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

A case of beta galactosidase deficiency is described in a 20-month-old boy. The child was hospitalized at 4 months of age for malabsorption syndrome. Biopsies of the small intestine and liver were performed and electron microscopy of the liver specimens strongly suggested a gangliosidosis. The cytoplasm of macrophages, Kupffer cells and hepatocytes contained membrane-bound lysosomes with a granular, fibrillar appearance and tubular structures interpreted as ganglioside deposits. Enzymatic deficiency was confirmed by biochemical investigation of leukocytes from both the patient and members of his immediate family. Although visceromegaly is typical of Landing disease, symptoms of malabsorption and hypertension have not been reported in its course.
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PMID:Landing disease, GM1 generalized gangliosidosis, and malabsorption syndrome. 250 73

To determine whether or not the previously reported association between alcohol intake and high blood pressure is influenced by differential intake of calcium and potassium in drinkers compared with nondrinkers and to assess the magnitude of the independent contributions of alcohol, calcium, and potassium to blood pressure, these associations were evaluated in 7,011 men of Japanese descent. Categorical analyses and multiple linear regression techniques were used to test the hypotheses that alcohol, calcium, and potassium were independent predictors of blood pressure. Alcohol consumption above a threshold of approximately 20 ml/day was found to be positively, strongly, and independently correlated with systolic and diastolic pressures, and this effect was completely independent of the effects of calcium and potassium. Calcium and potassium intake were highly correlated (r = 0.59) and were inversely related to blood pressure, and their combined effect was greater than the effect of either alone. However, in the subgroup of moderate and heavier drinkers, only potassium was inversely related to blood pressure. This finding is compatible with previous reports of malabsorption and increased excretion of calcium at higher levels of alcohol intake, and it indicates that a small portion of the alcohol-induced blood pressure elevation may be mediated through calcium depletion. In the range of dietary intake in this cohort, the effect of alcohol on blood pressure was stronger than was either the separate or combined effects of calcium and potassium.
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PMID:Dietary alcohol, calcium, and potassium. Independent and combined effects on blood pressure. 276 13

A new family syndrome is described that affected three of seven siblings and another patient who had been abandoned at birth but came from the same area of France. All four patients were young women with a very peculiar phenotype, poikiloderma and greying of the hair, and idiopathic non-arteriosclerotic cerebral calcifications. Pathological studies demonstrated small-vessel hyalinosis due to basal membrane thickening, mainly in the digestive tract, kidneys and calcified areas of the brain. The clinical and biological expressions of these vascular changes varied. Peripheral retinal ischemic syndrome and chorioretinal scars were found in the ocular fundi of three patients. Malabsorption and protein-losing enteropathy was the main problem in all four, and was the cause of one patient's death. A subarachnoid hemorrhage due to a right sylvian aneurysm also occurred in two of the three sisters and was lethal for one. Nephropathy with renal failure and systemic hypertension is the major problem of the two surviving patients.
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PMID:Retinal and choroidal ischemic syndrome, digestive tract and renal small vessel hyalinosis, intracerebral calcifications and phenotypic abnormalities: a new family syndrome. 277

Magnesium is an important element for health and disease. Magnesium, the second most abundant intracellular cation, has been identified as a cofactor in over 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Approximately half of the total magnesium in the body is present in soft tissue, and the other half in bone. Less than 1% of the total body magnesium is present in blood. Nonetheless, the majority of our experimental information comes from determination of magnesium in serum and red blood cells. At present, we have little information about equilibrium among and state of magnesium within body pools. Magnesium is absorbed uniformly from the small intestine and the serum concentration controlled by excretion from the kidney. The clinical laboratory evaluation of magnesium status is primarily limited to the serum magnesium concentration, 24-hour urinary excretion, and percent retention following parenteral magnesium. However, results for these tests do not necessarily correlate with intracellular magnesium. Thus, there is no readily available test to determine intracellular/total body magnesium status. Magnesium deficiency may cause weakness, tremors, seizures, cardiac arrhythmias, hypokalemia, and hypocalcemia. The causes of hypomagnesemia are reduced intake (poor nutrition or IV fluids without magnesium), reduced absorption (chronic diarrhea, malabsorption, or bypass/resection of bowel), redistribution (exchange transfusion or acute pancreatitis), and increased excretion (medication, alcoholism, diabetes mellitus, renal tubular disorders, hypercalcemia, hyperthyroidism, aldosteronism, stress, or excessive lactation). A large segment of the U.S. population may have an inadequate intake of magnesium and may have a chronic latent magnesium deficiency that has been linked to atherosclerosis, myocardial infarction, hypertension, cancer, kidney stones, premenstrual syndrome, and psychiatric disorders. Hypermagnesemia is primarily seen in acute and chronic renal failure, and is treated effectively by dialysis.
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PMID:Magnesium metabolism in health and disease. 328 51

To evaluate factors that might be related to the pathogenesis of hypertension in spontaneously hypertensive rats (SHR), mineral balance studies were conducted in SHR and control Wistar-Kyoto (WKY) rats at the ages of 9, 13 and 16 wk. During the first balance period, before onset of hypertension, Na, Ca, Mg and P balances were all significantly more positive in SHR than in WKY rats. Percentage of absorbed Na excreted in urine was correlated with the rise in blood pressure of SHR but not of WKY rats during the first 4 wk of the study. At 13 wk balances of all four nutrients still tended to be higher in SHR. During the 16th wk of life, after onset of hypertension, Na, Ca and P balances were similar in SHR and WKY rats, but Mg balance was significantly lower in SHR. The percent urinary excretion of absorbed Na was lower in SHR at 9 wk of age, but after onset of hypertension it was similar to that in WKY rats. Food intake was always greater in SHR, whereas growth during the study was less, and absorption of Ca, Mg and P declined more rapidly with age in SHR than in WKY rats. The data suggest that nutrient malabsorption in SHR, if it occurs at all, is most likely an effect of, rather than a cause of, hypertension.
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PMID:Mineral balance and blood pressure in the young spontaneously hypertensive rat. 333 33

Previous studies suggest abnormalities in PO4 and perhaps vitamin D metabolism in the spontaneously hypertensive rat (SHR) compared with normotensive Wistar-Kyoto (WKY) control rats. The mechanism for the hypophosphaturia obscure, but intestinal malabsorption of P and/or the possibility of linkage to renal Na avidity has not been evaluated. Furthermore, if sustained, the potential effects of the hypophosphaturia on P balance are not known. The present investigation examined these issues. We found that the reduced P excretion occurs as early as age 22 days, the second day after weaning in the SHR, well before the onset of detectable hypertension. This phenomenon is dissociable from renal Na avidity, and sustained through the 12th week of age, the last week of our studies. Since P absorption is normal, external P balance is increased relative to the WKY control rats. The greater cumulative P retention from infancy to adulthood may explain the age-dependent fall in serum 1,25 dihydroxyvitamin D3 [1,25(OH)2D3] reported in the SHR by some investigators.
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PMID:Nature and metabolic consequence of hypophosphaturia in spontaneously hypertensive rats. 347 94

A new familial syndrome that affected 3 of 7 siblings is described. All 3 patients were young women with a very peculiar phenotype, poikilodermia and hair greying, and idiopathic nonarteriosclerotic cerebral calcifications. Pathological studies demonstrated a marked and progressive hyalinosis involving capillaries and often arterioles and small veins of the digestive tract, kidneys, and calcified areas of the brain. Using electron microscopy, we found that the hyalin substance in the intestinal capillaries consisted of several concentric layers of basal membrane-like deposits within a finely granular fluffy material. Huge deposits of this material were present in the subepithelial and mesangial spaces of the kidneys. Endothelial cells and, in the kidneys, mesangial cells were markedly abnormal, and a true mesangiolysis pattern was present in 2 patients. The clinical and biologic expression of these vascular changes was variable. Diarrhea, rectal bleeding, malabsorption, and protein-losing enteropathy were the main and lethal clinical problems in the proband. Hypertension appeared in the early stage of a second pregnancy in 1 sister, and mild proteinuria was found in all 3 affected patients. Peripheral retinal ischemic syndrome and chorioretinal scars were found in the ocular fundi of both affected sisters of the proband. A subarachnoid hemorrhage, due to a right sylvian aneurism, also occurred in both sisters and was lethal in 1 sister. None of the known causes of distal vessel hyalinosis could be ascertained.
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PMID:Digestive tract and renal small vessel hyalinosis, idiopathic nonarteriosclerotic intracerebral calcifications, retinal ischemic syndrome, and phenotypic abnormalities. A new familial syndrome. 348 63

The authors describe their experience with four cases of dural arteriovenous malformation (AVM) which led them to analyze the clinical aspects of these lesions in an attempt to understand their pathophysiology. An additional 191 previously reported cases of dural AVM's were reviewed with special attention to the mechanism of intradural, central, and peripheral nervous system manifestations. Apart from the peripheral cranial nerve symptoms, which are most likely due to arterial steal, the central nervous system (CNS) symptoms appear to be related to passive venous hypertension and/or congestion. Generalized CNS symptoms can be related to cerebrospinal fluid malabsorption due either to increased pressure in the superior sagittal sinus, to venous sinus thrombosis, or to meningeal reaction resulting from minimal subarachnoid hemorrhages. These phenomena are not related to the anatomical type of venous drainage. On the other hand, focal CNS symptoms are specifically indicative of cortical venous drainage. Seizures, transient ischemic attacks, motor weakness, and brain-stem and cerebellar symptoms can be encountered depending on the territory of the draining vein or veins. Therefore, the localizing value of focal CNS symptomatology relates to the venous territory and not to the nidus or to the arterial supply characteristics of dural AVM's. Furthermore, the venous patterns of various dural AVM's at the base of the skull are expressed by differences in their clinical presentation. Dural AVM's of the floor of the anterior cranial fossa and of the tentorium are almost always drained by the cortical veins and, therefore, have a high risk of intradural bleeding. The remarkable similarities in the manifestations of dural and brain AVM's and the differences in the manifestations of dural and spinal dural AMV's are pointed out. High-quality angiograms and a multidisciplinary approach to the study of dural AVM's will provide the best understanding of their symptoms and, therefore, the most appropriate treatment strategy.
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PMID:Neurological manifestations of intracranial dural arteriovenous malformations. 370 21

To define the mechanism for the hypercalciuria in spontaneously hypertensive rats (SHR), Ca clearance was evaluated in fasted 23-wk-old SHR and normotensive Wistar Kyoto (WKy) controls. There was no exaggerated calciuria before or after parathyroidectomy. Ca balance was therefore measured in the nonfasted animals, which revealed hyperabsorption in SHR of both sexes with increments 10-fold that of Ca excretion, supporting the primacy of intestinal hyperabsorption. In situ duodenal Ca uptake was also increased in the SHR. Parathyroidectomy did not affect the hyperabsorption. Hypercalcemia (total and ionized) and hypercalciuria in SHR associated with reduced adenosine 3',5'-cyclic monophosphate excretion, were abolished by fasting. Correction of hypertension for 6 mo failed to abolish the hypercalciuria. Bone Ca deposits were increased in 1-yr-old SHR. Ten-week-old SHR, in contrast, displayed mild malabsorption. Our data do not support the "renal leak" hypothesis. Instead, the adult SHR is characterized by increased Ca retention due to primary hyperabsorption, absorptive hypercalciuria, and increased bone Ca deposition. These phenomena are independent of sex, parathyroid hormone, and treatment of the established hypertension.
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PMID:Evidence for an intestinal mechanism in hypercalciuria of spontaneously hypertensive rats. 649 32


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