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

Cardiac taurine levels are elevated in hypertension and congestive heart failure. A possible mechanism for this increase in taurine is an alteration of its uptake. We sought to identify and characterize a carrier-mediated transport system for taurine in the mammalian myocardium utilizing the fetal mouse heart in organ culture. Hearts from fetuses of 16-19 days gestational age used in these studies had an endogenous taurine content of 14.1+/-0.5 nmol/mg tissue. The uptake of [(3)H]taurine was linear for up to 8 h. Taurine was accumulated against a concentration gradient as demonstrated by a net increase in taurine concentration when hearts were incubated in 0.5 mM taurine. [(3)H]Taurine uptake was saturable, K(m) = 0.44 mM, temperature dependent, and required sodium. The close structural analogues, hypotaurine and beta-alanine, reduced [(3)H]taurine uptake by 87% when present in 100-fold excess. The alpha-amino acids alanine, alpha-aminoisobutyric acid, glycine, leucine, and threonine did not inhibit uptake. Other taurine analogues tested were guanidinotaurine, guanidinopropionic acid, gamma-aminobutyric acid, 2-aminoethane phosphonic acid, aminomethane sulfonic acid, 3-aminopropane sulfonic acid, N-acetyltaurine, and isethionic acid. We conclude that a carrier-mediated transport system for taurine exists in the fetal mouse heart based on the demonstration of (a) temperature dependence, (b) saturability, and (c) structural selectivity of the uptake process. Transport was demonstrated to be mediated by a beta-amino acid uptake system. In addition, taurine uptake was observed to be sodium dependent, energy dependent, and capable of accumulating taurine against a concentration gradient.
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PMID:Characterization of a carrier-mediated transport system for taurine in the fetal mouse heart in vitro. 65 83

The effect of manidipine on cardiac hypertrophy, coronary circulation, left ventricular weight and maximal coronary flow in hypertension was measured in DOCA/salt treated systolic hypertensive rats with and without manidipine treatment. Normotensive rats were used as controls. After feeding with 0.05% manidipine-containing food, blood pressure was reduced only in DOCA/salt hypertensive rats, but not in control rats. After 3 weeks of treatment, sodium excretion was significantly increased in DOCA/salt-treated rats with or without manidipine treatment. Hearts were removed and perfused with modified Krebs-Henseleit solution with adenosine (5 x 10(-5) M) in a Langendorff apparatus. Maximal coronary flow (MCF) was significantly decreased only in DOCA/salt hypertensive rats without treatment, while manidipine treatment restored MCF. Left ventricular weight/body weight was also markedly greater in DOCA/salt-treated rats not given manidipine. Left ventricular weight in DOCA/salt-treated rats given manidipine was significantly reduced compared with DOCA/salt hypertensive rats without treatment, although it was heavier than in the control animals. Morphological examination showed that the increased wall/lumen ratio in DOCA/salt hypertensive rats was reduced by manidipine treatment. These findings suggest that treatment with manidipine in DOCA/salt hypertensive rats lowered high blood pressure and improved impaired coronary circulation with a reduction in left ventricular and vascular hypertrophy.
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PMID:Effect of manidipine on cardiac hypertrophy and coronary circulation in DOCA/salt hypertensive rats. 134 89

There is evidence that cardiac hypertrophy in spontaneously hypertensive rats (SHR) occurs before the development of hypertension. 1,2-Diacylglycerol, which is thought to be a second messenger activating protein kinase C, is also produced in excess in SHR hearts at 4 weeks of age, before established hypertension. We determined myocardial 1,2-diacylglycerol content in SHR with and without prazosin and enalapril from 3 to 4 weeks of age. Hearts from untreated SHR had greater RNA and DNA synthesis and greater relative weights at 4 weeks of age than those from Wistar-Kyoto (WKY) rats. There was no difference in triglyceride content or phospholipid species between WKY rats and untreated SHR, except for a higher cholesterol content in SHR. Treatment of SHR with enalapril, but not prazosin, lowered not only 1,2-diacylglycerol content but also RNA synthesis to the levels of WKY rats. Moreover, fatty acids involved in 1,2-diacylglycerol were altered by enalapril despite the lack of a difference between WKY rats and untreated SHR. Prazosin did not have any effect on 1,2-diacylglycerol fatty acid composition. Enalapril may decrease cardiac hypertrophy in SHR by lowering myocardial 1,2-diacylglycerol production.
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PMID:Enalapril reduces the enhanced 1,2-diacylglycerol content and RNA synthesis in spontaneously hypertensive rat hearts before established hypertension. 138 Oct 46

Obesity is a major risk factor for cardiovascular disease. However, a direct link between these two states is difficult to establish, since obesity frequently occurs with other disease states such as diabetes, hypertension and atherosclerosis. Clinical studies have clearly shown that uncorrected obesity is associated with cardiac hypertrophy and compromised ventricular function. A number of rodent models of obesity have been studied in terms of cardiovascular adaptations. Cardiac function of the obese Zucker rat appears to be normal at a younger age. Only after several months is depression in cardiac function discernable. These animals are mildly hypertensive, but do not exhibit the characteristic increase in cardiac output associated with human obesity. A unique characteristic of JCR:LA-cp rat is that they develop atherosclerotic and myocardial lesions. Hearts from these animals will maintain normal function when perfused with physiological levels of calcium. At higher calcium concentrations, however, mechanical function becomes impaired. Dietary-induced obese rats exhibit many of the hemodynamic alterations associated with human obesity, but there is no evidence to-date that these animals will develop severe cardiac depression. Short-term weight reduction apparently has beneficial cardiovascular effects, but weight cycling may be harmful. Given the widespread occurrence of obesity, further studies are warranted to characterize the cardiac manifestations of this condition.
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PMID:Cardiovascular abnormalities associated with human and rodent obesity. 143 63

Echocardiography was used to asses parameters of cardiovascular function in order to identify the main cardiac adjustment mechanisms to arterial hypertension. In addition to morphological parameters of septal and parietal thickness and diameter, telesystolic (Ses) and telediastolic (Spk) stress, EF, Vcfm, the index of left ventricular mass (ILVM), hypertrophy ratio (h/r), contractility index (Do), peripheral resistances (RPT) and Tarazi's index (SAC) were evaluated. In comparison to control subjects, higher levels of PwTs, h/r, SAC, RPT and ILVM (at the limit of significance) were found in hypertensive patients, which were reflected by higher Spk and Do values. From the further analysis of data to identify patients with signs of left ventricular hypertrophy (h/r greater than 0.40 and/or ILVM greater than 140) it was concluded that the hypertrophy ratio (h/r) is the functional parameter which most closely reveals the type of myocardial adjustment. Irrespective of absolute values of ILVM, the adequacy of myocardial hypertrophy to the dimensions of the cavity is accompanied by the normalisation of stress and the return of Do values close to normal levels. Hearts with low h/r those with the highest stress levels, as well as preesting the lowest EF and the highest Do values.
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PMID:[Cardiovascular adjustments in hypertensive patients. An echocardiographic study]. 152 2

Hearts from 110 consecutive adult autopsies were examined to determine the frequency and predisposing clinical and pathologic features of acute left ventricular papillary muscle ischemia. Acute infarcts of papillary muscles were present in 23% of the hearts and were more frequent than acute infarcts of their corresponding ventricular walls. Patients with acutely infarcted papillary muscles were more likely to have significant stenosis of the corresponding coronary artery than were patients with normal papillary muscles. Increasing heart weight was also associated with increased frequency of papillary muscle acute infarction. Patients with acutely infarcted papillary muscles were more likely to have had hypertension and to have suffered significant hypotension prior to death than were patients with normal papillary muscles.
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PMID:Clinical and pathologic factors contributing to acute papillary muscle ischemia. 234 64

Hearts with advanced pressure-overload hypertrophy from systemic hypertension have been shown to have an increased susceptibility to the development of diastolic dysfunction in response to tissue hypoxia and ischemia. It is not known if this propensity to develop diastolic dysfunction in response to ischemia is dependent on the presence of a substantial increase in left ventricular mass, or alternatively, is characteristic of hearts subjected to mild chronic hypertension early in the development of cardiac hypertrophy. We tested the hypothesis that systemic hypertension associated with mild left ventricular hypertrophy increases the susceptibility to the development of diastolic dysfunction in response to demand ischemia. The effects of demand ischemia (6 minutes) were studied in hearts from New Zealand white rabbits with chronic systemic hypertension produced by the one-kidney, one-wrap method (n = 15) and compared with age-matched, sham-operated control rabbits (n = 11) with similar left ventricular mass (5.4 +/- 0.2 vs. 5.4 +/- 0.3 g, respectively). The hearts were studied using an isolated, isovolumic (balloon in left ventricle) preparation with absent pericardium that was perfused with fresh whole blood. At baseline, coronary perfusion pressure was 100 mm Hg with comparable coronary flow per gram left ventricular weight; the hearts were paced at a physiological rate of 3 Hz, and the left ventricular balloon volume was adjusted to achieve a left ventricular end-diastolic pressure of 15 mm Hg in both groups. Left ventricular balloon volume was similar in both groups and volume was thereafter held constant. At baseline, left ventricular systolic pressure (114 +/- 4 vs. 95 +/- 3 mm Hg, p less than 0.001) and developed pressure (18.9 +/- 1.2 vs. 15.1 +/- 0.9 mm Hg/g, p less than 0.05) were higher in the hearts from the hypertensive group in comparison with the control group. During the first minute of global ischemia produced by reducing coronary perfusion pressure from 100 to 20 mm Hg, there was an immediate fall in left ventricular systolic pressure in both groups without an increase in diastolic pressure. In response to the superimposition of pacing tachycardia (heart rate, 6 Hz) during the remaining 5 minutes of the period of ischemia, left ventricular developed pressure was comparable. However, isovolumic left ventricular end-diastolic pressure (measured during long diastoles obtained with transient cessation of pacing) rose to a significantly higher level in the hearts from hypertensive rabbits than in those from the control rabbits (29 +/- 3 vs. 18 +/- 2 mm Hg, p less than 0.01).(ABSTRACT TRUNCATED AT 400 WORDS)
Hypertension 1989 Apr
PMID:Influence of hypertension with minimal hypertrophy on diastolic function during demand ischemia. 252 16

Studies were carried out to determine if the release of atrial natriuretic factor (ANF) is altered in the inbred Dahl salt-sensitive (SS/Jr) rat. Isolated heart-lung preparations of prehypertensive young SS/Jr rats (6-8 weeks of age) and age-matched inbred Dahl salt-resistant (SR/Jr) rats were used. At this relatively young age the blood pressure difference between strains (SS/Jr, 108 +/- 3 mm Hg; SR/Jr, 103 +/- 2 mm Hg) was minor. ANF release was stimulated with preload-induced or afterload-induced atrial stretch. Increased preload produced increases in right and left atrial pressures that were equivalent between young SS/Jr and SR/Jr rats; increased afterload produced increases only in left atrial pressures, which again were equivalent for young rats of the two strains. At any preload-induced change in atrial pressure SS/Jr rat hearts released less ANF than those of SR/Jr rats. Similarly, at any afterload-induced increase in left atrial pressure, SS/Jr rat hearts released less ANF than those of SR/Jr rats. In contrast to the above results in young rats, the strain differences were dramatically reversed when older rats (5-6 months of age) were used; at this age SS/Jr rats were markedly hypertensive (SS/Jr, 211 +/- 8 mm Hg; SR/Jr 130 +/- 4 mm Hg). Hearts from adult hypertensive SS/Jr rats released more ANF than hearts from adult normotensive SR/Jr rats at any left atrial pressure as afterload was increased. This reversal of SS/Jr rats from hyposecreters to hypersecreters of ANF is probably a consequence of hypertension-induced changes such as cardiac hypertrophy and recruitment of the ventricles to produce ANF. It is concluded that the hyposecretion of ANF by prehypertensive SS/Jr rats may represent a genetic trait relevant to the pathogenesis of genetic hypertension and that this is obscured by adaptive changes in the heart as hypertension progresses.
Hypertension 1989 May
PMID:Hyposecretion of atrial natriuretic factor by prehypertensive Dahl salt-sensitive rat. 252 42

To investigate whether pressure-overloaded left ventricular hypertrophy is associated with changes in tissue composition of left ventricular subendocardial (ENDO) and subepicardial (EPI) myocardium, we studied post-mortem 19 normal hearts, 17 hearts of patients with systemic hypertension, and 5 hearts of patients with aortic stenosis. Coronary artery disease was present in 9 hearts of the hypertension group and all 5 hearts of the aortic stenosis group. By means of a grid-point method, volume percentages of nonmyocyte tissue were measured. In ENDO and EPI, nonmyocyte tissue contributed to 27 +/- 8% and 27 +/- 12% for normal hearts, 35 +/- 7% and 32 +/- 7% for hearts in the hypertension group without coronary disease, 40 +/- 10% and 29 +/- 8% for hearts in the hypertension group with coronary artery disease, and 38 +/- 9% and 40 +/- 7% for hearts with aortic stenosis, respectively. For the total group of 41 hearts the volume percentage of nonmyocyte tissue correlated with heart weight index in ENDO (r = 0.59: P less than 0.001), but not in EPI (r = 0.10; not significant). Hearts from patients with hypertension showed a significant increase in microscopical scar fibrosis in ENDO compared to normal, and this increase was amplified by the presence of coronary artery disease. Hearts from patients with aortic stenosis showed an increase in diffuse, non-scar interstitial tissue compared to normal, and occurred in ENDO and EPI. We conclude that the volume fraction of nonmyocyte tissue in ENDO increases as heart weight increases, independent of the type of pressure-overload. Only in the aortic stenosis group this increase of nonmyocyte tissue fraction was observed in EPI as well.
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PMID:Changes in nonmyocyte tissue composition associated with pressure overload of hypertrophic human hearts. 252 28

Cyclic GMP (cGMP) kinase is intimately involved in the regulation of vascular smooth muscle tone. Its tissue concentration was determined in normotensive and hypertensive rats by use of monospecific anti-cGMP kinase antibodies. Hearts of spontaneously hypertensive rats and renovascular (Goldblatt II) hypertensive rats contained half the concentration of cGMP kinase than those of the respective normotensive animals. The increase in blood pressure and the resulting left ventricular hypertrophy were correlated inversely with the left ventricular cGMP kinase concentration. This decrease was specific for the left ventricle and was not observed in other tissues. In addition, the cardiac concentration of cGMP kinase was unchanged in hyperthyroid animals that had comparable left ventricular hypertrophy and mild hypertension. This suggested that in severe renovascular hypertension the decrease in cardiac cGMP kinase concentration is caused by a relative lack of cardiac vessel growth during the development of hypertrophy. In agreement with this conclusion, immunohistochemistry of cardiac cross sections showed that cGMP kinase was exclusively located in cardiac vessels. In support of this localization, the maximal arterial blood flow of heart, liver, skeletal muscle, and kidney correlated excellently with the cGMP kinase content of the respective organ. These results suggest that the cGMP kinase concentration of nonsmooth muscle tissues depends on the amount of organ-specific vascular smooth muscle and may be used as an index for the vascularization of these organs.
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PMID:Decreased cardiac concentration of cGMP kinase in hypertensive animals. An index for cardiac vascularization? 253


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