Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

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

Cooperation between the family physician and the kidney-center begins with the recognition of a renal disease and pre-dialysis treatment. Our patients usually are sent for the preparation of an arterio-venous shunt operation (Cimino or modifications) when serum creatinin levels amount to 8 to 10 mg/100 ml. Peripheral veins on both forearms should be reserved for these procedures early in the course of renal disease and vascular punctures should be avoided. Dialysis treatment is performed either at the kidney-center, at one of our partner-centers, at the central self-care facility operating under the care and supervision of the kidney-center or as home-dialysis-treatment. Each patients continues to receive technical and medical services of the center. Central self-care dialysis as well as home-dialysis are organized by the Kuratorium for Heimdialyse e.V. in this area. This organization also provides an on-cell-service of technicians. Nurses and physicians take regular rotations to staff the dialysis- and the self-care-units. The family physician takes care of the hemodialysis patinet in cooperation with the hospital. In case of medical problems the patient is transferred to the kidney-center. The patient must be well instructued on problems and complications which might occur during hemodialysis, either due to the basic disease or in connexion with hemodialysis. In some cases of complications patients must be admitted to the center without delay. Emergency situations usually can be avoided as technical standard of dialysis equipment and standard of training of patients or their parners is high. Medications, such as phosphate binders (aluminium hydroxide), iron vitamins and allopurinol are provided if necessary. Patients are advised to limit intake of fluids and potassium containing foods. The sodium intake depends on blood pressure-values. In case of hypertension there will be salt restriction, in case of hypotension the salt intake is increased. Chronic intermittent hemodialysis treatment can result in successful rehabilitation. Further improvement concerning personal and medical problems can only be expected from kidney transplantation.
...
PMID:[Care of the hemodialysis patients by the family physician]. 84 54

The effect of prior hypertension on lipid synthesis in the thoracic aortae of normal-fed and cholesterol-fed rabbits was studied in vitro using[1(-14)C] acetate and [32P] phosphate as lipid precursors. In normally fed rabbits, prior hypertension did not increase the incorporation of the labelled precursors into either phospholipid or neutral lipid. In cholesterol-fed rabbits, hypertension increased the incorporation of [32P] phosphate into phosphatidyl-choline and of [1(-14)C-acetate into cholesterol ester. The increased incorporation of [1(-14)C] acetate into cholesterol ester was accompanied by an increase in intimal total cholesterol concentration. For both normotensive and hypertensive cholesterol-fed rabbits there was a close correlation between cholesterol esterification and total cholesterol concentration of the thoracic intima. It is concluded that the increase in aortic lipid synthesis in hypertensive cholesterol-fed rabbits is secondary to the increased cholesterol accumulation induced by hypertension rather than to a direct stimulation of arterial wall lipid synthesis by hypertension per se.
...
PMID:Incorporation in vitro of 14C-labelled acetate and 32P-labelled phosphate into lipid in thoracic aortae from hypertensive and nomotensive rabbits. 97 45

1. Indomethacin inhibits prostaglandin synthesis and interferes with renin release; these effects were studied in rabbit renovascular hypertension. 2. Ten intravenous injections (3 mg day-1 kg-1 after two initial doses of 9 mg/kg) of indomethacin were given daily to ten normal rabbits, ten rabbits with two-kidney Goldblatt hypertension (2KH), tension (1KH). Twelve appropriate control rabbits received diluent phosphate buffer without indomethacin. Plasma renin activity and plasma prostaglandin E2 were measured by radioimmunoassay. 3. In the normal group, indomethacin significantly decreased plasma prostaglandin E2 (1-15 to 0-2 ng/ml, SEM 0-2; P less than 0-01) and plasma renin activity (20 to 3 ng h-1 ml-1, SEM 1, P less than 0-01). Plasma creatinine increased slightly but the mean blood pressure was not significantly changed by indomethacin. 4. Six of ten rabbits with 2KH showed results similar to those in the normal rabbits. In four of ten rabbits in which development of 2KH was accompanied by increments in plasma renin activity (18 to 31-5 ng h-1 ml-1, SEM 3 and 4 respectively; P less than 0-01) and plasma prostaglandin E2 (1-2 to 3-4 ng/ml, SEM 0-2 and 0-4 respectively; P less than 0-05), treatment with indomethacin produced renal failure (plasma creatinine increasing to 7-6 mg/100 ml), oliguria, malignant hypertension (mean blood pressure, 168 mmHg, SEM 7-7) and death within 5 days. 5. In 1KH, indomethacin decreased plasma renin activity and plasma prostaglandin E2, but caused increased mean blood pressure (102 to 121 mmHg, SEM 4 and 6 respectively; P less than 0-01) and decreased renal function (plasma creatinine 0-9 +/- 0-04 to 3-5 +/- 1 mg/100 ml, SEM 0-04 and 1 respectively; P less than 0-01). 6. Aggravation of hypertension was conditioned by pre-existing levels of renal function and, to a lesser extent, by plasma renin activities. 7. These results suggest that prostaglandins exert a protective effect on renal function in renovascular hypertension.
...
PMID:Effects of indomethacin in rabbit renovascular hypertension. 107 20

In previous studies a decreased responsiveness to endothelin-1 (ET-1) of conduit arteries and resistance vessels of deoxycorticosterone acetate (DOCA)-salt hypertensive rats was found in comparison with uninephrectomized controls. Decreased isometric force, number of receptors, and inositol phosphate accumulation were reported in the DOCA-salt animals. In the present study effects of ET-1 on cytosolic free calcium, inositol phosphates, and 1,2-diacylglycerol were investigated in blood vessels of DOCA-salt hypertensive rats. Basal cytosolic free calcium, measured with the fluorescent dye fura-2, was 201 +/- 41 nmol/l in mesenteric arteries of DOCA-salt rats and 45 +/- 9 nmol/l in uninephrectomized controls (p less than 0.01). The maximal response of cytosolic free calcium (to 30 nmol/l ET-1) was 176 +/- 22% of the basal value for DOCA-salt and 242 +/- 6% for uninephrectomized rats (p less than 0.05). The concentration giving 50% of the maximum response was 9.0 and 6.5 nmol/l for DOCA-salt rats and controls, respectively. Inositol phosphate production after stimulation with 100 nmol/l ET-1 in the presence of LiCl was lower by at least 30% (p less than 0.01) in both aorta and mesenteric arteries of DOCA-salt hypertensive versus control rats. Basal levels of diacylglycerol in aorta were similar in DOCA-salt rats and in controls and did not respond to a 100 nmol/l ET-1 stimulation in the DOCA-salt rats, in contrast to the increase found in the control uninephrectomized rats (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Jun
PMID:Calcium, phosphoinositide, and 1,2-diacylglycerol responses of blood vessels of deoxycorticosterone acetate-salt hypertensive rats to endothelin-1. 131 55

Na+/K(+)-ATPase of the cell membrane is considered to be closely related to the pathology of various diseases including hypertension and heart failure. The activity of this enzyme in the erythrocyte membrane has been determined in earlier reports by the assay of inorganic phosphate generated from the substrate ATP or radioimmunoassay after binding 3H ouabain to the erythrocyte membrane, using a large volume of blood samples. However, as neither method was appropriate for wide routine use, we developed a method to assay this enzyme in a small volume (10 ml) of fresh human blood samples with re-evaluation of conditions for the inorganic phosphate assay. In this method, the coefficient value (CV) of membrane protein amount and the NA+/K(+)-ATPase activity were 2.2% and 2.5% respectively, indicating sufficient precision of the assay. Moreover, in 97 subjects without abnormalities in blood biochemical tests (77 males and 20 females) aged 35-59 years, the enzyme activity showed no differences according to age or sex, ranging from 0.217 to 0.071 mumols Pi/mg/hr with a mean of 0.130.
...
PMID:[Determination of human erythrocyte membrane Na+/K(+)-ATPase activity in small volume of blood sample]. 131 73

Endothelin is a 21 aminoacids peptide belonging to the family of endothelium-derived contracting factors. It exists as 3 isoforms which have similar actions. It is principally, but not exclusively, synthesized and secreted by the vascular endothelial cells. Hypoxia, physical stretching and various endogenous substances stimulate its secretion. Its specific receptors are widespread in tissues, and the endothelin-receptor binding process produces a rise of intracellular calcium through the formation of inositol phosphate. Endothelin is the most potent of known vasoconstrictor substances. In addition, it acts on the myocardium and has a contracturant effect on other smooth muscle fibres. It also contributes to the release of endogenous peptides, inhibits platelet aggregation and has mitogenic properties. Endothelin can be determined in biological fluids, such as plasma, urine and cerebrospinal fluid, using immunoanalysis methods. Several pathological situations are associated with an increase of plasma endothelin concentrations; these situations include arterial hypertension, myocardial infarction, cardiogenic shock and renal failure. Although not all physiopathological applications of endothelin have been elucidated, our current knowledge of this substance indicates that it will be of importance in human medicine.
...
PMID:[Endothelin, a peptidic vasoconstrictor]. 131 61

Vitamin D, a fat-soluble vitamin, can be associated with significant morbidity when prescribed in large doses. We describe a hypoparathyroid patient with vitamin D intoxication who developed painful periarticular calcinosis, nephrocalcinosis with hypertension and chronic renal failure in addition to band keratopathy and hearing loss. He was treated with combination therapy including prednisone, phosphate-binding antacid, phenytoin and disodium etidronate. After 20 months of follow-up there was a significant reduction of periarticular calcinosis, but no improvement in renal function, band keratopathy or hearing loss and possible calcification of the ossicles. The clinicopathologic features of metastatic calcification and the various treatment modalities are reviewed.
...
PMID:Calcinosis and metastatic calcification due to vitamin D intoxication. A case report and review. 139 78

Since arginine vasopressin may play a role in mineralocorticoid hypertension, we examined the effects of deoxycorticosterone acetate (DOCA)-salt on vasopressin V1 and V2 receptor binding and their second messengers, inositol phosphate and adenylate cyclase, respectively, in liver and kidney to determine whether altered vasopressin receptor binding is pathogenetic in mineralocorticoid hypertension. The mean arterial blood pressure of mineralocorticoid (DOCA-salt)-treated rats (163 +/- 1 mm Hg) was increased compared with control salt-treated rats (salt) (122 +/- 1 mm Hg) and water-treated rats (120 +/- 1 mm Hg; p less than 0.001). Mineralocorticoid treatment also increased plasma sodium, osmolality, and vasopressin concentration (p less than 0.001). In the hypertensive animals, there was a reduction in hepatic V1 (DOCA-salt, 91 +/- 12; salt, 132 +/- 13; and water, 145 +/- 13 fmol/mg protein; p less than 0.05) and renal V2 receptor binding density (DOCA-salt, 53 +/- 5; salt, 93 +/- 9; and water, 95 +/- 9 fmol/mg protein; p less than 0.01), although receptor affinities remained unaltered. In contrast, the density of renal V1 receptors was increased by mineralocorticoid treatment (DOCA-salt, 24 +/- 2; salt, 16 +/- 2; water, 18 +/- 1 fmol/mg protein; p less than 0.05), although the affinity was unchanged. Downregulation of V2 receptors was associated with a decrease in maximum cyclic adenosine monophosphate levels (DOCA-salt, 19 +/- 4; salt, 49 +/- 6; water, 53 +/- 9 pmol.mg protein-1.10 min-1; p less than 0.05), whereas changes in V1 receptor levels were not associated with changes in maximum inositol phosphate levels.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Oct
PMID:Regulation of vasopressin receptors in deoxycorticosterone acetate-salt hypertension. 139 92

Mechanisms of progression of chronic renal failure (CRF) have been well documented in the rat but may not be relevant in man. Factors which may modify clinical CRF include underlying disease, diet, hypertension, intercurrent events, and adverse or beneficial effects of drug therapy. It has been argued that progression in many forms of renal disease is inexorable below a certain level of renal function. In other diseases, eg primary malignant hypertension, analgesic nephropathy, function frequently improves in both the short and long term with appropriate management. Thus knowledge of the nature of the underlying disease is essential in assessing progression. The value of diet in preserving renal function has been debated, particularly the relative roles of protein and phosphate control. In our own unit, a prospective randomized study showed a benefit of protein restriction. Development of accelerated hypertension is an important cause of progression of renal disease and clinical and experimental evidence supports the view that non-accelerated hypertension is also a factor in progression, amenable to treatment. Various intercurrent events may accelerate progression and function may be lost permanently following sepsis, urinary tract obstruction, renal arterial or venous obstruction, hypotension and in some cases pregnancy. Numerous drugs can have deleterious effects on the kidney. The possibility that converting enzyme inhibitors might preserve renal function is attracting attention but in view of their side effects their place in therapy should be determined by prospective controlled studies in which the above factors are carefully considered.
...
PMID:Preservation of renal function in chronic renal failure. 141 42

Angiotensin II-induced phosphorylation of proteins was examined in isolated myocytes from hearts of Dahl rats. A high salt diet induced cardiac hypertrophy in Dahl salt-sensitive rats. Angiotensin II-induced phosphorylation of a 42-kd protein (pp42) was detected by two-dimensional electrophoresis in hypertrophic but not normal ventricular myocytes. Angiotensin II stimulation was time-dependent, with a peak effect at 30 minutes. The half-maximal and maximal concentrations of angiotensin II that stimulated pp42 phosphorylation were 1 and 10 nM, respectively. Phosphorylation of pp42 was a function of cardiac hypertrophy. Phorbol 12-myristate 13-acetate-induced phosphorylation of pp42 indicates the possibility of an association between protein kinase C and the signal transduction pathway of angiotensin II-induced pp42 phosphorylation. Ionomycin and A23187 (both at 1 microM) did not stimulate phosphorylation of pp42. Angiotensin II produced a small increase in the synthesis of myocyte proteins in both normal and hypertrophic cells as shown by [35S]methionine incorporation. However, this increase could not account for the increase in the phosphate content of pp42. This protein was not an isoform of actin nor was it of platelet origin. These results raise the possibility that angiotensin II may play a role in the activation of factors in hypertrophic myocytes; however, further study is required to define a link between phosphorylation of pp42 and the hypertrophic process.
Hypertension 1992 Nov
PMID:Angiotensin II-induced protein phosphorylation in the hypertrophic heart of the Dahl rat. 142 15


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

---