Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this research was to assess left ventricular myosin alterations of Sh, rats during the various phases in which primitive hypertension developed. Two groups of animals were examined: one comprised spontaneously hypertension rats (Shr) and the other controls. Both groups were studied from the 5th to 31st week of life. The Shrs became hypertensive at 9 weeks of age. The animals were sacrificed at: 5-7-9-12-16-24-31 weeks of age. The left ventricles were separated from their hearts and native myosin in non dissociated conditions was then obtained by polyacrylamide gel electrophoresis; heavy chains and light chains were separated with S.D.S. One of the findings showed that in the control rats the myosin iso-enzyme V1 always prevailed over the myosin iso-enzyme V3 during all the stages of life examined. In the Shrs, starting from the iso-enzyme V3 increased proportionally. The heavy chains showed the same behavior as the native protein while there were no significant differences for the light chains in both groups of animals. In conclusion, our findings show that the structural and biochemical compensation variations which several authors have demonstrated in other conditions of experimental hypertension occur in Sh rats as well.
 ...
PMID:[Changes of cardiac myosin in spontaneously hypertensive rats and control rats, during the various stages of development of essential arterial hypertension]. 252 46

In the myocardium, myosin and creatine kinase isoforms possess different capacities for using O2 and energy-rich phosphates. We studied electrophoretically the distribution of these isoforms in 19 hypertensive rats (two-kidney, one clip model of hypertension) and in age-matched controls. After 6 weeks of hypertension, seven rats were treated with captopril (2 mg/kg daily) for 4 weeks, six were left hypertensive for another 4 weeks, and the remaining rats were killed under ether anesthesia. In the latter, ventricular mass was significantly higher than in controls; V3 isomyosin was 32.3 +/- 6.8% versus 0%, and both creatine kinase-MB and -BB were increased at the expense of creatine kinase-MM (creatine kinase-MB = 29 +/- 2.8% vs. 14.7 +/- 1.8%, p less than 0.001; creatine kinase-BB = 3.1 +/- 0.6% vs. 1.7 +/- 0.8%, p less than 0.001). After 10 weeks of hypertension, ventricular mass, V3 isomyosin, and both creatine kinase-MB and -BB isoforms were found to be persistently higher than in controls. At the same time, captopril-treated rats showed reduced but not normalized blood pressure levels, normalized ventricular mass, and prevalence of the V1 isomyosin (56.9 +/- 22% vs. 47.9 +/- 23.8% in normotensive controls, p = NS). However, higher levels of creatine kinase-MB and -BB were still found in these rats in comparison with the normotensive controls (creatine kinase-MB = 22.4 +/- 5.4% vs. 15.8 +/- 2.8%, p less than 0.025; creatine kinase-BB = 2.3 +/- 0.1% vs. 1.8 +/- 0.3%, p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1989 Nov
PMID:Ventricular myosin and creatine-kinase isoenzymes in hypertensive rats treated with captopril. 268 Sep 63

The influence of the adrenergic system on the population of ventricular myosin isoenzymes under physiological conditions was assessed by subjection of normotensive and spontaneously hypertensive rats (SHR) to different types of physical exercise that increased the activity of the peripheral adrenergic system to varying degrees. The routines, which were 5-6 weeks in duration, involved the mild exercise of enforced swimming (2 x 90 min/day), spontaneous running (daily, about 15 km/10-12 hr) that resulted in absolute ventricular hypertrophy, and enforced running of low intensity (daily, 2 x 1.8 km/3 hr) but associated with marked stressors. Swimming and spontaneous running reduced the high blood pressure of SHR, whereas enforced running increased it. In both strains, the myosin isoenzymes were redistributed in the direction of V1 after swimming but not after running. In SHR, therefore, reduction of pressure load seems insufficient for induction of a higher proportion of V1. The unique and, until now, unexplained effect of swimming was attributed to the pronounced activation of the peripheral adrenergic system as judged from catecholamine stores of ventricles and adrenal glands. Only swimming increased the norepinephrine content of ventricles and adrenal glands in normotensive rats. Swimming also had the strongest influence in SHR. Further evidence for the influence of the adrenergic system came from the effect of selective cardiac beta-blockade with atenolol (50 mg/kg/day). The diminished adrenergic drive of the heart reduced the proportion of V1 to a greater extent in the swimming rats than in the sedentary rats. Taken together, the data demonstrate that substantial changes in adrenergic activity occur under physiological conditions associated with an altered myosin heavy-chain expression.
 ...
PMID:Differential effect of physical exercise routines on ventricular myosin and peripheral catecholamine stores in normotensive and spontaneously hypertensive rats. 275 46

The epidemiology and etiology, pathophysiology, diagnosis, and treatment of congestive heart failure (CHF) are reviewed. CHF affects as many as 4 million Americans and is one of the most prevalent causes of death in hospitalized patients. Major risk factors for developing CHF include advanced age, male sex, hypertension, coronary artery disease, smoking, hypercholesterolemia, diabetes mellitus, and rheumatic heart disease. Heart failure results from decreased intrinsic myocardial contractility caused by one or more of three changes: (1) altered adrenergic nervous system function, (2) impaired delivery of calcium to contractile elements in the heart, and (3) reduced myosin-ATPase activity in the myocardium. The disease is progressive, and no intervention has yet been found to stop it effectively. CHF is diagnosed based on subjective signs and symptoms and objective assessment using auscultation, ECG, chest roentgenogram, laboratory tests, and noninvasive and invasive tests. Treatment of CHF begins with restriction of physical activity and sodium intake. Pharmacologic interventions start with either digitalis glycosides or thiazide diuretics; both may be used concomitantly as the disease progresses. Current studies are focusing on the use of angiotensin-converting enzyme inhibitors as first-line agents for CHF. When CHF worsens, loop diuretics are substituted for or added to the thiazide diuretics, and vasodilators are added to reduce the workload on the heart. Other inotropic agents, including the new bipyridine derivatives, may also be used. In patients not responding to these and other aggressive therapeutic interventions, cardiac transplantation is the only option. Despite advances in management of CHF, little improvement in overall survival has been demonstrated, and no intervention has stopped or reversed the progression of CHF.
 ...
PMID:Current concepts in clinical therapeutics: congestive heart failure. 287 92

Effects of long term treatment of hypertension with bunitrolol on myocardial contractility and left ventricular myosin isoenzyme pattern were examined. Male 22-week-old spontaneously hypertensive rats were treated with bunitrolol (30-40 mg/kg/d, p.o.) for 8-10 weeks. The blood pressure of the bunitrolol-treated group did not differ from that of the untreated group, but ratio of ventricular weight to body weight was significantly lower in the treated group. There were no significant differences in isometric developed tension and dT/dtmax of isolated left ventricular papillary muscles between bunitrolol-treated and control groups. Myocardial mechanical responses to isoprenaline (isoproterenol) also showed no differences between the two groups. Left ventricular myosin isoenzyme pattern obtained by pyrophosphate gel electrophoresis was significantly shifted to VM-1 by bunitrolol treatment.
 ...
PMID:Effects of bunitrolol on myocardial contractility and left ventricular myosin isoenzyme pattern. 290 44

In order to investigate the cardiac effects of antihypertensive therapies in one-clip two-kidney hypertension in rats, we compared the consequences on myosin isoenzyme profile and on left ventricular hypertrophy of two treatments: one was a new converting enzyme inhibitor (S9490), the second a more standard tripletherapy associating clonidine, dihydralazine and furosemide. The two treatments were initiated 4 weeks after clipping and administered during 5 weeks. During the treatment period average systolic blood pressure was 215 +/- 32 mmHg in the hypertensive untreated group (HC2, n = 12) and 144 +/- 13 mm Hg in the CEI group (HT1, n = 13), which is not significantly different from the value found in the sham-operated group (139 +/- 4 mm Hg, C2, n = 13). Blood pressure was lowered only to 173 +/- 18 mm Hg in the group treated with tripletherapy (HT2, n = 12). The left ventricular weight decreased significantly in the CEI-treated group toward values similar to those of the sham-operated animals (2.2 +/- 0.13 mg/g vs. 1.9 +/- 10 mg/g, respectively NS), whereas it did not change in the tripletherapy group when compared to the untreated hypertensive animals despite the fall in blood pressure. In the hypertensive untreated rats the percentage of V1 isoenzyme of cardiac myosin was lower than in the sham-operated group (42.8 +/- 9.0% vs. 57.5 +/- 7.6% P less than .001). In parallel the V3 form of cardiac myosin increased (24.1 +/- 7.4% vs. 15.7 +/- 4.3%, P less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effect of antihypertensive treatment on the left ventricular isomyosin profile in one-clip, two kidney hypertensive rats. 293 25

The purpose of this study was to determine whether a chronic swimming program could reverse the decreased cardiac function and altered myosin biochemistry found in hearts of rats with established renal hypertension. Ten wk after the onset of hypertension [midpoint (m)], hearts from normotensive controls (C) and hypertensives (H) were studied in an isolated working heart apparatus, and myosin biochemistry was analyzed. Half of the control and hypertensive animals were then subjected to a 10-wk swimming program (Sw) and their hearts were compared with those from age-matched sedentary rats. Body weight was no different at the midpoint of the study between Cm and Hm or at the end point (e) of the study among Ce, Swe, He, or H-Swe. Swimming had no effect on blood pressure in either normotensive or hypertensive rats. Dry heart weight was increased by 46% in Hm compared with Cm and by 36% in He, 21% in Swe, and 61% in H-Swe when compared with Ce. Hypertension was associated in both the mid- and end-point studies, with decreases in coronary flow, stroke work (both per gram left ventricle), ejection fraction, and midwall fractional shortening. In addition, actin-activated myosin adenosinetriphosphatase (ATPase) activity was decreased in Hm and He associated with an increase in the content of the V3 myosin isoenzyme. Although the coronary deficit was not corrected in H-Swe, stroke work, ejection fraction, and fractional midwall shortening were normalized compared with control hearts. Myosin ATPase activity and the myosin isoenzyme distribution were similarly restored in H-Swe.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Chronic swimming reverses cardiac dysfunction and myosin abnormalities in hypertensive rats. 293 53

Male spontaneously hypertensive rats (SHR) and age matched Wistar Kyoto normotensive (WKY) rats of 5 weeks, 16 weeks, and 52 weeks of age were used to determine whether duration of hypertension has any effect on contractile protein ATPase and myosin isoenzyme distribution. Myofibrils, actomyosin, and myosin were isolated from the left ventricles of WKY rats and SHR and assayed for myosin ATPase activity and myosin isoenzyme distribution. Myofibrillar ATPase activity was assayed at various free [Ca++] ranging from 10(-7) to 10(-5) mol X litre-1. Ca++ stimulated actomyosin ATPase activity was determined at several Ca++ concentrations both at low ionic strength, which favours actin-myosin interaction, and at high ionic strength, which diminishes actin interaction with myosin. Purified myosin ATPase activity was assayed in the presence of K+-EDTA and in the presence of several concentrations of Ca++. Actin activated myosin ATPase activity was assayed using 26 mumol X litre-1 skeletal muscle actin. Under all these assay conditions no differences were observed in the contractile protein ATPase activity between SHR and WKY rats in any age group. On the other hand, in both SHR and WKY rats the contractile protein ATPase activity under all assay conditions was significantly decreased in 52 week old rats compared with 5 week old rats. The predominant myosin isoenzyme was Vi in 5 week and 16 week old WKY rats and SHR. In 52 week old WKY rats and SHR, however, significant amounts of isoenzymes V2 and V3 were present along with V1. Percentage distribution of V1, V2, V3 isoenzymes calculated from densitometric scans of gels did not show any differences between WKY rats and SHR in any age group. These results suggest that neither myosin ATPase activity nor myosin isoenzyme distribution is altered in the moderately hypertrophied left ventricles of SHR. Moreover, the data indicate that the myocardium of SHR, despite the persistence of pressure overload, undergoes a similar decrease in myosin ATPase activity and an increase in myosin isoenzyme V3 to age matched normotensive WKY rats.
 ...
PMID:Age dependent changes in myosin ATPase activity in the myocardium of spontaneously hypertensive rats. 293 54

Essential hypertension, with pressure overload leading to left ventricular hypertrophy, often results in coronary artery disease and congestive heart failure. The spontaneously hypertensive rat (SHR) is an attractive model for studying the effects of long-term antihypertensive therapy on the contractile properties of the myocardium. In this study we investigated differences in mechanical and biochemical characteristics of papillary muscles from SHR and normal (Wistar-Kyoto [WKY]) rats as a function of age and treatment. We found that the rate of delayed force redevelopment after rapid stretch was less in SHR than in WKY in every age group studied, even at 2 wk of age, before hypertension was evident in the SHR. In the treated SHR, blood pressure was lower, hypertrophy was reduced and the rate of delayed force redevelopment was increased compared with the untreated SHR. Finally, the pattern of myosin isoenzymes was different in treated than in untreated SHR, being shifted to more of the fast V1 and less of the slow V3 isomyosin. We conclude that long-term antihypertensive therapy not only prevents the development of left ventricular hypertrophy, but may do so by preventing the shift in myosin isoenzyme pattern normally found in hearts subjected to a long-term pressure overload.
 ...
PMID:Rapid transient analysis of myosin cross-bridge kinetics in hypertrophied hearts. 294 68

To evaluate the role of dietary sodium and antihypertensive drugs in the modulation of myocardial structure, especially myosin isozymic pattern, renal hypertensive rats (two-kidney, one clip) were treated with a sodium-deficient diet (7 mEq/kg), captopril, or atenolol. Native myosin was extracted under nondissociating conditions and separated by polyacrylamide gel electrophoresis. The percentage of myosin isozyme V1 was significantly decreased from 71.5 +/- 7.5 (Wistar controls) to 52.4 +/- 1.7% (p less than 0.05) in renal hypertensive rats and was associated with an increase in V3 component from 12.7 +/- 5.1 (Wistar controls) to 23.1 +/- 1.4% (renal hypertensive rats; p less than 0.05). There was a dramatic change in the myosin isozyme distribution pattern after treatment with low sodium and captopril. Six weeks of low sodium therapy in renal hypertensive rats resulted in an increase in V1 from 52.4 +/- 1.7 to 74.8 +/- 4.8% and a reduction in V3 from 23.1 +/- 1.4 to 9.5 +/- 2.4%. Normal rats treated with low sodium showed similar results. The percentage distribution of isozymes after low sodium therapy in the captopril-treated rats was not different from that in normal Wistar controls. Captopril therapy also caused an increase in V1 and a decrease in V3. Atenolol therapy, on the other hand, caused a significant increase in V3 and decrease in V1 with no change in blood pressure or heart weight. These data suggest that dietary sodium may play an important role in the modulation of myocardial mass and may modulate signals for synthesis of V1 or V3 myosin phenotypes.
Hypertension 1986 Oct
PMID:Role of sodium in modulation of myocardial hypertrophy in renal hypertensive rats. 294 27


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>