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)

In this study, 52 nonproteinuric Japanese patients with non-insulin-dependent diabetes (NIDDM) were followed from 1985 to 1990 to investigate the rate of development and progression of microalbuminuria and the factors which influence it. In 1985, 34 patients were normoalbuminuric, and 18 patients were microalbuminuric. Five years later, 11 of 34 initially normoalbuminuric patients (32.4%) developed microalbuminuria, and 6 of 18 initially microalbuminuric patients (33.3%) developed overt proteinuria. At the beginning of the study, hypertension existed more frequently in the patients who later developed microalbuminuria (8 of 11, 72.7%) than in the patients who stayed normoalbuminuric (4 of 23, 17.4%). Age-adjusted values of mean blood pressure (+/- SEM) at the beginning of the study in the patients who developed microalbuminuria (98.2 +/- 3.4 mm Hg, n = 11) were significantly higher than those in the patients who stayed normoalbuminuric (87.3 +/- 2.4 mm Hg, n = 23). In six patients who developed overt proteinuria, initial urinary albumin excretion rates (AER) were higher than those in the patients who stayed microalbuminuric, and four patients who presented with initial AER greater than 100 micrograms/min all developed overt proteinuria. These results indicate that, in Japanese patients with NIDDM, the rate of development of microalbuminuria is faster than that reported in Caucasian IDDM, and preexisting hypertension with relatively poor control of blood pressure may be a risk factor for the development of microalbuminuria.
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PMID:High blood pressure is a risk factor for the development of microalbuminuria in Japanese subjects with non-insulin-dependent diabetes mellitus. 147 44

Inheritance is a major determinant of increased sodium-lithium countertransport (SLC) activity in hypertension. However, hyperlipidaemia can also cause increased SLC activity in some individuals and it is difficult to distinguish this effect from the effect of hypertension. Erythrocyte SLC activity and its kinetic determinants sodium affinity (km) and maximum velocity (Vmax) were measured in 25 hyperlipidaemic patients and 15 normal controls (NC). Increased SLC activity (0.31 +/- SEM 0.03 mmol Li/(h x 1 cells) vs. NC 0.20 +/- 0.01, P < 0.01) in the hyperlipidaemic patients was associated with increased Vmax (0.59 +/- 0.07 vs. NC 0.41 +/- 0.03, P < 0.01) but normal km (median 120 range [40-324] mmol l-1 vs. 140 [108-260]. Lipid-lowering therapy resulted in decreased SLC activity secondary to a fall in Vmax. Km remained constant despite the changes in lipids and Vmax. The mechanism of increased SLC activity in hyperlipidaemia is different from that in essential hypertension where increased sodium affinity is found. Measurement of the kinetic characteristics of SLC may discriminate between the independent influences of hypertension and hyperlipidaemia on the sodium-lithium countertransporter.
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PMID:Plasma lipids affect maximum velocity not sodium affinity of human sodium-lithium countertransport: distinction from essential hypertension. 147 40

The present study was designed to evaluate the frequency of an increase in the urinary albumin excretion rate (UAER) and the factors involved in this parameter in non-diabetic obese patients; 122 non-diabetic obese patients were investigated. None had proteinuria or history of nephropathy or uropathy. Fourty of them had moderate hypertension. Compared with a group of 22 lean controls, UAER was significantly higher in the obese patients (19.0 +/- 2.0 (SEM) mg/24 h vs 3.2 +/- 0.6 mg/24 h, p < 0.001). UAER was elevated (> 20 mg/24 h) in 29 patients (23.7%). Prevalence of microalbuminuria was not significantly different in hypertensive than in normotensive patients. However UAER was significantly higher in the 32 patients with a family history of hypertension (29.6 +/- 6.3 mg/24 h vs 15.3 +/- 1.5 mg/24 h, p < 0.002). In patients with microalbuminuria, body weight was significantly higher (100.3 +/- 3.9 kg vs 91.8 +/- 1.9 kg, p < 0.05), plasma albumin was significantly lower (38.3 +/- 0.6 g/l vs 40.3 +/- 0.3 g/l, p < 0.005) and the estimated value of fractional albumin clearance was significantly higher. These results show the high frequency of microalbuminuria in non-diabetic obese patients. They suggest that UAER level may be an index of family hypertension in obese patients and that microalbuminuria is part of a widespread abnormality of the capillary permeability.
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PMID:[Microalbuminuria and hypertension in obese patients]. 148 58

Clentiazem, 8-chloro diltiazem, is a calcium channel blocker currently undergoing evaluation for the treatment of stable angina and hypertension. As patients with ischaemic disorders often present some degree of heart failure, the aim of this study was to investigate the effect of congestive heart failure on clentiazem (200 micrograms kg-1, i.v. bolus) pharmacokinetics in a canine model. Congestive heart failure was induced in six dogs by rapid ventricular pacing (240 beats min-1) for 3-5 weeks. Clentiazem pharmacokinetics was studied in each dog under the control condition and after the development of clinical signs of heart failure (ascites, dyspnea, fatigue). Blood samples were collected up to 480 min post-dose. Clentiazem plasma concentrations were determined by high performance liquid chromatography. The area under the plasma concentration versus time curves (AUC0-infinity) was significantly increased in congestive heart failure dogs (8.8 +/- 1.6 vs 21.8 +/- 1.4 micrograms min ml-1) (mean +/- SEM). These changes were related to a reduction of the volume of distribution of the central compartment (0.9 +/- 0.1 vs 0.2 +/- 0.11 kg-1) and total body clearance (1.9 +/- 0.4 vs 0.7 +/- 0.21 h-1 kg-1). It is concluded that, in our model, congestive heart failure significantly modifies clentiazem disposition. These results suggest that caution should be exercised when clentiazem is given to patients with a low ejection fraction and a compromised cardiac function. Reduced loading and maintenance doses might be recommended in patients with severe congestive heart failure.
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PMID:Effect of congestive heart failure on clentiazem pharmacokinetics in a dog model. 148 42

Glomerular hyperfiltration and hypertension induced by extensive loss of renal parenchyma are suspected to accelerate progression of renal failure. Amino acid infusion or protein ingestion also modify renal hemodynamics and increase glomerular filtration rate (GFR). This phenomenon was used to study the influence of two commonly used antihypertensive agents, captopril and nifedipine, on renal hemodynamics at rest and during glomerular hyperfiltration. Thirteen healthy volunteers were studied on three separate days (days A, B, and C) in random sequence: inulin and p-amino hippurate (PAH) clearance were measured first under glucose infusion and afterwards under stimulation by amino acid infusion (0.35 mmol/kg/min; 4 mg/kg/min). Day A served as a control, where no medication was given. On day B, 10 mg nifedipine, and on day C, 25 mg captopril, were administered orally before study. Without premedication (= day A, control) GFR increased from 108.0 +/- 6.9 mL/min (SEM) to 131.7 +/- 7.0 mL/min (P less than 0.05). On day B (nifedipine), GFR before stimulation by amino acids was already elevated to 121.8 +/- 4.2 mL/min (P less than 0.05 compared with day A) and increased to 132.6 +/- 6.3 mL/min with infusion of amino acids, thus to the same range as on day A without medication. On day C, after captopril, GFR did not increase with infusion of amino acids (from 112.5 +/- 7.2 to 117.3 +/- 6.3 mL/min). Our results indicate the calcium channel antagonist nifedipine and the angiotensin-converting enzyme (ACE) inhibitor captopril differ in their effect on intrarenal hemodynamic parameters. Nifedipine induces hyperfiltration at rest and allows maximal hyperfiltration to develop under amino acid infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of nifedipine and captopril on glomerular hyperfiltration in normotensive man. 149 65

In normal pregnancy, increased production of platelet thromboxane A2(TXA2) parallels increased biosynthesis of vascular prostacyclin (PGI2). An imbalance in the formation of these prostaglandins is believed to be associated with the pathogenesis of pregnancy-induced hypertension (PIH). Recent evidence suggested that aspirin in low doses was effective in reducing the incidence of PIH, by selective inhibition of platelet-derived TXA2 biosynthesis. In this communication, we determined the urinary 11-dehydro TXB2 and 6-keto-PGF1 alpha, which are major metabolites of TXA2 and PGI2, respectively, from early to late pregnancy of normal pregnant women and of women complicated with PIH. The ratio of 11-dehydro TXB2 to 6-keto-PGF1 alpha decreased significantly from as early as 10wks of gestation when compared with that in non-pregnant controls (1.43 +/- 0.15 vs 1.99 +/- 0.13: Mean +/- SEM, p less than 0.05), and increased in later pregnancy to the control values at term. No significant difference was found in the excretion of 11-dehydro TXB2 between normal pregnant women and women with PIH. In contrast, urinary excretion of 6-keto-PGF1 alpha decreased in women with PIH. The ratio of 11-dehydro TXB2 to 6-keto-PGF1 alpha increased significantly as compared with that of pregnant controls. These results demonstrated that disturbed production of vascular PGI2 may be the primary cause of PIH, and affect the vascular responsiveness to pressor inducers such as angiotensin II.
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PMID:[Urinary 11-dehydrothromboxane B2 and 6-keto-prostaglandin F1 alpha in normal pregnant women and in women complicated with pregnancy-induced hypertension]. 150 26

The goal of the current study was to determine whether treatment of hypertension reduces cerebral infarction after occlusion of the middle cerebral artery in stroke-prone spontaneously hypertensive rats (SHRSPs). Three-month-old SHRSPs received untreated drinking water or drinking water containing cilazapril, an angiotensin converting enzyme inhibitor, or hydralazine and hydrochlorothiazide. After 3 months of treatment, the left middle cerebral artery was occluded and neurological deficit was evaluated. Infarct volume was measured 3 days after occlusion using computer imaging techniques from brain slices. Cilazapril and hydralazine with hydrochlorothiazide were equally effective in reducing systolic blood pressure in SHRSPs. One day after occlusion of the middle cerebral artery, neurological deficit was decreased by both cilazapril and hydralazine with hydrochlorothiazide compared with untreated SHRSPs, and the deficit 3 days after occlusion was decreased significantly only by cilazapril. Infarct volume was 178 +/- 7 mm3 (mean +/- SEM) in untreated SHRSPs, and it was significantly reduced to 117 +/- 15 mm3 by hydralazine with hydrochlorothiazide and to 101 +/- 17 mm3 by cilazapril. Infarct volume in Wistar-Kyoto rats was 27 +/- 16 mm3. Thus, reduction in arterial pressure by hydralazine with hydrochlorothiazide or an angiotensin converting enzyme inhibitor is protective against focal cerebral ischemia in SHRSPs.
Hypertension 1992 Jun
PMID:Effect of antihypertensive treatment on focal cerebral infarction. 153 16

Eleven anemic children and adolescents with a median age of 14 years (range six months-20 years) on chronic hemodialysis were treated with recombinant human erythropoietin (rHuEPO) intravenously three times a week for an average of 9.2 months. After eight weeks of therapy, hematocrit rose from 20.3 +/- 1.4% to 31.7 +/- 0.7% (0.20 +/- 0.01 to 0.31 +/- 0.007, p less than 0.001, mean +/- SEM). After reaching the target hematocrit of 30% to 33% (0.30 to 0.33), doses were adjusted individually. Blood transfusions were eliminated in all but one patient. All patients experienced an increase in appetite and energy level. Serum ferritin concentrations decreased in all patients who reached target hematocrit and seven required iron supplementation. Hypertension worsened in two patients and developed in two others. One patient's vascular access clotted. Dialysis efficiency and heparin requirements during dialysis did not change significantly. We conclude that rHuEPO is safe, effective, and should be recommended as treatment for anemia in children and adolescents on hemodialysis, but close monitoring for the development of hypertension and/or iron deficiency is necessary.
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PMID:Therapy of renal anemia in children and adolescents with recombinant human erythropoietin (rHuEPO). 154 82

The activity of Na-Li countertransport (CT), a marker of the risk of essential hypertension, was determined in 55 primigravid women during pregnancy, together with urinary 11-dehydro-thromboxane B2 (11-dehydro-TXB2) as a marker of thromboxane A2 synthesis. The mean Na-Li CT (mean +/- SEM) value was increased significantly at 20 weeks gestation and thereafter, and reached higher levels in late pregnancy than in non-pregnant controls (0.31 +/- 0.02 vs. 0.21 +/- 0.01mmol per hr per liter RBC, p less than 0.05). Fifty five primigravid women could be divided into two groups, depending upon Na-Li CT activity either higher or lower than the value of 0.25mmol per hr per liter RBC at any time in the pregnancy up to term. At 20 weeks gestation all but one of 13 women in the lower-activity group had Na-Li CT activity less than 0.20 mmol per hr per liter RBC, and none developed PIH, whereas out of 42 women in the higher-activity group, all but one had Na-Li CT activity more than this value, and 8 developed PIH. Urinary 11-dehydro-TXB2 increased as pregnancy progressed, maximum levels being attained in women at term, about 3 times higher than in controls (4.19 +/- 0.35 vs. 1.36 +/- 0.10 ng per mg creatinine, p less than 0.05). Although the formation of thromboxane A2 was reported to be higher in pregnancy complicated by hypertension, no significant difference existed in the levels of 11-dehydro-TXB2 between women with PIH and women with uncomplicated pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Increased red-cell sodium-lithium countertransport activity and urinary 11-dehydrothromboxane B2 during pregnancy]. 154 69

The present study examined whether the dual cyclooxygenase/lipoxygenase inhibitor phenidone would protect stroke-prone spontaneously hypertensive rats (SHRSP) from stroke and hypertensive renal disease. Vehicle-treated SHRSP (N = 6), fed stroke-prone rodent diet and 1% saline, exhibited severe systolic blood pressure elevation (261 +/- 10 mm Hg, mean +/- SEM), marked proteinuria (90 +/- 12 mg/day), and stroke, with an average age at death of 14 +/- 1 weeks. In a second group of six saline-loaded SHRSP, treatment with phenidone (60 mg/kg/day) was started at 8.4 weeks of age. Despite establishment of severe hypertension in this group (274 +/- 10 mm Hg), proteinuria remained at basal levels (28 +/- 13 mg/day), and signs of stroke were absent (P less than .01 v vehicle) through at least 16 weeks of age. Phenidone treatment also prevented the declines in body weight and food intake observed in vehicle-treated SHRSP, and maintained urine volume and saline intake. Serum 12-hydroxy-eicosatetraenoic acid (12-HETE) generation was significantly inhibited greater than 50% in incubates of whole blood from phenidone-treated SHRSP. We have previously shown that agents which interfere with the renin-angiotensin system afford protection from renal and cerebrovascular injury in saline-loaded SHRSP; cyclooxygenase inhibition alone will hasten the onset of these pathologic changes. Whether phenidone, which has been reported to attenuate angiotensin II-mediated effects, affords vascular protection by interference with a lipoxygenase-mediated action of angiotensin II remains to be elucidated.
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PMID:The lipoxygenase inhibitor phenidone protects against proteinuria and stroke in stroke-prone spontaneously hypertensive rats. 155 Jun 66


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