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

This study investigated hemodynamic changes in diabetic rats and their relationship to changes in vascular albumin permeation and increased metabolism of glucose to sorbitol. The effects of 6 wk of streptozocin-induced diabetes and three structurally different inhibitors of aldose reductase were examined on 1) regional blood flow (assessed with 15-microns 85Sr-labeled microspheres) and vascular permeation by 125I-labeled bovine serum albumin (BSA) and 2) glomerular filtration rate (assessed by plasma clearance of 57Co-labeled EDTA) and urinary albumin excretion (determined by radial immunodiffusion assay). In diabetic rats, blood flow was significantly increased in ocular tissues (anterior uvea, posterior uvea, retina, and optic nerve), sciatic nerve, kidney, new granulation tissue, cecum, and brain. 125I-BSA permeation was increased in all of these tissues except brain. Glomerular filtration rate and 24-h urinary albumin excretion were increased 2- and 29-fold, respectively, in diabetic rats. All three aldose reductase inhibitors completely prevented or markedly reduced these hemodynamic and vascular filtration changes and increases in tissue sorbitol levels in the anterior uvea, posterior uvea, retina, sciatic nerve, and granulation tissue. These observations indicate that early diabetes-induced hemodynamic changes and increased vascular albumin permeation and urinary albumin excretion are aldose reductase-linked phenomena. Discordant effects of aldose reductase inhibitors on blood flow and vascular albumin permeation in some tissues suggest that increased vascular albumin permeation is not entirely attributable to hemodynamic changes. We hypothesize that 1) increases in blood flow may reflect impaired contractile function of smooth muscle cells in resistance arterioles and 2) increases in vascular 125I-BSA permeation and urinary albumin excretion reflect impaired vascular barrier functional integrity in addition to increased hydraulic conductance secondary to microvascular hypertension associated with decreased vascular resistance.
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PMID:Prevention of hemodynamic and vascular albumin filtration changes in diabetic rats by aldose reductase inhibitors. 250 78

The cause of the thrombotic tendency in nephrotic patients is unknown. Recent reports of thrombotic complications in patients with deficiencies of protein C or protein S (natural inhibitors of coagulation) have raised the possibility that decreased levels of these proteins may play a role in the hypercoagulable state of nephrotic patients. We measured the levels of protein C, total protein S, and free protein S antigens in 42 patients (21 nephrotic and 21 non-nephrotic) with one of four types of glomerular pathology: diabetic nephropathy (DM), focal glomerular sclerosis (FGS), membranous glomerulonephritis (MGN), and chronic renal failure due to hypertension (CRF). Protein C and total protein S antigen levels were significantly higher in FGS and MGN than they were in DM or CRF. Free protein S levels were lower in DM than they were in MGN. Protein C, total protein S, and free protein S levels did not significantly correlate with either serum albumin or degree of proteinuria. The mean levels of the three proteins did not differ between nephrotic and non-nephrotic patients. Free protein S and protein C were, however, significantly correlated (P less than .005 and P less than .002, respectively) with the type of glomerular pathology, independent of differences in age, sex, serum albumin, or degree of proteinuria. These data suggest that abnormalities of free protein S and protein C are related to the nature of the underlying renal disease, rather than to the degree of proteinuria.
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PMID:Protein S and C antigen levels in proteinuric patients: dependence on type of glomerular pathology. 252 34

Numerous studies have suggested that a functional relationship may exist between the kallikrein-kinin and the renin-angiotensin systems within the kidney. We investigated the effects of glandular kallikrein on renin release by using an in vitro preparation of isolated rat glomeruli with their attendant arterioles. The effect of kallikrein was studied in the presence or absence of 0.1% bovine serum albumin (BSA) in Krebs superfusion fluid. We also studied the effect of inactivating kallikrein by treatment with phenylmethylsulfonyl fluoride or by inhibiting it with aprotinin. In the absence of BSA, kallikrein caused a 12-fold increase in renin release, from 5.1 +/- 1.2 ng angiotensin I (ANG I)/min to 66.0 +/- 2.27 ng ANG I/min (p less than 0.025). In the presence of BSA, renin release increased twofold, from 13.0 +/- 1.8 ng ANG I/min to 24.3 +/- 4.8 ng ANG I/min (p less than 0.025). The basal level of renin measured when the glomeruli were superfused with BSA-Krebs was two to three times greater than when they were superfused with Krebs alone (p less than 0.001). This finding suggests that media protein inhibited renin loss during either the superfusion or storage of renin samples. Neither phenylmethylsulfonyl fluoride-inactivated nor aprotinin-inhibited kallikrein stimulated renin release. We propose that kallikrein can stimulate renin release in isolated glomeruli.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:Effect of glandular kallikrein on renin release in isolated rat glomeruli. 257 3

1. The authors elaborated an original concept for the interpretation of vasomotor disorders in subjects with an artificial heart. 2. This concept is based on the regeneration of nervous elements in the walls of the atria (in particular the right one) after implantation of the artificial heart and on comparison of their activity with the venous pressure which revealed the interrelationship of the two phenomena. 3. Both therapeutic methods based on this concept, the method of influencing the afferentation and efferentation of vasomotor nervous regulations leading to a reduction of the central venous pressure proved valid and effective. 4. Evaluation of the effectiveness of this therapy is based on regular assessment of the central venous pressure, on the laboratory assay of enzymes (AST, ALT, GMT and LDH), on the assessment of serum albumin and finally on the morphological and histological examination of the liver incl. assessment of the hepatic index. 5. The nervous pathogenesis is closely linked with hormonal factors. The latter are conceived as the participation of associated factors in the pathogenesis of venous hypertension in recipients with an artificial heart.
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PMID:[Therapy of venous hypertension in animals with an artificial heart and long-term survival]. 268 92

We studied the long-term effect of an angiotensin converting enzyme (ACE) inhibitor, captopril, on the progression of chronic renal failure and on the rate of urinary protein excretion. When compared with standard triple therapy, captopril slowed the progression of renal failure. Captopril was also able to reduce the proteinuria of non-diabetic glomerular origin. This reduction was not dependent on the presence or absence of arterial hypertension but was limited by the presence of low serum albumin levels, and only occurred in patients with proteinuria in excess of 3 g/24 h.
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PMID:Effects of angiotensin converting enzyme inhibitors on the progression of renal failure and proteinuria in humans. 269 57

In previous studies, administration of adrenocorticotrophin (ACTH; 0.5 mg i.m. b.d. for 5 days) to normal subjects produced an adrenally dependent rise in blood pressure (BP) of some 20 mmHg, accompanied by an increase in cardiac output and an increase in plasma volume. The BP and metabolic effects of ACTH (increase in plasma glucose, fall in eosinophils, increase in body weight and urine sodium retention) were reproduced by infusion of the glucocorticoid (GC) cortisol at rates (6-8 mg/h) which reproduced the blood concentrations of the steroid achieved with ACTH administration. Oral administration (hydrocortisone 200 mg daily) produced similar changes qualitatively, although the cortisol concentrations and increase in pressure (12 mmHg) were less. Plasma volume was increased. To determine the role of urine sodium retention and plasma volume expansion in the hypertension, we gave synthetic steroids to six normal subjects for 5 days, at doses which were calculated to be similar for GC activity, but which had little or no mineralocorticoid (MC) activity. Prednisolone (40 mg/day), methylprednisolone (32 mg/day), triamcinolone (40 mg/day) and dexamethasone (8 mg/day) all produced equivalent GC effects (increase in plasma glucose, increase in total white cell count, fall in direct eosinophil count). There were no MC effects with any of the steroids. Body weight did not increase and urinary sodium excretion increased rather than decreased. Plasma volume (125I human serum albumin) and haematocrit were unchanged. BP rose with all four steroids: systolic BP rose by 13 mmHg with prednisolone, by 9 mmHg with methylprednisolone, by 10 mmHg with triamcinolone, and by 6 mmHg with dexamethasone. Diastolic BP increases were 8, 11, 8 and 7 mmHg, respectively. Thus, neither MC activity nor an increase in plasma volume is essential for steroids to induce an increase in blood pressure. Therefore, screening of synthetic GCs to minimize MC activity will not prevent hypertensive complications.
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PMID:The hypertensive effect of synthetic glucocorticoids in man: role of sodium and volume. 276 Apr 58

The effect of cyclosporin A in acute and chronically active inflammatory bowel disease was tested in 11 patients with Crohn's disease and two with ulcerative colitis who had exhibited a poor response to at least eight weeks of conventional therapy. Trough levels of the drug in the therapeutic range were obtained in 12 of 13 patients. Cyclosporin A, which was usually added to the continued previous medication, including corticosteroids (11 of 13) or metronidazol (1 of 13), prompted an apparent clinical improvement in all but one patient. In six of the nine Crohn's disease patients with an initial Best index of greater than 150, a definite fall by at least 100 points was observed after 2-10 weeks of treatment, but the van Hees index declined only in two patients. All four patients with chronic perineal fistulation experienced symptomatic relief. Both patients with ulcerative colitis had a clinical remission. Erythrocyte sedimentation rate or serum albumin improved in eight of 13 patients. However, two of the nine responders with Crohn's disease relapsed during cyclosporin A therapy and three immediately after the medication was discontinued. Common side effects included hypertrichosis, tremor, and hyperesthesia; hypertension and epigastric pain each occurred only in one patient.
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PMID:Cyclosporin A treatment in inflammatory bowel disease. 276 6

In 485 long-term geriatric inpatients (mean age 80 years), serum ionized calcium (CaI) concentrations were significantly associated with 2-year mortality. The cumulative 2-year survival was 37% in the hypocalcaemic group (CaI less than 1.17 mmol/l), 49% in the hypercalcaemic group (CaI greater than 1.29 mmol/l) and 57% in the normocalcaemic group. The association of calcaemia and survival remained significant even when patients with low serum albumin and high serum creatinine were excluded. However, serum total calcium concentrations, whether or not 'corrected' for albumin, were not significantly associated with survival. The use of diuretics may have had some influence on the calcaemic grouping of the patients, but the excess mortality in the hypercalcaemic group was not explained by heart failure or hypertension. The impaired survival in dyscalcaemic groups was not associated with sex, age, immobility, diabetes, hypertension, or renal failure.
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PMID:Association of calcaemic status with survival of elderly inpatients. 281 55

Six elderly patients with established hypertension and six young healthy subjects were studied after 8 days of treatment with atenolol 50 mg day-1, metoprolol 50 mg day-1, oxprenolol 80 mg day-1 and propranolol 80 mg day-1. The area under the blood concentration-time curve was increased in the elderly group for each drug, but the difference was statistically significant only for atenolol. The lower serum albumin concentrations in the elderly group did not result in a decrease in the percentage of propranolol or oxprenolol bound to serum proteins.
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PMID:A comparison of the pharmacokinetics of atenolol, metoprolol, oxprenolol and propranolol in elderly hypertensive and young healthy subjects. 286 83

Hypertension has been associated with an enhanced transport of macromolecules from the vasculature to the interstitium. The first objective of this study was to determine if, under control conditions, there is an enhanced leakage of macromolecules from the cremaster vasculature of the hypertensive rat. The second objective was to determine if the response to a mediator of macromolecular leakage (histamine) was altered in the renovascular hypertensive rat. A third objective was to determine if a calcium entry blocker, verapamil, could inhibit histamine-induced leakage and, if so, was the sensitivity to verapamil different in the renovascular hypertensive rat. Rats were anesthetized with pentobarbital, and the cremaster preparation was used for in vivo television microscopy studies. Fluorescein isothiocyanate was tagged to rat serum albumin (FITC-RSA), and the leakage of this albumin from the vasculature to the interstitium was quantitated by the use of fluorescent microscopy techniques. There was no difference during control conditions in macromolecular leakage between the normotensive and hypertensive rats. However, histamine induced a greater leakage in the renovascular hypertensive rat than in the normotensive controls. In addition, verapamil, in the presence of normal calcium levels, inhibited the histamine-induced leakage in the hypertensive rats but not in the normotensive controls. These data suggest that enhanced macromolecular leakage during hypertension may be due to an increased sensitivity to mediators of protein leakage. These agents may produce protein leakage by enhancing entry of extracellular calcium into endothelial cells.
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PMID:Histamine-induced protein leakage in hypertensive rats: inhibition by verapamil. 308 Sep 1


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