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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate cardiac performance in renal hypertension more precisely we determined cardiac function curves for 12 normotensive rats and 11 other rats with two-kidney Goldblatt hypertension. The hypertensive group (BP = 134 +/- 8 mm Hg) showed significant cardiac hypertrophy (44 +/- 1% increased ratio of heart weight to body weight, P less than 0.01) and markedly increased left ventricular stroke work with a moderate but not significant increase in left ventricular end-diastolic pressure (LVEDP) (5.9 +/- 0.8 vs. 4.7 +/- 0.4 mm Hg). We evaluated cardiac function by recording left ventricular end-diastolic pressure, stroke volume (SV), and cardiac output (CO) (by electromagnetic flowmeter) during rapid alteration in venous return. Analysis of variations of stroke volume vs. left ventricular end-diastolic pressure showed that renal hypertension is accompanied by a significant decrease in ventricular performance [SV = 0.0190 + 0.0509 LVEDP - 0.0025 (LVEDP)2 + 0.0001 (LVEDP)3] compared to the normotensive group [SV = 0.0430 + 0.0644 LVEDP - 0.0040 (LVEDP)2 + 0.001 (LVEDP)3]. The alterations in stroke volume and cardiac output were associated with a lack of significant changes in the work performed at matched end-diastolic pressures. The data indicate that chronic renal hypertension is accompanied by a depression of cardiac reserve which is not revealed by measurements of cardiac output and left ventricular end-diastolic pressure at rest. This impairment in cardiac function might be related to either diminished cardiac contractility or reduced left ventricular compliance; the latter possibility is in accord with our finding of a 2-fold increase in the hydroxyproline content (P less than 0.001) and a significant decrease in the DNA concentration of ventricular tissue.
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PMID:Cardiac performance in rats with renal hypertension. 13 Oct 7

Oxidative phosphorylation was measured polarographically in mitochondria isolated from rat heart. With regard to ADP/O ratio and respiratory control index, no differences were found among mitochondria isolated from normal, acutely (increased pneumatic resistance of the heart-lung preparation) and chronicly (renal hypertension) stressed heart. However, the acute stressed heart induced by strangulating the outflow tract of the heart-lung preparation showed clear depression and tendency to depression, respectively, in the level of ADP/O ratio and respiratory control index in mitochondria. The results indicate that there is no change in the oxidative phosphorylating mechanism of the myocardial mitochondria of nonfailed heart despite acute or chronic pressure loadings; however, there is an uncoupling of oxidative phosphorylation in mitochondria of the failed heart after acute strangulation of the outflow tract.
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PMID:Oxidative phosphorylation in mitochondria isolated from stressed rat heart. 121 39

This study demonstrates the suppression of chronotropic component and activation of vascular component of baroreceptor reflex evoked by v.cava inferior occlusion in the conscious chronically instrumented cats with renal hypertension. Infusion of nitroprusside caused the depression of both components in the normotensive and hypertensive animals. The values of system hemodynamics indices permit considering that new model of orthostatic hypotension is worked out.
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PMID:[The characteristics of the cardiovascular reactions in modelling a state of orthostatic hypotension in waking hypertensive animals]. 156 90

The factors regulating calcium homeostasis in the cardiac plasma membrane of renal hypertension in the rat (two kidney-one clip, Goldblatt model) have been studied. Comparison of the cardiac sarcolemma from control (C) and hypertensive (H) rats indicates similar protein yield and purity. Study of longer term hypertension (4 to 12 weeks) shows a decrease in the number of calcium channel receptor binding sites (Bmax C: 549 +/- 122 fmol/mg; H: 334 +/- 74 fmol/mg) as well as a depressed calcium pumping ATPase activity (C: 7.6 +/- 2.5 nmol/mg/min; H: 3.8 +/- 1.5 nmol/mg/min). Furthermore, there is a decreased rate of Na+-Ca2+ exchange (C: 5.4 +/- 1.9 nmol/mg/5 s; H: 2.3 +/- 0.9 nmol/mg/5 s). Study of short-term hypertension (1 to 4 weeks) indicates that the earliest change occurs at 1 week with decreased calcium pumping ATPase due to a change of the Vmax of Ca2+ transport (C: 9.7 +/- 1.6 nmol/mg/min; H: 5.4 +/- 1.4 nmol/mg/min). This is then followed by the decreased calcium channel receptor binding. However, the rate and the extent of depression in Ca2+-ATPase activity are much greater than that of Ca2+ channel receptor binding. Since alteration of Ca2+-ATPase is accompanied by an increase in intracellular Ca2+ concentration and there is a temporal association with the onset of myocardial lesions in the hypertensive rats, it is suggested that elevated intracellular calcium concentration as a result of altered Ca2+-ATPase activity may play a significant role in the development of hypertensive cardiomyopathy.
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PMID:Altered calcium regulation in the cardiac plasma membrane in experimental renal hypertension. 284 6

The influence of a 6-week treatment of female Wistar rats with one-kidney, one clip (1-K, 1 C) renal hypertension, with the calcium antagonist nifedipine on plasma volume, red cell Na+ handling and plasma atrial natriuretic peptide immunoreactivity (ANP-IR) was studied. Measurements were performed at 2 and 6 weeks after surgery. In 1-K, 1 C rats plasma volume was increased and red cell Na+ pump activity was reduced only after 2 weeks. Blood pressure, heart weights and plasma ANP were massively increased after both 2 and 6 weeks. 1-K, 1 C-rats treated with nifedipine had normal plasma volume, plasma ANP, and red cell Na+ pump activity in comparison with sham-operated rats. Increases in blood pressure and heart weights were attenuated. It is concluded that 1-K, 1 C hypertension in the rat is associated with cardiomegaly, rise in plasma ANP, initial hypervolemia and depression of the membrane Na+ pump. Nifedipine prevents the occurrence of hypervolemia and secondary phenomena such as rises in plasma ANP and cardiomegaly. This may play an important contributory role in the prevention of pathological sequelae.
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PMID:Modulation by chronic nifedipine of plasma atrial natriuretic peptide, cell Na+ transport and plasma volume in rats with renal hypertension. 284 89

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

In normotensive, barodenervated rats and those with experimental renal hypertension, arterial BP, heart rate and behaviour were recorded during aversive emotional stress. Cardiochronotropic component of the baroreceptor reflex and the activity of the energy metabolism enzymes were tested in structures of the medulla oblongata. The depression of the baroreceptor reflex in hypertensive rats was accompanied by no significant changes of enzymatic activity in the nucleus tractus solitarii but led to biphasic reactions of the BP during emotional stress. A possible role of the baroreceptor reflex suppression in genesis of hypertension is discussed.
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PMID:[Character of the baroreceptor reflexes in experimental arterial hypertension]. 324 78

The changes of the anterior cerebral artery/olfactory artery junction, one of the favorite sites of aneurysm formation, in rats treated with unilateral ligation of the common carotid artery and renal hypertension were investigated by light microscopy. The initial changes of aneurysm occurred not at the apex itself, but on the distal side of the major branch adjacent to the apex, at the intimal pad and the neighboring distal portion. Here the internal elastic lamina showed various degenerative changes and disappearance. The neighboring distal portion adjacent to the intimal pad showed a shallow depression associated with a thinning of the media due to a decrease of medial smooth muscle cells in number even in some control animals. Such degenerative changes of the internal elastic lamina and medial smooth muscle cells caused by hemodynamic stress due to branching structure, including intimal pads, augmented by the experimental treatment, are supposed to be the basis for aneurysm formation.
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PMID:Early changes of experimentally induced cerebral aneurysms in rats. Light-microscopic study. 376

Alterations in the number and reactivity of thymic and splenic lymphocytes were studied during the development of experimental renal hypertension in Sprague-Dawley rats. The mitotic responses of thymocytes and splenic T and B lymphocytes were tested by the T cell mitogen concanavalin A and the B cell mitogen dextran sulfate 3, 8, 12, and 36 days after the initiation of hypertension. At 3 days, hypertensive rats showed a fourfold increase in plasma corticosteroid levels, marked thymic atrophy, and a 50% reduction in the total number of thymocytes. The mitotic reactivity of the cells remaining in the organ was depressed 60% when compared to sham-operated controls. At 8 days a similar reduction in thymus size was accompanied by similarly decreased lymphocyte populations. Twelve days after initiation of hypertension structural recovery of the gland, lymphoid proliferation, and slightly increased thymocyte populations were observed. Differences with sham-operated controls were, however, still remarkable. Hypertensive rats sacrificed at 36 days showed thymus hypertrophy, and the thymocyte populations were larger than those of sham-operated animals. Despite the fluctuations in the number of thymocytes registered during the development of renal hypertension, the impaired mitotic reactivity of these cells to concanavalin A was sustained throughout the 36 days of the experiment. A similar reduction in the total number of cells and a similar depression in T lymphocyte reactivity was observed in the spleen between 8 and 36 days of hypertension. In contrast, after an initial depressed response, splenic B lymphocytes showed a slight but sustained increase in reactivity throughout the entire experimental period. These results indicate that with evolving renal hypertension there is a reduction in the number of lymphocytes as well as a depression in the ability of the remaining T lymphocytes to react with concanavalin A. Since T lymphocytes are important regulators of immunological homeostasis, this reduction in T cell reactivity may suggest the existence of an immunological imbalance accompanying the development of experimental renal hypertension.
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PMID:Lymphoid alterations and impaired T lymphocyte reactivity in experimental renal hypertension. 698 32

From before treatment throughout its course a new hypotensive drug ebrantil was studied for clinical efficacy in 52 patients with essential, renal and thyrogenic arterial hypertension. Clinical instrumental and biochemical findings support the drug efficacy in management of a hypertensive crisis and sudden AF rise. The response was registered in 83.3% of the cases. A persistent hypotensive effect of 180 mg/day course ebrantil became obvious within the first week of the treatment, passing ahead of relevant changes in central hemodynamics and myocardial contractility. The drug acts by reducing both cardiac pre- and postload, the reduction being brought about due to diuretic effect. In response to AP decrease there was neither myocardial contractility depression nor reflex tachycardia. Psychoemotional testing confirmed the central effect of ebrantil promoting adaptation of patients to stress under long-term administration. The drug demonstrated good tolerance when used orally and intravenously. No bronchial pulmonary, carbohydrate and lipid metabolism, renal and hepatic function side effects were reported. 24-h AP monitoring proved ebrantil efficacy in essential and renal hypertension patients.
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PMID:[A clinical assessment of ebrantil efficacy in arterial hypertension patients]. 779 Dec 94


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