Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cells were isolated from the outer medulla of the rabbit kidney, primarily from the thick ascending limb of Henle's loop (mTALH). These mTALH cells are heavily invested with a cytochrome P450-linked monooxygenase that represents the third pathway by which arachidonic acid is metabolized. After cell separation, approximately 80% of the cells proved to be mTALH in origin, based on electron microscopic criteria and immunofluorescent localization of Tamm-Horsfall protein, a specific marker for mTALH cells. The specific activity of alkaline phosphatase, a marker for proximal tubular cells, decreased threefold after separation of mTALH cells from outer medullary cells, associated with a fourfold increase in the capacity of the separated mTALH cells to metabolize arachidonic acid. Incubation of mTALH cells with 14C-arachidonic acid resulted in formation of oxygenated metabolites, identified as two peaks (P1 and P2), which accounted for 30 to 40% of the recovered radioactivity. Formation of prostaglandin E2 and F2 alpha accounted for only 3 to 5%. The chromatographic retention times of P1 and P2 were different from products of lipoxygenases. An inhibitor of cytochrome P450-dependent enzymes, SKF-525A (50 microM), reduced product formation by mTALH cells by more than 70%, while induction of cytochrome P450 increased product formation. Formation of P1 and P2 by cell-free homogenates of mTALH was totally dependent on the presence of nicotinamide adenine dinucleotide phosphate, reduced form (NADPH), which suggests a NADPH-dependent cytochrome P450-linked monooxygenase pathway. Vasopressin and calcitonin (10(-10) M to 10(-7) M) stimulated release of arachidonic acid metabolites from mTALH cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:Renal arachidonic acid metabolism. The third pathway. 298 23

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

A 56-year-old female patient on verapamil for hypertension experienced two episodes of jaundice, pruritus and upper abdominal pain with transaminase elevated up to six-fold and alkaline phosphatase up to four-fold when inadvertently re-challenged with the drug. Liver biopsy showed marked cholestasis. Verapamil can occasionally cause mixed cytotoxic-cholestatic liver injury.
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PMID:Liver injury due to verapamil. 318 62

The vascular extracellular matrix (ECM) plays an important role in the histopathology of cerebral microcirculation, but its characterization is still incomplete. For that reason we investigated paraffin-embedded and cryostat sections of intracerebral and meningeal vessels from eight normotensive and six hypertensive humans using monospecific affinity-purified polyclonal antibodies against human/monkey amino-terminal procollagen I + III peptide (P I P, P III P), collagen IV (7-S and NC1 domains), VI, and laminin (P 1 fragment) by applying peroxidase-antiperoxidase- and alkaline phosphatase-antialkaline phosphatase techniques. In normotensives, laminin and collagen IV were codistributed in the basal lamina of meningeal and intraparenchymal vessels. Collagen VI was only present in the adventitia of meningeal vessels and larger intraparenchymal arteries and veins, whereas it was absent from cortical vessels including capillaries. Intensive staining for collagen VI was observed in the choroid plexus, the superficial glia and sheath of cranial nerves. In hypertensives, the basement membrane constituents laminin and collagen IV appeared ubiquitously increased. Here, collagen VI was also deposited in the broadened vascular intima and media of larger arteries and in cortical vessels. In both groups collagen VI and P III P appeared to be codistributed. Our results indicate that significant qualitative change sin ECM of cerebral blood vessels are taking place during the development of hypertension, such as (1) an atypical deposition or an increase of collagen VI which by interconnecting collagen fibrils (I and III) might exert a stabilizing (sclerosing) function in the ECM, and (2) a thickening of vascular basement membranes caused by an accumulation of its major components laminin and collagen IV.
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PMID:Altered expression of collagen type VI in brain vessels of patients with chronic hypertension. A comparison with the distribution of collagen IV and procollagen III. 323 76

To determine the factors associated with low-output left ventricular failure (LVF) in endstage renal disease (ESRD), we performed echocardiography and gated cardiac scan on 217 nondiabetic dialysis and transplant patients. The prevalence of low-output LVF (ejection fraction less than 55% and left ventricular end diastolic diameter greater than or equal to 5.5 cm) in dialysis patients was 18% and in transplant patients 2%. The 26 patients with LVF were compared to 52 controls without LVF, matched by age, sex and year of starting treatment for ESRD, but not for current ESRD therapy. Mean age was 55 +/- (SEM) 14 years; 73% of the patients in both groups were males. Duration of treatment for ESRD was 5.6 +/- 4.3 years in patients, compared to 5.1 +/- 4.1 years in controls. Significant differences between LVF patients and controls included current treatment (73% of cases were on hemodialysis and 8% were transplanted, compared to 48 and 42%; chi 2 = 9.9, p less than 0.01), high serum creatinine, smoking and high serum alkaline phosphatase. There were no differences for current blood pressure, proportion on treatment for hypertension, left ventricular wall thickness, symptomatic ischemic heart disease, proportion with functioning vascular access, degree of weight gain between dialyses, hemoglobin level or high transfusion requirement. Multiple logistic regression demonstrated the most significant and independent variables associated with LVF were high alkaline phosphatase (suggestive of hyperparathyroidism), smoking and high serum creatinine levels (reflecting degree of uremia). Dialysis patients with LVF (n = 23) were compared to dialysis patients who had normal echocardiograms (n = 29).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Low-output left ventricular failure in end-stage renal disease. 330 13

Twenty-seven patients with mild to moderate essential hypertension were randomized to receive therapy with either hydrochlorothiazide or diltiazem. After a placebo run-in period of 2 weeks, patients received increasing doses of either drug for 14 weeks. Those in whom hypertension was effectively controlled continued for 26 weeks of total treatment. Those not controlled, i.e. blood pressure greater than 140/90 mm Hg or less than 10 mm Hg reduction of pressure, were unblinded and crossed over to therapy with both drugs. Eleven of 14 patients (79%) were effectively treated with diltiazem alone, and 8 of 13 patients (62%) were effectively treated with hydrochlorothiazide alone. Supine blood pressures fell from 152 +/- 5/97 +/- 1 to 142 +/- 4/87 +/- 3 mm Hg in the 11 patients treated with diltiazem, from 152 +/- 2/99 +/- 1 to 134 +/- 3/88 +/- 2 mm Hg in the 8 patients treated with hydrochlorothiazide, and from 151 +/- 4/104 +/- 3 to 140 +/- 5/92 +/- 1 mm Hg in the 8 patients who received both drugs (p less than 0.01 for each group). Diltiazem patients had significant increases in alkaline phosphatase and urinary magnesium. Hydrochlorothiazide patients had increases in serum uric acid, serum globulin, CO2 content, and plasma renin activity. Serum potassium, serum chloride, urinary osmolality, and urinary calcium decreased after treatment with hydrochlorothiazide. Patients receiving both drugs had increases in serum glucose, serum BUN, serum uric acid, serum globulin, and CO2 content. These patients had decreased serum chloride and urinary calcium. Diltiazem monotherapy was comparable to hydrochlorothiazide in efficacy of lowering blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal-metabolic consequences of antihypertensive therapy with diltiazem versus hydrochlorothiazide. 332 Jul 20

Sixty-eight patients with mild primary hyperparathyroidism were studied for a mean period of 4.5 years (median 3.3). Seven of these patients presented with renal colic while the rest had no symptoms. There was no significant deterioration in mean serum creatinine, total calcium or ionized calcium concentrations during this period. No patient had progressive renal stone or parathyroid bone disease. Hypertension was defined as a systolic or diastolic blood pressure greater than one standard deviation from the age-sex mean, or if hypotensive drugs were required. Thirty-nine per cent were hypertensive at presentation and 42 per cent became hypertensive later. Four patients died from causes unrelated to hypercalcaemia and three required parathyroidectomy when serum calcium concentration rose above 3.0 mmol/l. Patients over 55 with mild asymptomatic primary hyperparathyroidism may be managed conservatively for several years without significant renal impairment, progressive stone disease, parathyroid bone disease or worsening hypercalcaemia. We suggest that observation in these patients could be restricted to six-monthly checks of physical state, blood pressure and serum biochemistry, particularly concentration of calcium creatinine and alkaline phosphatase.
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PMID:The conservative management of primary hyperparathyroidism. 345 52

The first reported Spanish family with autosomal dominant endosteal hyperostosis is presented and two members in two different generations studied. Neurological involvement with sensorineural hearing loss, chronic intracranial hypertension, and mild corticospinal tract abnormalities were found in one case with radiological evidence of progressive bone disease at follow-up. In addition to mild hydrocephalus, CT-scan of the head documented a reduction in size of the posterior fossa and encroachment of the foramen magnum. A pattern of selective increase in the bone fraction of serum alkaline phosphatase was also recorded. This family supports the view that severe forms of endosteal hyperostosis are not confined to the autosomal recessive variant, as individuals with the autosomal dominant form may also show relentless progression to neurological involvement during adulthood.
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PMID:Autosomal dominant endosteal hyperostosis. Report of a Spanish family with neurological involvement. 356 43

From 1965 to 1985, 412 patients were operated on for primary hyperparathyroidism (pHPT). Of these, 35 (8.7%) were without specific symptoms and findings. The follow-up investigations after six months to 14 years (median: 31 months) revealed a normalization of the preoperative pathological parameters of alkaline phosphatase, uric acid, creatinine and hypertension in the majority of patients apart from the improvement of their general condition. All patients were normocalcemic. According to these results, the indication for early surgical therapy of the asymptomatic pHPT is to be advocated in order to avoid long-term complications.
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PMID:[Asymptomatic hyperparathyroidism. An indication for surgery?]. 356 55

Activity of some enzymes in the cerebral cortex of rats with experimentally induced renal arterial hypertension (AH) was studied histochemically. Histologic data provide the evidence for the disturbances in water-salt metabolism in AH. Morphometric study revealed an increase in the specific volume of smaller microvessels and moderate decrease in the specific volume of bigger microvessels. Vascular markers show different time course of activity changes in AH: the activity of alkaline phosphatase increases, while that of alpha-glycerophosphate dehydrogenase remains unchanged. The development of AH is accompanied by the increase in succinic dehydrogenase activity and the decrease in the activity of lactate dehydrogenase in neurons. The changes in the neuron-capillary relationship arising in AH can be one of the possible pathogenetic factors in the pathologic process progression.
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PMID:[Characteristics of the morphofunctional status of the tissue in the rat cerebral cortex in experimental renal arterial hypertension]. 366 63


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