Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was designed to clarify the state of beta-adrenergic signal transduction and the disordered level of its transduction in hypertensive hearts, using myocardium from spontaneously hypertensive rats (SHR) as a generic model of essential hypertension. Beta-adrenergic receptor binding sites and dissociation constants in the extracted membranes of adult (70-100 days of age) SHR heart were not significantly different from those of Wistar-Kyoto (WKY) rats, the non-hypertensive control. The adenylate cyclase activities stimulated by isoproterenol with GTP, NaF and forskolin were significantly higher in SHR compared to those in WKY. To determine whether differences in signal transduction are natural or are a result of hypertension, we evaluated chronotropic responses in cultured cells of fetal hearts which had not been exposed to hypertension. Fetal cardiac muscle cells of SHR were more sensitive than WKY to isoproterenol stimulation over a wide concentration range. However, there were no statistically significant differences between these two strains with respect to the density of binding sites. These results suggest that in the transduction of adrenergic signals, alterations distal to the beta-receptors are present in the adult hearts of hypertensive rats, and, that the adrenergic signal transduction is already exaggerated in the pre-hypertensive fetal stage.
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PMID:Enhanced myocardial adenylate cyclase activity in spontaneously hypertensive rats. 131 19

In 103 hearts with various forms of cardiac muscle hypertrophy the following parameters were estimated: diameter, length, volume, density and number of myocytes, as well as the density of nuclei of myocytes. The values of all histometric parameters correlated well with the LV weight up to 350 g. In heavier hearts these parameters were approximately at the same magnitude. The number of myocytes was significantly higher in hearts with LV weight above 250 g than in hearts below 250 g: 5.53 x 10(9) vs 4.31 x 10(9), p less than 0.001. The influence of coronary artery diameters, degree of atherosclerosis, weight and percent of fibrous tissue and age on LV weight were evaluated as well. Only coronary artery diameters significantly influenced on LV weight. On the basis of linear discriminant function, three classes of hearts were separated: 1) LV weight 250 g - absence of hyperplasia, only hypertrophy 2) LV weight 251-350 g - hypertrophy + signs of hyperplasia 3) LV weight 350 g - marked signs of hyperplasia Among 18 patients with the LV weight above 350 g (all patients with congestive heart failure), 11 suffered from valvular disease, 3 were postinfarction patients, 2 suffered from primary hypertension and 2 from primary congestive cardiomyopathy. It indicates that, irrespective to the etiologic factor, hyperplasia is a simple result of the cardiac muscle mass increase.
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PMID:[Myocardial structure in various forms of hypertrophy. II. Myocyte hypertrophy or hyperplasia? Results of the study]. 215 Jun 80

Nicardipine has high affinity for the dihydropyridine-binding site and has been shown to inhibit the influx of extracellular calcium through membrane slow channels. The calcium antagonist activity of nicardipine is greater in vascular smooth muscle than in cardiac muscle. Nicardipine has also been shown to possess greater activity in coronary than in peripheral vascular smooth muscle. This in vitro profile accounts for the decreased blood pressure and increased coronary blood flow in animal models in vivo. These pharmacologic properties are the basis for nicardipine's clinical utility in essential hypertension and acute myocardial ischemia. Nicardipine has been shown to be more vascular selective than other calcium antagonists and, therefore, possibly less inclined to produce negative inotropicity. This latter property has been confirmed in human hemodynamic studies. Nicardipine is effective in models of acute myocardial ischemia and hypertension. These results have been confirmed in antianginal and antihypertensive studies in humans. This new calcium antagonist has been shown to limit myocardial infarct size in both dogs and baboons subject to left anterior descending coronary artery ligation and to reduce the extent of ischemia-induced cerebral neuronal death in rats. Other protective effects of nicardipine have been demonstrated in paracetamol overdose in mice, chloroform-induced hepatotoxicity in rats and cerebral ischemia in gerbils and baboons. The mechanism of this cell protection of nicardipine may be related to physicochemical effects.
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PMID:Animal pharmacology of nicardipine and its clinical relevance. 244 Feb 94

Research on the etiology of essential hypertension has led to many reports of altered ion transport in cells from hypertensive patients and animal models. Abnormalities in sodium and calcium ion gradients and transport in vascular smooth muscle, neuronal tissue, cardiac muscle as well as erythrocytes have been extensively investigated. It is not clear whether these abnormalities are of primary or secondary nature. The current knowledge of sodium and calcium ion transport in essential hypertension is briefly reviewed here. Furthermore, evidence is presented which suggests a role of calcium in the regulation of sodium transport activity.
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PMID:A role of calcium in altered sodium ion transport of hypertensives? 245 43

Using column chromatography with phenylcepharase, calmodulin was isolated from the brain of rats with spontaneous hypertension (SHR) and control normotensive rats (NKWR). As judged from the findings of electrophoresis in polyacrylamide gel, UV-spectroscopy and spectrofluometry, the obtained samples of calmodulin contained no significant admixture of other proteins. The Ca-binding capacity of calmodulin of the brain of SHR and NKWR estimated by the method of fluorescent probes were identical. There were also no differences in their capacity to interact with troponine I and to activate the Ca-pump of the erythrocytic membrane and phosphodiesterase of the cardiac muscle. A study on the dependence of activity of phosphodiesterase on the protein content of the brain homogenate from SHR and NKWR revealed no differences in the calmodulin levels in this tissue. On the basis of these data a conclusion was made that impairments of the intracellular distribution of calcium in primary hypertension described earlier are not related to disorders in the metabolism of the universal Ca-binding protein-regulator.
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PMID:[Isolation and characteristics of calmodulin from the brains of rats with spontaneous genetic hypertension]. 398 65

M-mode echocardiography was used in 12 patients with essential hypertension to study changes in cardiac anatomy during long-term therapy with hydrochlorothiazide (50 to 100 mg) and alpha-methyldopa (500 to 1,750 mg). Echocardiographic examination was performed after six weeks of treatment with hydrochlorothiazide alone and after four to six weeks, six months, and nine months of treatment with both hydrochlorothiazide and alpha-methyldopa. Hydrochlorothiazide alone induced a small, and not significant, change in blood pressure (from 157 +/- 16 (SD)/105 +/- 9 to 150 +/- 14/101 +/- 5 mm Hg). Changes in echocardiographic parameters of cardiac anatomy were not observed during short-term diuretic therapy. Addition of alpha-methyldopa further reduced blood pressure (to 133 +/- 11/90 +/- 6 mm Hg, p less than 0.001), which was maintained throughout the study. Gradual decreases in diastolic septal thickness (from 10.9 +/- 1.1 to 9.5 +/- 1.0 mm, p less than 0.01), relative wall thickness (from 0.40 +/- 0.06 to 0.36 +/- 0.06, p less than 0.05) and left ventricular cross-sectional area (from 18.9 +/- 2.9 to 17.3 +/- 2.6 cm2, p less than 0.05) were observed. Posterior wall thickness did not change significantly during the study. The results provide evidence for regression of echocardiographic parameters of cardiac muscle mass during long-term antihypertensive treatment with a diuretic and a centrally-acting sympatholytic drug. Regression of left ventricular mass was not clearly related to changes in casual blood pressure. However, patients who showed a decrease in septal thickness tended to have a greater decrease in systolic blood pressure than those in whom septal thickness did not change during therapy. Moreover, patients in whom a decrease in left ventricular transverse dimension was observed, had a greater decrease in both systolic and diastolic blood pressure than those in whom left ventricular diastolic dimension did not change.
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PMID:Effect of long-term antihypertensive therapy on cardiac anatomy in patients with essential hypertension. 622 88

A polygraphic study involved 122 patients with acute myocardial infarction mostly of transmural nature. In 42 cases using parallel catheterization, barograms of the right portion of the heart and pulmonary artery were recorded. The above non-invasive techniques were tested in relation to their suitability for the indirect determination of the pulmonary circulation pressure. Mathematically substantiated formula are presented designed for the indirect measurement of right atrium and pulmonary pressure. The localization of the primary infarction in the left ventricle anterior wall, recurrent necrosis of the cardiac muscle, attendant essential hypertension and diabetes mellitus are shown to be associated with a more pronounced pulmonary hypertension. An attempt is made to elicit the mechanisms of pulmonary hypertension by correlating the phasic structures of the systole of the right and left ventricles.
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PMID:[Changes in blood pressure in the pulmonary artery in myocardial infarct]. 654 90

We have used 23Na nuclear magnetic resonance spectroscopy to examine the relationship between intracellular sodium and cardiac muscle alterations in genetic hypertension. In the spontaneously hypertensive rat (SHR) compared with the normotensive Wistar-Kyoto rat (WKY) (aged 15 to 19 weeks), mean systolic blood pressures (measured using the tail-cuff method) were significantly (P < .05) different (WKY: 118 +/- 8 mm Hg, n = 5; SHR: 185 +/- 9 mm Hg, n = 5). Heart weights were also increased significantly (P < .05) in SHR (grams dry heart to kilograms body weight ratio was 0.73 +/- 0.04, n = 5, for SHR and 0.55 +/- 0.02, n = 5, for WKY). Intracellular sodium levels, measured using shift-reagent-aided and triple quantum filtered (TQF) nuclear magnetic resonance techniques, were significantly increased (P < .05) in the isolated Langendorff perfused hypertensive rat hearts (17.3 +/- 3.6 mmol/L, n = 5) compared with normotensive rat hearts (8.4 +/- 2.3 mmol/L, n = 5). These data demonstrate increased sodium in cardiac muscle in essential hypertension. We also investigated the effect of pacing on cardiac TQF 23Na nuclear magnetic resonance and found an increase in TQF Na+ content in both WKY and SHR hearts on stepped up pacing. These results support the existence of sodium pump lag in the rat heart perfused at physiologic Ca2+ concentration and suggest that the hypertensive rat heart has adapted to compensate for increased basal intracellular Na+ and maintain a normal response to increased heart rate. Our data appear to suggest an ionic contribution to the cardiac hypertrophy of genetic hypertension in the rat.
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PMID:Nuclear magnetic resonance measurement of intracellular sodium in the perfused normotensive and spontaneously hypertensive rat heart. 806 May 76

Insulin-like growth factor-1 (IGF-1) and insulin stimulate cardiac growth and contractility. Recent evidence suggests a relationship between essential hypertension, left ventricular hypertrophy, and circulating IGF-1 levels. Advanced age alters cardiac function in a manner similar to hypertension. The aim of this investigation was to evaluate the effects of IGF-1 and insulin on the force generating capacity of cardiac muscle in hypertension and the influence of age on this response. Contractile responses to IGF-1 and insulin were examined using papillary muscles from Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) at 10 and 25 weeks of age. Muscles were electrically stimulated at 0.5 Hz, and contractile properties, including peak tension development (PTD), time-to-peak tension, time-to-90% relaxation, and the maximal velocities of contraction and relaxation, were evaluated. PTD was similar in WKY and SHR myocardium at both age groups. At 10 weeks of age, IGF-1 (1-500 ng/ml) caused a dose-dependent increase in PTD in WKY but not SHR myocardium, whereas insulin (1-500 nM) had no effect on PTD in either group. At 25 weeks of age, the positive inotropic effect of IGF-1 was attenuated in the WKY group, and IGF-1 exerted no inotropic action in the SHR group. Pretreatment with the nitric oxide synthase inhibitor, N-omega-nitro-L-arginine methyl ester (L-NAME, 100 microM), did not alter the IGF-1-induced positive inotropic response in 10-week-old WKY myocardium, whereas it unmasked a positive inotropic action in muscles from age-matched SHR animals. At 25 weeks of age, L-NAME abolished IGF-1-induced a positive inotropic response in WKY myocardium, and did not unmask an IGF-induced inotropic response in SHR myocardium. Our results suggest that alterations in nitric oxide modulation of IGF-1-induced contraction may underlie resistance to this inotropic peptide with advancing age, and/or hypertension.
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PMID:Influence of age on inotropic response to insulin and insulin-like growth factor I in spontaneously hypertensive rats: role of nitric oxide. 1032 Jun 31

Patients with cerebral stroke develop electrocardiographic changes concerning the period of ventricular muscle repolarization and cardiac arrhythmias, which may results in the possibility of acute circulatory arrest. ECG monitoring by means of Holter method provides not only information concerning arrhythmias, episodes of ischaemia of the cardiac muscle, but it is also a recognised and generally accepted method of investigation of the autonomic system. The aim of the study was to assess the incidence of arrhythmias and heart rate variability in patients suffering from recent cerebral stroke. The studies involved 36 patients, in that 22 women (mean age 67.7 +/- 7.2 years) and 14 men (mean age 66.5 +/- 11.3 years) within first 24 hours after cerebral stroke confirmed by computerised tomography (CT). One the basis of CT scan haemorrhagic stroke was diagnosed in 7 patients and ischaemic stroke, after ruling out haemorrhagic stroke and neurological consultations, in 29 patients. Moreover, all patients revealed hypertension, 12 of them mild degree (1 degree), and 21 of moderate degree (2 degrees), and 3 of severe degree (3 degrees). The control group comprised 65 patients suffering from primary hypertension without concomitant cerebral stroke, matching the study group as to sex and age as well as the degree of hypertension. All of them were submitted to 24-hour Holter monitoring on tape by means of 3-channel registrator MR45, analysis of ECG tracings was carried out according to Optima Jet system manufactured by Oxford. In order to facilitate further analysis, the automatic recording was verified visually and next heart rate variability (HRV) was estimated within 24 hours and separately for day hours 6:00-22:00 and night hours 22:00-6:00. In comparison to patients with hypertension, but without stroke, subjects with hypertension and accompanying cerebral stroke more often reveal premature supraventricular beats, pairs of ventricular beats as well as episodes of nonsustained ventricular tachycardia; they also reveal lower 24-hours heart rate variability.
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PMID:[Studies of arrhythmia incidence and heart rate variability in patients suffering from cerebral stroke]. 1040 64


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