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 activities of the Na+--K+-ATPase, succinic dehydrogenase (SDH/, lactic dehydrogenase (LDH/ and glucose-6-phosphat dehydrogenase (G-6-PDH/ were studied in the cortex outer and inner medulla of the kidneys of rats with spontaneous hypertension (SHR) and were compared with those of control normotensive Wistar rats. The SHR aged 6--8 weeks had durint the prehypertensive and the early hypertensive stage the same enzymatic activities as control rats. Rats with a steady SH aged 16-22 weeks had low specific activity of the, Na+--K+-ATPase, SDH and LDH in the outer medulla. The latter can be associated with decreased intensity of the energy metabolism and a reduction of the active sodium transport in the ascending limb of the loop of Henle in the SHR rats and cold cause the phenomenon of exaggerated natriuresis characteristic of hypertension.
 ...
PMID:[Na+--K+-adenosine triphosphatase and some oxidoreductases in the kidney of rats with spontaneous hypertension]. 12 6

The rats with chronic renal hypertension caused by constricting one renal artery, exhibit a decrease in the activity of Na-K-ATPase in the outer medulla of the "untouched" kidney, as compared to this activity in the kidneys of intact normotensive rats and in the "untouched" kidney of the rats where renal artery constriction did not result in hypertension. There were no differences between the control normotensive Wistar rats and the spontaneously hypertensive rats (SHR) in the prehypertensive and early hypertensive stages (at the age of 6-8 weeks) as far as the activities of Na-K-ATPase and oxidoreductases (SDH and LDH) in the renal cortex, the outer and inner medulla are concerned. The spontaneously hypertensive rats with chronic hypertension had at the age of 16-20 and 27-29 weeks lower activity of Na-K-ATPase, SDH, and LDH in the outer renal medulla than the control normotensive Wistar rats. The experimental results indicate that in chronic arterial hypertension there is a decrease in the activity of Na-K-ATPase, in the outer renal medulla, which suggests a reduction in the resorpo sodium and water.
 ...
PMID:Na-K-adenosine triphosphatase in the kidney of rats with renal hypertension and spontaneously hypertensive rats. 13 Jun 15

The elevated blood pressure of spontaneously hypertensive rats (SHR) was further exacerbated by subjecting these animals to surgically induced adrenal-regeneration hypertension (ARH). When chronic abnormally high blood pressure had been in effect for 12 weeks, the animals were subjected to an acute and massive myocardial infarction with isoprenaline. Hypertensive but intact SHR survived better than ARH-treated animals. Circulating enzyme (CPK, SGOT, SGPT and LDH), lipid and glucose levels and BUN manifested much greater excursions commensurate with more extensive myocardial infarction in ARH-treated than in intact SHR. ARH-treated SHR displayed a high incidence of atrial and ventricular thrombi associated with frequent left ventricular aneurysm formation. It is suggested that the more extensive myocardial connective tissue and ground-substance degeneration in ARH-treated SHR is due to the impoverished steroidogenic capacity of their regenerated adrenal glands.
 ...
PMID:Myocardial infarction in spontaneously hypertensive rats with superimposed adrenal-regeneration hypertension. 50 86

Repeatedly-bred, male and female Sprague-Dawley rats which develop hyperglycemia, hyperlipidemia, hypertension, and arteriosclerosis spontaneously were killed at sequential time intervals, i.e., when the females had completed 1, 2, 3 and 4 pregnancies. The control breeders received no treatment; the experimental animals were given 113 mg of clofibrate/100 g of b.w., subcutaneously, daily, 5 times per week. Clofibrate-treated breeders manifested reduction in blood pressure and in the incidence and severity of arterial disease characteristic of repeatedly-bred rats. The aortic lesions of the clofibrate-treated breeders showed attenuation of the usual severe ground substance alterations, the degenerative changes in connective tissue elements, e.g., fibrosis and elastosis, and absence of calcification and cartilaginous metaplasia. Clofibrate-treated breeders did not show any unusual elevation in serum enzymes, e.g., CPK, SGOT, SGPT and LDH, or significant reduction of their hyperlipidemia. They manifested a definite reduction in adrenocortical and medullary histopathology and their circulating corticosterone levels were subnormal compared to non-treated breeders. It is suggested that the protective effect of clofibrate was mediated through its ability to block normal adrenal steroidogenic pathways rather than through its antilipemic action.
 ...
PMID:Clofibrate retardation of naturally-occurring arteriosclerosis in repeatedly-bred male and female rats. 66 83

27 aortic histoenzymatic activities and 6 aortic macromolecular substances were comparatively studied in spontaneous hypertensive rats (SHR) and normotensive Wistar rats (3, 5, 13 and 16 month-old). The earlier aortic changes (3rd month) were only histoenzymatic: 5 Nase and LDH were increased in the entire aorta: some oxido-reductases increase near the intima. These early minor changes might represent some of the factors of the functional disturbance of the arterial smooth muscle cell. At the stage of stable hypertension (5th-13th month) two lesion patterns were seen: 1) metabolic: increase of the histoenzymatic activities involved in lipolysis, GAG anabolism, glycolysis, cell respiration, energizing metabolism and nucleotides-esterolysis. 2) Structural: cell hypertrophy and hyperplasia, interstitial fibrosis. The stimulus of the metabolic changes seems to be dual: 1) the hypertensive factor acting upon smooth muscle cells and/or vasa vasorum. 2) The intraarterial pressure increasing endothelial crossing and stimulating myocyte contraction. The structural change is more probably the reaction to elevated pressure; it has led to diffuse medial thickening providing a balance between hypertension and arterial wall stress. On the 16th month, the cell reaction developed in two ways: 1) increase of metabolic and morphogenetic activation of some cells. 2) irreversible degeneration in some other cell groups (media necrosis, cicatricial fibrosis, decrease of oxidoreductases and lipolytic activities, increase of lysosomal enzymes). Aortic lesions during spontaneous hypertension were less dramatic and occurred later than after experimental hypertension. Some of the observed histometabolic changes might lead to maintenance and worsening of hypertension.
 ...
PMID:[Hypertensive arteriopathy: aortic histo-metabolic changes during postnatal ontogenesis in spontaneous hypertensive rats (Okamoto-Aoki strain) (author's transl)]. 78 45

Adrenal regeneration hypertension (ARH) was induced in virgin and breeder, spontaneously hypertensive (SHR) and Sprague-Dawley (SD) rats. The blood pressure of the previously normotensive, virgin, SD rats and the SD breeder rats with preexistent mild hypertension became greatly elevated. ARH caused an increase in the preexisted severe hypertension in SHR virgin and breeder rats. Serum enzymes, e.g., CPK, SGOT and LDH, were greatly elevated concomitant with the finding of old and new foci of myocardial necrosis. ARH produced a dichotomous metabolic effect, i.e., elevated cholesterol, glucose, and corticosterone levels in SD rats but reduced levels in SHR rats. The zonae glomerulosae of the the regenerated adrenal glands of SD rats were devoid of lipid whereas the zonae glomerulosae of SHR rats were full of lipid. Intact SHR breeder rats develop arterial lesions confined to their reproductive organs but after ARH treatment, they were found to have aortic, coronary and renal arterial lesions which were similar to those which occur, spontaneously, in SD breeder rats. It is suggested that changes in the spectrum of adrenal steroids produced during ARH may contribute to the diverse metabolic changes and the alterations in the usual cardiovascular degenerative changes found in these two strains.
 ...
PMID:Comparative effects of adrenal regeneration hypertension on non-arteriosclerotic and arteriosclerotic Sprague-Dawley vs spontaneously hypertensive rats. 83 44

Repeatedly bred male rats which develop arteriosclerosis spontaneously were subjected to unilateral nephrectomy, 1% saline drinking water, and 2 mg subcutaneous injections of deoxycorticosterone acetate per animal weekly for 7 weeks to induce severe hypertension (+/- 175 mmHg systolic). Acute cerebral ischemia was induced by ligating one carotid artery. Two days later, experimental animals were subjected to acute myocardial ischemia by injecting them subcutaneously with a single dose of isoproterenol (25 mg/100 g body weight). All of the experimental animals died within 4 hours of the injection of isoproterenol. During this same period, blood pressure, body weight, thymus, kidney, and testicular weights were reduced, whereas heart and adrenal gland weights increased markedly. Serum enzymes (CPK, SGOT, and LDH), lipids (triglycerides and free fatty acids), glucose, BUN, and corticosterone rose progressively. Fatty infiltration of the liver, adrenal hyperplasia, myocardial thrombi, renal degenerative changes, and cerebral edema became progressively more severe. A hypothalamic-pituitary-adrenal axis component may be involved in the reaction to the stress of acute cerebral or myocardial ischemia, which is intensified when the two ischemias are combined, and chronic hypertension may exacerbate both.
 ...
PMID:Acute cerebrovascular and myocardial ischemia superimposed upon chronically hypertensive and arteriosclerotic male Sprague-Dawley rats. 90 14

Healthy virgin and breeder rats (Sprague-Dawley) with naturally occurring hypertension and arteriosclerosis were fed 5% oxonic acid and 1% uric acid added to their regular diet for 30 days. Although rats are able to convert uric acid into excretable allantoin, abnormal urinary and serum urate levels appeared. Males and females, virgins and breeders, differed in the severity of their increased urate levels. Animals with elevated urate levels developed hypertension, hyperglycemia, and hypertriglyceridemia, with only slight changes in cholesterol and free fatty acids. The kidneys were greatly enlarged and manifested medullary streaking indicative of urate deposits but were free of significant damage; BUN levels in these animals were abnormally high. Adrenal glands were reduced in size and depleted of lipid, circulating corticosterone levels were subnormal, and thymi were involuted. Serum enzymes CPK and LDH were greatly increased, whereas SGOT and SGPT levels were not elevated. The abnormal urate levels did not induce de novo arterial disease in the formerly healthy virgin rats and did not cause exacerbation of the pre-existing, naturally occurring arteriosclerosis characteristic of repeatedly bred rats. It is suggested that Sprague-Dawley rats are endowed with an especially efficient hepatic and renal capacity to metabolize uric acid. Increased urate levels in rats may have some direct metabolic relationship to the production of hypertension, hyperglycemia, and hypertriglyceridemia.
 ...
PMID:Effect of increased serum urate levels on virgin rats with no arteriosclerosis versus breeder rats with preexistent arteriosclerosis. 92 65

The authors examined dynamicaly from the third day to the third month the activity of enzymes, participating in glycolysis (ALD, PK, LDH), pentosemonophosphate shunt (G6P-DH), citric cycle (MDH, INDH) in the myocardium of rats with hypertension, induced by the method of Selye, modified by Kolarova. There were phase changes in enzymatic activity in the myocardium, manifested at the first stages by lowering (LDH, ALD, INDH) or elevation (MDH, PK, G6-DH). The activity of all examined enzymes was over that of the control group on the thirteenth day, while there were also oscillations on the nineteenth day. Only the actimity of G6-DH revealed a progressive elevation during the whole experimental period. The changes in the enzymic activity of the myocardium at the first stages were interpreted as a sign of nonspecific adaptation to the changed conditions of heart activity. The later changes were manifestations of the disturbances at various metabolic links, which were unevenly involved in the processes of myocardial hypertrophy.
 ...
PMID:[Changes in myocardial activity of several enzymes of glycolysis, the tricarboxylic acid cycle and pentosephosphate shunt in rats with experimental hypertension]. 101 10

The study was carried out on rats of the Wistar strain with experiments hypertension by the method of Selye, modified by Kolarova. These authors examined the activity of the enzymes of protein metabolism (GOT, GPT, AP), of glycolysis (ALD, LDH, alpha-HBDH) and of the citric cycle (MDH) in the left and right kidney at various intervals after modeling the process (3th, 15th, 30th and 90th day). The activity of the enzymes of the glycolytic chain and the cycle of Krebs in the left kidney was lowered at all stages of the experiment. Transaminase activity diminished progressively. Such a dynamics revealed the activity of adenosine phosphate as well. The activity of all examined enzymes of the right kidney showed phase changes-after initial elevation on the third day there was a lowering at the later stages of the experiment. The altered activity off the left kidney was connected with the disturbed vascularization with subsequent metabolic changes. The changes in the enzymic activity in the right kidney were assumed as a consequence of the occurred adaptive hyperfunction.
 ...
PMID:[Changes in renal enzyme activity in rats with experimental hypertension]. 102 9


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