransferase (PNMT) served to monitor chronic alterations of catecholamine turnover in myocardium. Redistribution in favour of VM-1 (ventricular myosin isoenzyme 1) occurred as early as 2 weeks after the onset of intermittent swimming and was observed under several experimental conditions. The redirection of genetic expression of the isoenzymes was not linked to the presence of an increased ratio of right to left ventricular weight, most probably arising from intermittent hypoxia during drownproofing. The myosin isoenzyme population of swimming spontaneously hypertensive rats (SHR) resembled that of sedentary Wistar rats. The enzyme activities of MAO and PNMT were both significantly reduced following 6 weeks intermittent swimming in Wistar rats and SHR. This can most probably be attributed to the exercise component of swimming which, on average, led to reduced catecholamine turnover in heart. Electrostimulation of rats in pairs for 6 weeks, which resulted in aggressivity and aggressions, did not alter the myosin isoenzyme population in Wistar rats; in SHR, it further augmented the proportion of VM-3 (ventricular myosin isoenzyme 3), which had already increased in the sedentary state. Furthermore, electrostimulation increased PNMT activity, but did not affect MAO activity. Electrostimulation in pairs, followed by swimming, altered the myosin isoenzyme population in the same way as did swimming alone. However, the activities of PNMT and MAO seemed to be governed by the routine involving stress and not by the exercise routine. This demonstrates that stressors supplementing exercise can decisively modify or even prevent reactions of the organism in response to exercise.(ABSTRACT TRUNCATED AT 400 WORDS)     

Cardiac dysfunction in isolated perfused hearts from spontaneously diabetic BB rats

The purpose of this investigation was to examine cardiac function and biochemistry in spontaneously diabetic BB rats, a strain in which diabetes occurs spontaneously and closely resembles insulin-dependent diabetes in humans. The study involved two groups: nondiabetic littermates of BB rats and BB diabetic rats treated daily with a very low insulin dose such that the rats were severely hyperglycemic and hyperlipidemic. The hearts from these two groups were isolated and heart function (using isolated perfused working hearts) and biochemistry were examined 6 weeks after the onset of diabetes. BB diabetic rats exhibited a lower calcium-stimulated myosin ATPase activity and depressed left ventricular developed pressure, cardiac contractility, and ventricular relaxation rates compared with BB nondiabetic littermates. These results suggest that the chronically diabetic state in the BB rat produces cardiac changes similar to those demonstrable after chemical diabetes induced by alloxan or STZ, or that seen during human diabetes mellitus.     

Determinants of energy utilization in the activated myocardium

This is a review of work dealing with the effect of pressure overload and thryotoxic hypertrophy of rabbit hearts on the production of total activity related (TA) and initial (I) heats during isometric contraction. Pressure overload hypertrophy is produced by constricting the pulmonary artery with a spiral monel metal clip. Thyrotoxic hypertrophy is produced by 14 daily i.m. injections of 0.2 mg L-thyroxine per kilogram. Heat output is measured with Hill-type planar vacuum deposited bismuth and antimony thermopiles, and force is measured with a capacitance strain gauge. The pressure overload results in a depressed velocity of unloaded shortening, a depressed rate of isometric force development, and an increased time-to-peak tension. These changes are associated with a decreased myosin ATPase, a heart with no V1 myosin isoenzyme, and an increase in the economy of isometric force development (integral of Pdt/TA, integral of Pdt/I). The thyrotoxic hearts exhibit an increased velocity of shortening and rate of force development, and a decrease in time-to-peak tension. These changes are associated with an increase in myosin ATPase activity, a heart with increase in the V1 isoenzyme composition (88% V1), and a decrease in the economy of isometric force development (integral of Pdt/TA, integral of Pdt/I). The changes in the two types of hypertrophied hearts are interpreted in terms of altered cross-bridge cycling rates and changes in cross-bridge tension time integral as well as excitation contraction coupling phenomena. In the thyrotoxic hearts there is an increase in the economy of the recovery processes. Both types of hypertrophy are considered to be adaptive and involve the coordinated restructuring of the excitation-contraction, contractile, and recovery systems.     

Exercise alters cardiac myosin isozyme distribution in obese Zucker and Wistar rats

Recent evidence suggests that exercise training may significantly increase the expression of the cardiac myosin isozyme V1 in the diabetic heart, a change associated with improved cardiac functional capacity. To test this hypothesis, cardiac myofibrillar adenosinetriphosphatase (ATPase) activity and myosin isozyme profiles were determined in trained and sedentary male hyperinsulinemic obese Zucker (OZT, OZS) and obese Wistar (OWT, OWS) rats. Lean sedentary (LZS, LWS) animals served as age-matched controls. Myofibrillar ATPase activity and the relative quantity of the high-ATPase isozyme V1 was significantly lower in both strains of sedentary obese rats than in the respective lean sedentary controls (P less than 0.05). Both 5 (OZT) and 10 wk (OWT) of moderate treadmill training increased these markers of cardiac myosin biochemistry in the obese animals (P less than 0.05). Thus, endurance exercise training remodels the cardiac isomyosin profile of hyperinsulinemic rats and, in doing so, may enhance cardiac contractility and functional capacity. Such changes may reflect an improvement in glucose availability and utilization in these hearts.     

Effects of chronic swimming training on cardiac sarcolemmal function and composition

Cardiac contractile function is dependent on the integrity and function of the sarcolemmal membrane. Swimming exercise training is known to increase cardiac contractile performance. The purpose of the present study was to examine whether a swimming exercise program would alter sarcolemmal enzyme activity, ion flux, and composition in rat hearts. After approximately 11 wk of exercise training, cardiac myosin and actomyosin Ca2+-adenosinetriphosphatase (ATPase) activity was significantly higher in exercised rat hearts than in sedentary control rat hearts. Glycogen content was increased in plantaris and gastrocnemius muscles from exercised animals as was succinic dehydrogenase activity in gastrocnemius muscle of exercised rats in comparison to sedentary rat preparations. Sarcolemmal vesicles were isolated from hearts of exercise-trained and control rats. Sarcolemmal Na+-K+-ATPase and K+-p-nitrophenylphosphatase activities, Na+-Ca2+ exchange, and passive Ca2+ binding did not differ between the two groups. ATP-dependent Ca2+ uptake and 5'-nucleotidase activity were elevated in the cardiac sarcolemmal vesicles isolated from exercised animals compared with sedentary control rats. Sarcolemmal phospholipid composition was not altered by the exercise training. Our results demonstrate that swimming training in rats does not affect most parameters of cardiac sarcolemmal function or composition. However, the elevated sarcolemmal Ca2+ pump activity in exercised rats may help to reduce intracellular Ca2+ and augment cardiac relaxation rates. The enhanced 5'-nucleotidase activity may stimulate adenosine production, which could affect myocardial blood flow. The present results further our knowledge on the subcellular response of the heart to swimming training in the rat.     

Reduced cardiac myofibrillar Mg-ATPase activity without changes in myosin isozymes in patients with end-stage heart failure

In this study we tested the hypothesis that reduced myofibrillar ATPase activities in end-stage heart failure are associated with a redistribution of myosin isozymes. Cardiac myofibrils were isolated from left ventricular free wall from normal human hearts and hearts at end-stage heart failure caused by coronary artery diseases, cardiomyopathy or immunological rejection. The hearts had been excised in preparation for a heart transplant. Myofibrillar Ca^2–-dependent Mg-ATPase and myosin Ca^–- and K^–EDTA-ATPase activities were compared. Possible changes in myosin isozyme distribution in the diseased heart were investigated using polyacrylamide gel electrophoresis of native myosin in the presence of pyrophosphate. Significant reduction in myofibrillar Ca²⁺-dependent Mg-ATPase with no changes in the sensitivity of the myofibrils to Ca⁺ was observed in heart with coronary artery diseases (25.2 to 27.1% at pCa 5.83 to pCa 5.05), cardiomyopathy (21.1 to 25.5% at pCa 5.41 to pCa 5.05), and in the immunologically rejected heart (18.4 to 22.8% at pCa 5.41 to pCa 5.05). Significantly lower myosin Ca²⁺-ATPase was observed with coronary artery diseases only and myosin K-EDTA activities did not differ in diseased and normal hearts. Polyacrylamide gel electrophoresis of native myosin from the normal and three models of end-stage heart failure revealed two distinct bands in the human left ventricle and one diffuse band in the human right atria. No apparent differences in myosin isoenzyme pattern were observed between the normal and diseased hearts. Further evaluation is needed to clarify the ATPase nature of the two bands.     

Changes in myocardial contractile protein ATPases in chronically adrenalectomized rats with and without glucocorticoid replacement

Studies were conducted to examine the effects of chronic adrenalectomy (Adx) and adrenalectomy plus glucocorticoid replacement therapy on rat cardiac contractile protein ATPase activities. The Ca2+-dependent Mg-ATPase activity of myofibrils isolated from rat ventricles 3 weeks postadrenalectomy (Adx) was significantly decreased at all pCa2+ concentrations (P less than 0.01), compared to sham-operated (SO) rats. Similarly, Ca2+-, K+-EDTA, and actin-activated myosin ATPase activities of Adx rat hearts were markedly decreased below that of SO rats (P less than 0.01). Dexamethasone administration to Adx rats prevented the decrease of Ca2+- and K+-ATPase activities of myosin, but not of myofibrillar Ca2+-dependent Mg-ATPase or actin-activated myosin Mg-ATPase activities. These studies suggest that glucocorticoid insufficiency induced by adrenalectomy results in altered myocardial contractile protein ATPase activity which may underlie impaired cardiac performance.     

Effects of systolic overload and swim training on cardiac mechanics and biochemistry in rats

We have previously shown that swim conditioning corrects the depressed mechanical function and myosin adenosinetriphosphatase (ATPase) activities associated with renovascular hypertension (HTN) in the rat. The present study was designed to assess the effects of swim conditioning on another form of systolic overload, subdiaphragmatic suprarenal aortic stenosis. Cardiac mechanics in an isolated working heart apparatus and myosin enzymology were studied in four groups of rats: controls (C), animals with chronic systolic overload secondary to aortic constriction (St), swim-conditioning animals (Sw), and animals exposed to a combined load (St-Sw). Heart weight was increased by 23% in St, 27% in Sw, and 36% in St-Sw. In contrast to HTN, cardiac pump and muscle function were not depressed in St. Sw was associated with improved cardiac output, stroke work, and velocity of circumferential fiber shortening. St-Sw showed improved mechanical cardiac performance relative to both C and St. The percent of ventricular myosin of the V1 type and Ca2+-activated myosin ATPase activity relative to C was unchanged in Sw but was depressed in St and St-Sw. These data demonstrate that the salutory mechanical effects of Sw can be superimposed on the systolic overload of St. However, the dissociation between mechanics and myosin enzymology suggests that factors in excitation-contraction coupling other than myosin isoenzyme shifts are responsible for this finding.     

Troponin subunits contribute to altered myosin ATPase activity in diabetic cardiomyopathy

Our group has documented that myocardial performance is impaired in the hearts of chronically diabetic rats and rabbits. Abnormalities in the contractile proteins and regulatory proteins may be responsible for the mechanical defects in the streptozotocin (STZ)-diabetic hearts. Previously, the major focus of our research on contractile proteins in abnormal states has concentrated on myosin ATPase and its isoenzymes. Our present study is based on the overall hypothesis that regulatory proteins, in addition to contractile protein, myosin contribute to altered cardiac contractile performance in the rat model of diabetic cardiomyopathy. The purpose of our research was to define the role of cardiac regulatory proteins (troponin-tropomyosin) in the regulation of actomyosin system in diabetic cardiomyopathy.For baseline data, myofibrillar ATPase studies were conducted in the myofibrils from control and diabetic rats. To focus on the regulatory proteins (troponin and tropomyosin), individual proteins of the cardiac system were reconstituted under controlled conditions. By this approach, myosin plus actin and troponin-tropomyosin from the normal and diabetic animals could be studied enzymatically. The proteins were isolated from the cardiac muscle of control and STZ-diabetic (4 weeks) rats. Sodium dodecyl sulfate gel electrophoretic patterns demonstrate differences in the cardiac TnT and TnI regions of diabetic animals suggesting the different amounts of TnT and/or TnI or possibly different cardiac isozymes in the regulatory protein complex. Myofibrils probed with a monoclonal antibody TnI-1 (specific for adult cardiac TnI) show a downregulation of cardiac TnI in diabetics when compared to its controls. Enzymatic data confirm a diminished calcium sensitivity in the regulation of the cardiac actomyosin system when regulatory protein(s) complex was recombined from diabetic hearts. Actomyosin ATPase activity in the hearts of diabetic animals was partially reversed when myosin from diabetic rats was regulated with the regulatory protein complex isolated from control hearts. To our knowledge, this is the first study which demonstrates that the regulatory proteins from normal hearts can upregulate cardiac myosin isolated from a pathologic rat model of diabetes. This diminished calcium sensitivity along with shifts in cardiac myosin heavy chain (V1V3) may be partially responsible for the impaired cardiac function in the hearts of chronic diabetic rats. (Mol Cell Biochem151: 165–172, 1995)     

The ATPase activity of subfragment-1 from the hypertrophied heart.

Myosin and subfragment-1 were prepared from rabbit hearts hypertrophied secondary to pulmonary artery constriction. The Ca2+ -stimulated ATPase activity was reduced while the potassium/EDTA-stimulated ATPase activity was unchanged in both the myosin and subfragment 1 (S-1) from hypertrophied hearts. When hypertrophy myosin was mixed with an equal quantity of control myosin, the ATPase activity of the mixed protein fell halfway between control and hypertrophy values. Similar results were obtained with control and hypertrophy S-1. The actin-stimulated ATPase activity of hypertrophy S-1 was slightly depressed but unlike hypertrophy myosin this depression was not significant when compared to normal S-1. This suggests that papain cleavage may have removed part of the conformational difference that exists between control and hypertrophy myosins.     

Influence of long-term swimming training on the structure and enzyme activity of myosin in the rat myocardium (author's transl)]

Intermittent hemodynamic loading of the rat myocardium due to swimming training for several weeks leads to a significant increase in the specific ATPase activity of myosin. This enzymatic alteration of the myosin molecule is accompanied by changes in the stoichiometry of its light chains which are of great significance for the ATPase activity. The maximum shortening velocity of the unloaded myocardium (Vmax), estimated on the basis of afterloaded contractions, shows a slight increase as a result of the physical training. Since, on the other hand, the increase is not significant using the quick release technique, a close relationship between the specific ATPase activity and the augmented cross-sectional contractile capability cannot be proved in our experiments.     

Sucrose feeding prevents changes in myosin isoenzymes and sarcoplasmic reticulum Ca2+-pump ATPase in pressure-loaded rat heart

Pressure-overload due to banding of the abdominal aorta in rats for 10 weeks resulted in cardiac hypertrophy, redistribution of myosin isoenzymes and reduction in the sarcoplasmic reticulum (SR) Ca2+-stimulated ATPase activity. Administration of sucrose in the drinking water (0.8%, w/v) to rats prevented changes in myosin isoenzymes and SR Ca2+-stimulated ATPase in hypertrophied hearts. This beneficial effect of sucrose feeding with respect to remodeling of the subcellular organelles in the myocardium was not associated with any significant changes in plasma glucose or thyroid hormone levels. It is suggested that the prevention of subcellular changes in the hypertrophied hearts due to sucrose feeding may be due to a shift in fuel utilization by the myocardium.     

慢性缺氧对大鼠左右心室功能、心肌肌原纤维Ca~（2＋），Mg~（2＋）－ATP

模拟５０００ｍ中度缺氧时,大鼠右室功能显著加强,而左室功能加强不显著;左右心室肌原纤维Ｃａ２＋,Ｍｇ２＋－ＡＴＰ酶活性下降,肌球蛋白同功酶Ｖ２和Ｖ３百分含量增加,Ｖ１百分含量减少。８０００ｍ重度缺氧时,右室功能减弱,但无统计学意义,左室功能减弱有显著性;ＡＴＰ酶活性和同功酶的变化超过５０００ｍ组。此外,右室ＡＴＰ酶活性与ＰＡＰ呈反比且有显著性,左室ＡＴＰ酶活性与ＣＡＳＰ虽也呈反比但无显著性;右室同功酶Ｖ３百分含量与ＰＡＰ呈正比,左室同功酶Ｖ３百分含量与ＣＡＳＰ不呈比例。上述结果表明,因短期突发严重缺氧引起的心肌供氧不足对左心室心肌的直接损伤作用大于右心室心肌。     

Protein synthesis, myosin ATPase activity and myofibrillar protein composition in hearts from tumour-bearing rats and mice.

Growing rats and adult weight-stable mice bearing a transplantable methylcholanthrene-induced sarcoma were compared with animals with various states of malnutrition. Heart protein synthesis was measured in vivo. Myocardial RNA, myofibrillar protein composition and the Ca2+-activated ATPase activity in heavy chains of native myosin were measured. 'Fingerprints' were made from myosin by trypsin treatment to evaluate possible structural changes in the protein. Cardiac protein-synthesis rate was decreased by 20% in growing tumour-bearing rats, by 35% in protein-malnourished (rats) and by 47% in starved rats, compared with freely fed controls (P less than 0.05). Adult tumour-bearing mice showed no significant decrease in myocardial protein synthesis. Pair-weighed control mice had significantly depressed heart protein synthesis. Protein translational efficiency was maintained in both tumour-bearing rats and mice, but was decreased in several groups of malnourished control animals. The Ca2+-activated myosin ATPase activity was decreased in all groups of malnourished animals, including tumour-bearing mice and rats, without any evidence of a change in cardiac isomyosin composition. We conclude that loss of cardiac muscle mass in tumour disease is communicated by both depressed synthesis and increased degradation largely owing to anorexia and host malnutrition. Increased adrenergic sensitivity in hearts from tumour-bearing and malnourished animals is not communicated by increased Ca2+-activated ATPase activity. This may be down-regulated in all groups with malnutrition, without any observable alterations in the isomyosin profile.     

Prevention of diabetes-induced myocardial dysfunction in rats by methyl palmoxirate and triiodothyronine treatment

Diabetes results in myocardial functional alterations which are accompanied by a depression of biochemical parameters such as myosin ATPase and calcium uptake in the sarcoplasmic reticulum. Methyl palmoxirate, a fatty acid analog, is reported to decrease circulating glucose levels by inhibiting fatty acid metabolism, thus forcing carbohydrate utilization. In the present study, we attempted to prevent streptozotocin diabetes-induced myocardial alterations in the rat. Using the isolated working heart preparation, we observed a depression of myocardial function in rats 6 weeks after the induction of diabetes, which was characterized by the inability of these hearts to develop left ventricular pressures and rates of ventricular contraction and relaxation as well as control hearts at higher left atrial filling pressures. Methyl palmoxirate treatment (25 mg kg-1 day-1 po daily) was unable to control diabetes-induced changes in plasma glucose, triglycerides, insulin, and total lipids. Also, the functional depression seen in diabetic rat hearts was present despite the treatment. However, depression of calcium uptake and elevation of long chain acyl carnitines seen in sarcoplasmic reticulum (SR) prepared from diabetic rat hearts could be prevented by the treatment. As triiodothyronine (T3) treatment has been shown to normalize depression of cardiac myosin ATPase in diabetic rats, we repeated the study using a combination of T3 (30 micrograms kg-1 day-1 sc daily) and methyl palmoxirate. While diabetic rats treated with T3 alone did not show significant improvement of myocardial function when compared with untreated diabetics, the function of those treated with both T3 and methyl palmoxirate was not significantly different from that in control rat hearts.(ABSTRACT TRUNCATED AT 250 WORDS)     

The roles of myosin ATPase activity and myosin light chain relative content in the slowing of type IIB fibers with hindlimb unweighting in rats

We tested the hypothesis that slowing of shortening velocity generated by type IIB fibers from hindlimb-unweighted (HU) rats resulted from a reduced ATPase activity and/or a reduction in the relative content of myosin light chain 3f isoform content (MLC_3f). After 2, 3, and 4 wk of HU, maximal unloaded shortening velocity (V_o) of single permeabilized semimembranosus muscle fibers was determined by the slack test. Subsequently, the myosin heavy chain and the relative content of MLC were determined by SDS-PAGE. The ratio of MLC_3f to MLC_2f was determined by densitometric analysis. In addition, myofibrils were prepared from permeabilized fibers (soleus and semimembranosus muscles) and assayed for resting myosin ATPase and Ca²⁺-activated myosin ATPase. After HU, V_o declined by 28–40% and the MLC_3f/MLC_2f ratio decreased by 32 to 48%. A significant correlation between the relative amount of MLC_3f and V_o was found (r = 0.48, P < 0.05). Resting myosin ATPase rates were not different between myofibrils prepared from corresponding muscles of control and HU rats (P = 0.86). Ca²⁺-activated myosin ATPase activities also were not different between myofibrils prepared from corresponding muscles of control and HU rats (P = 0.13). These data suggest that the slowing of maximal unloaded shortening velocity in type IIB fibers with HU is, at least in part, due to a relative change in the essential light chain composition, a decrease in the relative amount of MLC_3f and most likely a concomitant increase in MLC_1f. However, this reduction in V_o is independent of myosin ATPase activity. unloading shortening velocity; myosin light chain 3f     

Effect of hypertension on hearts of rats trained by swimming

To determine whether a prior chronic swimming program would alter the heart's response to chronic hypertension, female rats were made to swim for 10 wk, and then the left renal artery was stenosed. Heart perfusions were performed 10 wk later. The five groups studied were: control (C), normotensive swimmers (Sw), sedentary hypertensives (H), swimming rats made hypertensive and then allowed to be sedentary (Sw-H-Sd); and swimming animals made hypertensive and continued in a swimming program (Sw-H-Sw). Total heart and left ventricular weights were increased in increasing degrees in the sequence Sw, H, Sw-H-Sd, and Sw-H-Sw. Right ventricular weight was only increased in Sw and Sw-H-Sw. Swimming before the onset of hypertension enhanced total cardiac output and stroke work. Ejection fractions and mean velocity of circumferential fiber shortening (Vcf) were increased in Sw-H-Sd or Sw-H-Sw vs. controls. Myocardial O2 extraction was increased and coronary flow and myocardial O2 consumption were diminished in all hypertensive groups. However, lactate production was similar in all groups. Myosin adenosinetriphosphatase activity was increased in Sw but decreased in the three H groups. The percent of V1 myosin isozyme was greater and the percent of V3 less in Sw than in C; V1 was diminished and V3 increased in H and Sw-H-Sd; isozymes were normal in Sw-H-Sw.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ouabain-sensitive and -insensitive ATPase activities in the kidney and the liver of spontaneously hypertensive rats.

Ouabain-sensitive and-insensitive ATPase activities were measured in the kidneys and the kidneys and the liver of male and female rats of the Lyon hypertensive (LHS) and Lyon normotensive strain (LNS). At the age of 48 +/- 2 weeks, hypertensive rats exhibited a significantly higher blood pressure and body weight than age-matched normotensive rats. Ouabian-insensitive ATPase activity was decreased in the kidney, but not in the liver of hypertensive rats compared to normotensive rats. Ouabian-sensitive ATPase activity was non significantly decreased in the kidney of hypertensive rats.