Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intestinal Ca2+ malabsorption has been described in spontaneously hypertensive rats (SHRs), but the molecular basis for this defect is unknown. In this study, we measured intestinal alkaline phosphatase and vitamin D-dependent Ca(2+)-binding protein (calbindin-D9k), two proteins implicated in the active pathway of intestinal Ca2+ absorption. Both proteins were measured in the small intestines of SHRs and their normotensive controls, Wistar-Kyoto rats, before, during, and after development of hypertension (4, 9, 14, 18, and 28 wk of age). At all ages, alkaline phosphatase activity in duodenum (0-6 cm) was decreased by 30-57% (P less than 0.001) and by 47-75% in the 2nd intestinal segment (6-12 cm) (P less than 0.001-0.05). Calbindin-D9k was decreased similarly. The decreases of calbindin were statistically significant (P less than 0.001-0.05) in the duodena at 4, 14, 18, and 28 wk (9-30% decreases) and in the 2nd segment at 4, 14, and 18 wk (38-69% decreases; P less than 0.001-0.005). Decreased calbindin in SHRs was documented in animals from two suppliers. The deficiencies of calbindin-D9k and alkaline phosphatase could not be attributed to malnutrition or to a generalized brush-border defect as indicated by body weights and the intestinal marker enzyme sucrase. Although calbindin-D9k was decreased in young SHRs, the serum 1,25-dihydroxycholecalciferol [1,25(OH)2D3] was increased by 59 and 129% in 4- and 9-wk-old SHRs (P less than 0.001), respectively; by contrast, serum 1,25(OH)2D3 was unchanged or decreased in older SHRs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intestinal vitamin D-dependent calbindin-D9k and alkaline phosphatase in spontaneously hypertensive rats. 203 38

Alkaline phosphatase, sucrase, Na+,K+-ATPase and Mg2+-ATPase specific activities of crude membrane fractions, prepared from duodenal, jejunal, ileal and colonic mucosa, have been estimated in three types of hypertensive rats: the spontaneously hypertensive rat (SHR), the DOCA-saline treated rat and the renovascular rat (Goldblatt one-kidney, one-clip rat; 1K-1C). Alkaline phosphatase and sucrase specific activities have been measured in purified jejunal brush-border membranes. When compared with its normotensive age-matched control (WKY rat), the SHR has a lower activity of alkaline phosphatase in duodenal and jejunal crude membrane fractions, whereas a higher activity in colonic Na+,K+-ATPase is recorded. In purified jejunal brush-border membranes, lower alkaline phosphatase activity and higher sucrase activity were found. These differences occur in the young prehypertensive SHR as well as in the adult animal. In the DOCA-treated rat, the only significant alteration in crude membrane fractions is a decreased Mg2+-ATPase activity at all regions of intestinal mucosa. In purified jejunal brush-border membranes both alkaline phosphatase and sucrase activities are increased at 4 or 7 weeks but especially at 13 weeks of hypertension. In the 1K-1C rat, no significant modification appears in crude membrane fractions or in purified jejunal brush-border membranes, but a decrease in alkaline phosphatase and in sucrase activities is probable after 13 weeks of hypertension. Since alterations of the intestinal enzymes are different in the three types of hypertensive rats it is concluded that the changes are not secondary to the hypertension condition. In the SHR, these alterations are present in the young prehypertensive animal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alterations of intestinal membrane-bound enzymes in three types of hypertensive rats. 301 51

Recently, hypertension research has focused on altered cytosolic free Ca2+, [Ca2+]i, in cells of spontaneously hypertensive rats (SHR). In this work, a mechanism(s) responsible for regulating [Ca2+]i was studied with duodenal epithelial cells isolated from SHR and their control, normotensive Wistar-Kyoto rats (WKY). The equal specific activity of sucrase, an enzyme characteristic of microvilli, in both mucosal scrapings and isolated cells from SHR and WKY suggested that mucosal density of enterocytes was not largely different between the two strains. [Ca2+]i of the isolated cells was estimated with fura-2. Upon incubation in the presence of CaCl2, [Ca2+]i increased to a larger extent in SHR than in WKY cells. Ca2+ efflux based on measurements of [Ca2+]i was decreased in SHR cells. Correspondingly, it was found that 45Ca efflux at 10 sec was lower for SHR cells than for WKY cells. Specific activities of Ca(2+)-stimulated and Ca2+/calmodulin-stimulated ATPases in basolateral plasma membrane preparations were reduced in SHR cells. These results indicated that Ca2+ efflux was decreased by reduction in Ca(2+)-pumping ATPase activity in SHR enterocytes.
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PMID:Decreased calcium pump activity in duodenal epithelial cells from spontaneously hypertensive rats. 839 87

The obese spontaneous hypertensive rat/NIH-corpulent (SHR/N-cp) rat exhibits some of the metabolic and pathologic alterations associated with non-insulin-dependent diabetes mellitus and hypertension. The current study was conducted to investigate the influence of phenotype (ob versus In) and source of dietary carbohydrate (sucrose versus starch) on intestinal sucrase, maltase, lactase, and alkaline phosphatase activity in SHR/N-cp rats. For 3 months, lean and obese male SHR/N-cp rats were fed isocaloric diets containing as the sole source of carbohydrate either 54% cooked corn starch or sucrose. Serum and urine markers for diabetes were observed in obese rats. Wet weight and length of intestines were significantly increased in obese rats compared with lean littermates. Among the intestinal enzymes measured, statistical tests confirmed that sucrase activity was significantly increased (P < 0.01) by both phenotype (ob > In) and feeding a sucrose diet. Diet alone (sucrose > starch) significantly increased (P < 0.05) maltase activity in obese rats, but had no effect on lean rats. Lactase activity was significantly higher (P < 0.05) in obese sucrose-fed rats compared with obese starch-fed and/or lean littermates. Statistical tests revealed that intestinal alkaline phosphatase activity was significantly altered (P < 0.05) by both phenotype and diet. Intestinal alkaline phosphatase was higher in starch-fed lean rats compared with lean littermates fed sucrose and to starch or sucrose-fed obese rats. These results are not indicative of a simple, nonspecific increase in intestinal enzyme activity, since the effects observed in intestinal alkaline phosphatase contrast the effects observed in intestinal sucrase, maltase, and lactase activity. These results indicate that both phenotype and diet alter structural and enzymatic intestinal activities of SHR/N-cp rats. Distinct variations in the observed intestinal enzymatic activities suggest that these enzymes are under the control of genetic, hormonal, and dietary factors. Rationale for these differences are discussed.
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PMID:Effect of dietary carbohydrate and phenotype on sucrase, maltase, lactase, and alkaline phosphatase specific activity in SHR/N-cp rat. 843 90

The current studies explore the effect of hypertension on D-glucose transport into jejunal brush-border membrane vesicles (BBMV). Spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats, as a control group, were used. The purity of the BBMV from both groups of animals was validated by the finding that the specific activity of brush-border enzyme marker, sucrase, was severalfold greater in membrane vesicles compared with corresponding values in mucosal homogenate. D-glucose uptake was Na+ dependent in both groups of animals, with a transient increase in the intravesicular concentration of D-glucose. However, the initial rate and the magnitude of the accumulation of Na+-dependent D-glucose was significantly higher in SHR compared with WKY rats. In order to investigate the mechanism(s) for the increase in Na+-dependent D-glucose transport in SHR, several experiments were performed: (1) an experiment that indicated 22Na uptake, as an indicator for Na+ permeability, was similar between SHR and WKY rats, (2) kinetic studies that indicated that Vmax values of SHR were significantly greater that those of WKY rats. In contrast, similar Km values for glucose were found between SHR and WKY rats, (3) Na+-dependent phlorizin binding measurements that were not altered by hypertension and (4) a study of the brush-border membrane lipid composition that showed a significant increase in the free cholesterol/phospholipid ratio in SHR. We conclude that altered membrane cholesterol content and consequently altered lipid fluidity could be, at least in part, responsible for the observed increase in Na+-dependent D-glucose transport in SHR.
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PMID:Increased sodium-dependent D-glucose transport in the jejunal brush-border membrane of spontaneously hypertensive rat. 866 84

Intakes of some macronutrients can comprise risk factors for life-style-related diseases such as obesity, hyperlipidemia, diabetes, hypertension, and atherosclerosis. In this study, we examined the effects in C57BL/6J mice of consuming excess fat or sucrose for a long period of time (55 wk). Another group of mice consumed a low-fat, low-sucrose (LL) diet. Mice fed the high-fat (HF) diet gained weight and developed hyperlipidemia and hyperleptinemia. At 25 wk, but not at 55 wk, hepatic glucose-6-phosphatase (G6Pase) activity of the mice fed the high sucrose (HS) diet was greater than that of mice fed the LL or HF diet. Those fed the HS diet were not obese and had greater hepatic lipogenic and gluconeogenic enzyme activities. The HF and HS diets resulted in different types of glucose intolerance. In an oral glucose tolerance test, mice fed the HF diet had a delay in the clearance of glucose compared with those fed the LL diet, perhaps due to the peripheral insulin resistance that resulted from higher levels of circulating free fatty acids. Feeding the HS diet for 55 wk induced hyperglycemia 10 min after oral glucose administration, although blood glucose declined rapidly after i.p. insulin injection. This finding suggests that the effects of chronic HS diet intake may be due to the reduction in early insulin secretion from pancreatic islets and the increase in sucrase activity in the small intestine. It is important to consider the effects of macronutrients in lean as well as obese mice to clarify the pathogenesis of the metabolic disorders.
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PMID:Chronic intake of high-fat and high-sucrose diets differentially affects glucose intolerance in mice. 1648 28

Buckwheat has been shown to have various health benefits such as reduction of hypertension and improvement of hypercholesterolemia; however, its effect on diabetes has not been fully elucidated. In this study, buckwheat bran extracts (BBE) inhibited sucrase activity in vitro more effectively than buckwheat. Balb/c mice pretreated with BBE showed dose-dependent reductions of blood glucose, greater than those observed with control mice, within 60 min following oral sucrose administration. Blood glucose levels in mice pretreated with buckwheat extracts were also significantly lower compared to those in control mice within 30 min following oral administration of sucrose. However, rutin, one of the abundant polyphenols of BBE, did not lower blood glucose level. Our data indicate that components of BBE other than rutin have inhibitory activity against sucrase in vivo. These results suggest that BBE could have beneficial effects on diabetes.
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PMID:Extracts of common buckwheat bran prevent sucrose digestion. 2247 88