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

The effect of chronic physical exercise on the development of hypertension was measured in spontaneously hypertensive rats (SHR) and their progenitor normotensive wistar-kyoto controls (WK). Starting 4--5 weeks after birth groups of rats were subjected to swimming exercise 1 h x day-1, 4 days x week-1 for a total period of 11 weeks. Control rats were handled daily without exercise. Both in trained SHR and WK a significant delay in increase in body weight was observed. Physical training caused a small, but significant (P less than 0.001) reduction in systolic blood pressure of SHR, whereas it did not affect blood pressure in WK. Heart rate was significantly (P less than 0.001) lower in both trained SHR and WK than in their non-trained controls. At the end of the training period the degree of training was tested by measuring muscle cytochrome oxidase activity and relative heart weight. Cytochrome oxidase activity in gastrocnemius muscle was higher in the trained animals, although the difference was only significant (P less than 0.05) for WK. Training also caused a significant (P less than 0.01) increase in the ratio heart weight to body weight in WK. Both trained and non-trained SHR have a ca. 25% higher relative heart weight than WK controls. SHR hearts did not further hypertrophy as a consequence of physical exercise. These data indicate that swim training induces a trained state in both SHR and WK. Moreover, this form of training causes a slight, but significant attenuation of the development of hypertension in SHR.
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PMID:Effect of physical training on the development of hypertension in the spontaneously hypertensive rat. 22 25

Parameters of tissue oxygen regime measured by polarography and serum lactate dehydrogenase (LDG) and cytochrome oxidase (CO), oxidation-reduction enzymes, were studied in 23 patients with stable hypertension of various hemodynamic types. The nature of the tissue oxygen regime and changes observed in the isoenzymic spectra of LDG and CO were found to be associated with BP levels, hemodynamic types and BP reduction degree. The time course of these values may be useful in assessing whether the antihypertensive therapy is appropriate and in determining an optimal level of BP decrease.
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PMID:[Evaluation of the adequacy of hypotensive therapy based on the status of the tissue oxygen system and serum lactate dehydrogenase and cytochrome oxidase activities in patients with hypertension]. 285 75

The influence of endurance training on functional capacity [maximal O2 consumption (VO2 max)], caudal arterial blood pressure, and myocardial capillary density were investigated in normotensive rats and rats made hypertensive using the two-kidney one-clip approach (Goldblatt's hypertension). Male Sprague-Dawley rats were assigned to sham (N: 120-140 mmHg), moderately hypertensive (MH = 0.30-mm clips, 150-170 mmHg), or severely hypertensive (SH = 0.25-mm clips, 190-230 mmHg) groups. Rats designated to be runners (T) were exercised on a motor-driven treadmill equal to 50-70% of their VO2 max values for 8-12 wk. Compared with their nontrained (NT) controls, training was associated with significantly higher VO2 max values (12-15%) and muscle cytochrome-c oxidase activities (33-78%). Resting systolic blood pressure was not significantly changed in the N-and MH-T subgroups; however, it was 20-30 mmHg higher in the SH-T subgroup. Mean absolute heart weight for only the N-T group was significantly heavier than their NT controls. However, the mean predicted heart weights (heart wt = 0.639 X body wt of N-NT + 0.001 g) of the two SH groups were significantly higher than expected. The SH-T group had a lower (11%) subepicardial capillary density mean than its NT control and significantly fewer capillaries in the subendocardial region than the other five subgroups. It was concluded that moderate exercise training appeared to be detrimental to rats with severe hypertension because it increased resting blood pressure and decreased myocardial capillary density, even though it improved their functioning capacity.
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PMID:Exercise training and its effects with renal hypertensive rats. 299 59

A study of associations between lactate dehydrogenase and cytochrome oxidase isoenzymes and total cytochrome oxidase activity, on the one hand, and the type of arterial hypertension, the magnitude of blood pressure and its response to treatment, on the other, was carried out in 143 patients with varying stages of essential hypertension and in renal hypertension. The examined parameters were found to be valuable indicators of adequate hypotensive effect and an optimum BP fall. A 20-24% BP drop below the baseline is optimal for patients with renal hypertension. A 30% BP drop is acceptable for patients with stable essential hypertension. Attaining normal BP level is acceptable and desirable for cases of labile essential hypertension.
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PMID:[Criteria for assessing the adequacy of a hypotensive effect by data on the lactate dehydrogenase and cytochrome oxidase isoenzyme spectra of patients with different forms of arterial hypertension]. 303 54

In order to test the effect of aerobic training on blood pressure, and to examine the putative mechanisms involved, stroke-prone spontaneously hypertensive rats (SHR-SP), borderline hypertensive rats (BHR), and Wistar-Kyoto control rats (WKY) were swim-trained for up to 1.5 h twice-daily for 22 weeks. The BHR were F1 back-cross SHR-SP, WKY. A training effect was observed in the trained rats compared to controls, as demonstrated by slower heart rates, heavier hearts and increased cytochrome oxidase activity in their skeletal muscle. Trained SHR-SP and BHR had significantly lower blood pressures at the end of the intervention period (approximately 10 mmHg) compared to controls. Acute increases in blood pressure with swimming were less in trained than in untrained rats. Trained rats had higher extracellular sodium values than untrained rats. Further, trained SHR-SP and BHR had lower intra-erythrocyte sodium values than controls. Increases in corticosterone, epinephrine and norepinephrine with swimming were less in trained rats than in controls. We conclude that exercise conditioning ameliorates hypertension in rats. The mechanism may involve an effect on cation transmembrane transport, as well as decreased, adrenosympathetic tone. Moreover, these effects may be related.
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PMID:Blood pressure, electrolyte and adrenal responses in swim-trained hypertensive rats. 361 73

The metabolic activity in the brains of adult spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY), and Wistar (W) rats was assessed before and after fasting using cytochrome oxidase (COX) histochemistry. Before fasting, metabolic activity in the paraventricular (PVH) and supraoptic (SON) nuclei of the hypothalamus in SHR was greater than in control rats. Fasting elicited a decrease in arterial pressure (AP) in SHR and WKY; in SHR the decrease in AP was accompanied by a decrease of metabolic activity in the PVH and SON. The findings of this study support the hypothesis that the PVH and SON are involved in the hypertension and in the increased levels of sympathetic nervous activity and vasopressin production known to occur in SHR. In addition, the PVH and possibly the SON may be involved in the suppression of sympathetic nervous system activity and the lowering of arterial pressure which are associated with fasting.
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PMID:Cytochrome oxidase activity in the hypothalamus of SHR and normotensive rats before and after fasting. 609 37

It is not known why alcohol ingestion poses a risk for development of hypertension, stroke and sudden death. Of all drugs, which result in body depletion of magnesium (Mg), alcohol is now known to be the most notorious cause of Mg-wasting. Recent data obtained through the use of biophysical (and noninvasive) technology suggest that alcohol may induce hypertension, stroke, and sudden death via its effects on intracellular free Mg2+ ([Mg2+]i), which in turn alter cellular and subcellular bioenergetics and promote calcium ion (Ca2+) overload. Evidence is reviewed that demonstrates that the dietary intake of Mg modulates the hypertensive actions of alcohol. Experiments with intact rats indicates that chronic ethanol ingestion results in both structural and hemodynamic alterations in the microcirculation, which, in themselves, could account for increased vascular resistance. Chronic ethanol increases the reactivity of intact microvessels to vasoconstrictors and results in decreased reactivity to vasodilators. Chronic ethanol ingestion clearly results in vascular smooth muscle cells that exhibit a progressive increase in exchangeable and cellular Ca2+ concomitant with a progressive reduction in Mg content. Use of 31P-NMR spectroscopy coupled with optical-backscatter reflectance spectroscopy revealed that acute ethanol administration to rats results in dose-dependent deficits in phosphocreatine (PCr), the [PCr]/[ATP] ratio, intracellular pH (pHi), oxyhemoglobin, and the mitochondrial level of oxidized cytochrome oxidase aa3 concomitant with a rise in brain-blood volume and inorganic phosphate. Temporal studies performed in vivo, on the intact brain, indicate that [Mg2+]i is depleted before any of the bioenergetic changes. Pretreatment of animals with Mg2+ prevents ethanol from inducing stroke and prevents all of the adverse bioenergetic changes from taking place. Use of quantitative digital imaging microscopy, and mag-fura-2, on single-cultured canine cerebral vascular smooth muscle, human endothelial, and rat astrocyte cells reveals that alcohol induces rapid concentration-dependent depletion of [Mg2+]i. These cellular deficits in [Mg2+]i seem to precipitate cellular and subcellular disturbances in cytoplasmic and mitochondrial bioenergetic pathways leading to Ca2+ overload and ischemia. A role for ethanol-induced alterations in [Mg2+]i should also be considered in the well-known behavioral actions of alcohol.
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PMID:Role of magnesium and calcium in alcohol-induced hypertension and strokes as probed by in vivo television microscopy, digital image microscopy, optical spectroscopy, 31P-NMR, spectroscopy and a unique magnesium ion-selective electrode. 784 86

Oxygen consumption and cytochrome oxidase activity of aortas of rats with experimental hypertension were found to be higher than the corresponding values for aortas of normotensive animals. The higher metabolic activity of aortas of hypertensive animals appeared to be due both to an increase in the proportion of muscle cells to connective tissue fibers and to a higher activity of the intracellular portion of the tissue.
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PMID:The respiration and cytochrome oxidase activity of rat aorta in experimental hypertension. 1362 Aug 48

Angiotensin II can induce oxidant stress by stimulating vascular superoxide production. Hypertension promotes mitochondrial function decline in brain, liver and heart. The aim of this study was to investigate whether a) hypertension is associated to kidney mitochondrial dysfunction, and b) angiotensin II blockade can reverse potential mitochondrial changes in hypertension. Four-month-old male spontaneously hypertensive rats (SHR) received drinking water containing candesartan (7.5 mg/kg/day, SHR+Cand), or no additions (SHR) for 4-months. Eight-month-old Wistar-Kyoto rats (WKY), that received water with no additions, were used as control. Systolic blood pressure, proteinuria, cortical glomerular area, and glomerular and tubulointerstitial alpha-smooth muscle actin labeling, were significantly higher, and creatinine clearance was significantly lower, in SHR relative to WKY and SHR+Cand. In SHR, kidney mitochondria membrane potential, and nitric oxide synthase and cytochrome oxidase activities were significantly lower than in WKY and SHR+Cand. In SHR, mitochondrial hydrogen peroxide production was significantly higher than in WKY and SHR+Cand. The results suggest that, in hypertension, increased mitochondrial oxidant production may mediate kidney mitochondria dysfunction. Candesartan preserved mitochondrial function, probably favoring the maintenance of adequate cellular and tissue function in the kidney. The known renal protective effects of candesartan in hypertension may be related to the improvement of mitochondrial function. This may be an additional or alternative explanation for some of the beneficial effects of AT1 receptor antagonists.
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PMID:Angiotensin II blockade improves mitochondrial function in spontaneously hypertensive rats. 1630 82

Mitochondrial dysfunction is associated with cardiovascular damage; however, data on a possible association with kidney damage are scarce. Here, we aimed at investigating whether 1) kidney impairment is related to mitochondrial dysfunction; and 2) ANG II blockade, compared with Ca2+ channel blockade, can reverse potential mitochondrial changes in hypertension. Eight-week-old male spontaneously hypertensive rats (SHR) received water containing losartan (40 mg.kg-1.day-1, SHR+Los), amlodipine (3 mg.kg-1.day-1, SHR+Amlo), or no additions (SHR) for 6 mo. Wistar-Kyoto rats (WKY) were normotensive controls. Glomerular and tubulointerstitial damage, systolic blood pressure, and proteinuria were higher, and creatinine clearance was lower in SHR vs. SHR+Los and WKY. In SHR+Amlo, blood pressure was similar to WKY, kidney function was similar to SHR, and renal lesions were lower than in SHR, but higher than in SHR+Los. In kidney mitochondria from SHR and SHR+Amlo, membrane potential, nitric oxide synthase, manganese-superoxide dismutase and cytochrome oxidase activities, and uncoupling protein-2 content were lower than in SHR+Los and WKY. In SHR and SHR+Amlo, mitochondrial H2O2 production was higher than in SHR+Los and WKY. Renal glutathione content was lower in SHR+Amlo relative to SHR, SHR+Los, and WKY. In SHR and SHR+Amlo, glutathione was relatively more oxidized than in SHR+Los and WKY. Tubulointerstitial alpha-smooth muscle actin labeling was inversely related to manganese-superoxide dismutase activity and uncoupling protein-2 content. These findings suggest that oxidant stress is associated with renal mitochondrial dysfunction in SHR. The mitochondrial-antioxidant actions of losartan may be an additional or alternative way to explain some of the beneficial effects of AT1-receptor antagonists.
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PMID:Renal mitochondrial dysfunction in spontaneously hypertensive rats is attenuated by losartan but not by amlodipine. 1641 Apr 2


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