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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the changes in ventricular isomyosin composition and Ca2+-activated ATPase activity during progression and regression of hypertension and cardiac hypertrophy. Eight control male Wistar rats and 14 Goldblatt-II (two-kidney, one clip) hypertensive rats were studied from the 5th week of age. Five of the Goldblatt-II rats underwent nephrectomy of the ischaemic kidney after 5 weeks, with normalization of blood pressure. The hypertensive rats showed a higher biventricular weight to body weight ratio (P less than 0.02), a lower ATPase activity (P less than 0.005), and an increased expression of 'slow' isomyosins in comparison with the age-matched controls. These changes were more pronounced at 15 than at 10 weeks of age. The 15-week-old nephrectomized rats showed the same degree of cardiac hypertrophy, ATPase activity and isomyosin pattern as the age-matched controls. In conclusion, the changes in ventricular myosin observed during the progression of cardiac hypertrophy regressed after normalization of blood pressure and ventricular mass.
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PMID:Progression and regression of cardiac hypertrophy in hypertensive rats: biochemical and molecular changes in ventricular myosin. 294 23

Cardiac hypertrophy in hypertensive subjects, its biochemical markers, and functional consequences are of great clinical importance but still unclear. We observed a shift of the ventricular isomyosin of adult spontaneously hypertensive (H) rats of both sexes to the V3 form and a decreased myofibrillar ATPase activity in the H animals when compared to normotensive (N) controls. Compared to the male H rats, age-matched female H animals revealed a lower blood pressure, the same or even an elevated magnitude of cardiac hypertrophy, a different ventricular isomyosin pattern, and a higher myofibrillar ATPase activity. In female H rats the V1 and V3 isomyosins were equally distributed (35% V1 and 35% V3), but in male H animals the V3 was predominant (24% V1 and 45% V3). The Ca2+-regulated Mg2+-dependent myofibrillar ATPase of the rat ventricle correlated positively with the amount of V1 when measured at pCa 5 (maximum activation). At submaximum Ca2+-concentrations (pCa 6.9-5.9) the myofibrillar ATPase activities were not changed with the proportion of V1. The cooperativity of the Ca2+-activation of the myofibrillar ATPase increased with increasing amount of V1 (Hill-coefficient 3.7 with 100% V1) and decreased with increased proportion of V3 (Hill-coefficient 1.3 at 45% V3). Two myosin isoenzymes were detected in the aorta of rats, a slow migrating (S2) and a fast migrating (S1) form having both a higher mobility than the ventricular isomyosins. Only one band was observed in the portal vein, which revealed the same mobility as S2. Hypertension did not change the appearance of these vascular smooth muscle isomyosins neither in male nor in female animals.
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PMID:Myosin isoenzymes of vascular smooth and cardiac muscle in the spontaneously hypertensive and normotensive male and female rat: a comparative study. 294 38

Evidence for the existence of factor(s) other than blood pressure responsible for modulation of myocardial hypertrophy accompanying hypertension is well documented. A factor that has been isolated from the myocardium of the spontaneously hypertensive rat and partially purified has been shown to stimulate protein synthesis in vitro. Three indexes of protein synthesis, namely incorporation of 3H-leucine into myocyte myosin, specific activity of the leucyl tRNA, and rate of protein synthesis, also were observed to significantly increase on exposure to this factor, which may play a key role in the modulation of myocardial hypertrophy that accompanies hypertension. Evidence has also been presented demonstrating the role of unknown factors that control the shift of myosin isozymes from V1 (a high-ATPase, high-contractile protein type) to V3 (a slow ATPase type myosin), and vice versa. This study demonstrates that the modulation of the myocardial mass can be controlled at different levels: first at an intrinsic intracellular level by the mechanism of a local growth factor, and then at the level of the contractile protein, the quality rather than quantity of which was found to be important. Both of these were observed to be modulated by factor(s) independent of blood pressure and myocardial mass. However, it remains to be determined what is responsible at the genetic level for transmitting the signal that selects what type of protein will be synthesized and whether there is a common pathway among all the controlling factors.
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PMID:Factors regulating myocardial hypertrophy in hypertension. 294 54

The changes in ventricular isomyosin composition and Ca2+-activated ATPase activity occurring with regression of both hypertension and cardiac hypertrophy were investigated by using polyacrylamide gel electrophoresis under nondenaturing conditions, heavy chain peptide mapping, and an enzymatic assay. Eight control male Wistar rats and 14 two-kidney, one clip (Goldblatt II) hypertensive rats were studied from the fifth week of age. At 10 weeks of age, five Goldblatt II rats and four normotensive controls were killed. Five other Goldblatt II rats underwent nephrectomy of the ischemic kidney, which resulted in subsequent normalization of blood pressure. The remaining four control, four Goldblatt II rats, and five nephrectomized rats were killed at 15 weeks of age. Both the 10- and 15-week-old hypertensive rats had a significantly higher (p less than 0.001) biventricular weight to body weight ratio than the age-matched controls (3.84 +/- 0.76 X 10(-2) vs 2.75 +/- 0.25 X 10(-2); 5.93 +/- 2.26 X 10(-2) vs 2.65 +/- 0.17 X 10(-2]. The 15-week-old nephrectomized rats had a biventricular weight to body weight ratio (2.90 +/- 0.25 X 10(-2] close to that of age-matched controls and significantly lower (p less than 0.05) than that of age-matched hypertensive rats. In both the 10- and 15-week-old hypertensive rats left ventricular myosin Ca2+-activated ATPase activity was significantly lower (p less than 0.001) than in the age-matched controls (0.44 +/- 0.03 vs 0.59 +/- 0.06; 0.24 +/- 0.05 vs 0.48 +/- 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1986 Dec
PMID:Changes in rat ventricular isomyosins with regression of cardiac hypertrophy. 294 51

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)
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PMID:Effect of hypertension on hearts of rats trained by swimming. 295 61

Previous studies in hearts of female rats have demonstrated that ventricular hypertrophy due to systolic overload, when combined with hypertrophy induced by a chronic swimming program, results in increased cardiac performance and enhanced contractile protein activity compared with the effects of hypertension alone. To explore how a chronic running program affects the function of hypertensive hearts, renal hypertension was created in female rats, and the animals were subjected to a program of chronic treadmill running. Running alone caused enhanced cardiac function, an increase in myosin adenosinetriphosphatase (ATPase) activity, and an increase in the percent of the V1 myosin isoenzyme. Hypertension alone caused cardiac hypertrophy with a depression in myosin ATPase activity and a decrease in the percent of the V1 isoenzyme. Running improved cardiac function in hearts of normotensive rats but had no effect in hearts of hypertensive rats. Despite the diminished myosin ATPase activity in hearts of hypertensive runners and the decrease in percent of the V1 isoenzyme, cardiac function was well maintained. The results demonstrate that a chronic running program in hypertensive rats, in contrast to a chronic swimming program, had virtually no effect on cardiac performance or contractile proteins. The dissociation between myocardial performance and the contractile proteins implicates other biochemical mechanisms in the adaptations observed.
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PMID:Combined effects of hypertension and chronic running program on rat heart. 295 51

The influence of isoenzyme pattern of myosin on cardiac energetics was investigated in a modified in situ heart-lung preparation in the rat. Chronic pressure load (spontaneous hypertension, aortic stenosis, Goldblatt hypertension), intermittent feeding, and swim-training elicited redistribution in the concentration of alpha chains of myosin ranging from 18 to 94%. The influence of isoenzyme pattern of myosin on cardiac energetics could be quantitatively assessed by extrapolation of the regression line of oxygen and substrate consumption related to tension time index. Fast myocardium with 100% alpha chains had an ATP and oxygen consumption which exceeded that of slow myocardium with 0% alpha chains by about 60%. This corresponds well to the state of activity of myofibrillar ATPase of fast myocardium which also exceeds that of slow myocardium by about 50%. Furthermore it could be shown that acute increase in the ATPase activity depends on the isoenzyme pattern of myosin. Under the influence of catecholamines the oxygen consumption related to tension time index increased by 30-40% in fast myocardium, whereby in a myocardium with 40% alpha chains no increase in oxygen consumption per unit tension time index was observed, when catecholamines were applied.
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PMID:Implications of myocardial transformation for cardiac energetics. 295 58

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.
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PMID:Effects of systolic overload and swim training on cardiac mechanics and biochemistry in rats. 296 13

We have previously shown that physical conditioning in the rat improves cardiac mechanics and biochemistry and normalizes the cardiac contractile protein abnormalities associated with renovascular hypertension. Since chronic adrenergic stimulation with dobutamine simulates some aspects of physical conditioning, this study was undertaken to investigate the effects of chronic dobutamine administration on normal and hypertensive rat hearts. Four groups of female animals were studied: controls, dobutamine-treated (2 mg/kg twice daily), renovascular hypertensives, and dobutamine-treated hypertensives. Animals were killed after 8-10 weeks and cardiac histology, myosin biochemistry, and mechanics in an isolated heart perfusion apparatus were studied. Dobutamine, unlike hypertension, was not associated with histological evidence of myocardial damage but did increase cardiac mass by 10% and calcium-activated myosin ATPase activity by 13%. Hypertension was associated with a 24% increase in mass, a 24% decrease in ATPase activity, and a shift in the myosin isoenzyme pattern from V1 to V3. The combined stimuli caused additive hypertrophy (44%) and normalized myosin biochemistry and isomyosin distribution. Dobutamine treatment was not associated with significant improvements in pump or muscle function in control or hypertensive hearts. Thus chronic dobutamine treatment, like physical conditioning, induces a physiological cardiac hypertrophy in rats that is associated with improved myosin enzymology and normalization of the contractile protein abnormalities associated with hypertension. Unlike physical conditioning, however, these biochemical alterations do not result in improved contractile function as measured in an isolated buffer-perfused heart apparatus.
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PMID:Effects of chronic dobutamine administration on hearts of normal and hypertensive rats. 296 93

A monoclonal antibody specific for cardiac troponin T has been used to investigate troponin changes during development in the rat heart. Specificity of the antibody was determined by immunoblot analysis with purified bovine cardiac troponin. In the rat heart, immunoblot analysis shows that anticardiac troponin T reacts with a 42.5-kDa band in fetal ventricles and with a 41-kDa band in adult ventricles. The faster migrating troponin T is present in traces in the fetal heart and increases markedly during the first 2 weeks after birth, concomitantly with the progressive decrease of the slower migrating form that is no longer detectable in the adult. The pattern of reactivity of the monoclonal antibody is not modified by alkaline phosphatase pretreatment, suggesting that the antibody is not specific for a phosphorylated epitope. Conditions known to affect cardiac myosin composition, such as hypothyroidism and hypertrophy secondary to systemic hypertension, do not change the troponin T isoform profile of adult rat ventricles. The expression and accumulation of the adult isoforms of troponin T are not suppressed by propylthiouracil treatment of pregnant and nursing rats.
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PMID:Troponin T switching in the developing rat heart. 297 62


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