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)

Hypertension has been reported to occur in 50 to 75 percent of subjects with autosomal dominant polycystic kidney disease (ADPKD) prior to the onset of marked renal insufficiency but concurrent with cystic deformation of the renal parenchyma. The present study was undertaken to examine whether the renal structural abnormalities are greater in hypertensive (HBP) versus normotensive (NBP) male and female patients with ADPKD who were matched within gender groups for age, body surface area, serum creatinine concentration (males HBP 1.2 +/- 0.02 vs. NBP 1.1 +/- 0.03 mg/dl. NS: females HBP 0.9 +/- 0.03 vs. NBP 0.9 +/- 0.02 mg/dl, NS) and creatinine clearance (males HBP 100 +/- 3 vs. NBP 108 +/- 3 ml/min/1.73 m2, NS: females HBP 97 +/- 3 vs. NBP 96 +/- 2 ml/min/1.73 m2, NS). Renal volume was significantly greater in the HBP compared to the NBP group (males HBP 624 +/- 47 vs. NBP 390 +/- 43 cm3, P less than 0.0005; females HBP 446 +/- 32 vs. NBP 338 +/- 24 cm3, P less than 0.002). Since increased renal volume is due to increased cysts, the results indicate that the early high incidence of hypertension in ADPKD correlates with the renal structural abnormalities in this disorder.
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PMID:Renal structure and hypertension in autosomal dominant polycystic kidney disease. 207 59

In a baseline survey of 4,936 school children aged 6-16 years, 199 children with systolic blood pressure (SBP) values equal or greater than the 95-th percentiles for age and sex were chosen as the hypertensive group (HBP), and were matched for age and sex with 197 children with SBP from the 5-th through the 50-th percentiles as the control (normotensive) group (NBP). For both groups the intra-RBC and plasma sodium and potassium contents, 8-hour night urinary sodium, potassium and creatinine excretions for three days, and an oral saline-water load test were performed. The results show that (1) intra-RBC potassium level in the HBP was lower than that in NBP. The level in those with positive hypertension family history (FH+) was lower than that with negatives (FH-). The intra-RBC potassium contents correlated inversely with diastolic BP. No correlation between intra-RBC sodium and BP was found; (2) Plasma sodium concentration in HBP was much lower than that in NBP. No difference was found between the FH+ and FH- in the plasma sodium concentrations; (3) Mean 8-hour night urinary potassium excretion expressed as mmol/g creatinine, was lower in HBP than in NBP; (4) After the saline load test the 4-hour urinary sodium excretion was significantly higher in HBP. Of those children with FH- the 4-hour sodium excretion in HBP was higher than that in NBP, but no significant difference was found between HBP and NBP of the FH+ children in the 4-hour urinary sodium excretions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sodium and potassium levels in hypertensive children. 251 56

On a baseline survey of 4936 school children, age ranged from 6 to 16 years, 199 children with the systolic blood pressure (SBP) value equal or greater than 95-th percentiles for age and sex were chosen as the hypertensive group (HBP), and the same number of children with the SBP lower than 50-th percentiles were matched as the normotensive group (NBP). For both groups the intra-RBC and plasma Na and K content, three sequential nights 8-hour urinary Na, K and creatinine excretion, and an oral saline-load test were performed. The results show that: (1) The intra-RBC K in the HBP was lower than in NBP, 259 +/- 57 vs 291 +/- 78 mumol/g-protein, P less than 0.01. That in those with positive hypertensive family history (FH+) was lower than in those of negatives (FH-). The intra-RBC K content was correlated inversely with diastolic BP, r = -0.43, P less than 0.001. No correlation between intra-RBC Na and BP was found; (2) Plasma Na concentration in HBP was much lower than in NBP, 137.5 +/- 7.9 vs 142.6 +/- 6.9 mmol/L, P less than 0.001. No difference was found between FH+ and FH-; (3) Mean 8-hour urinary K excretion at night was lower in HBP than in NBP, 23.9 +/- 11.5 vs. 28.2 +/- 14.7 mmol/g-creatinine, P less than 0.01; (4) After a load of oral saline the 4-hour urinary Na excretion was significantly higher in HBP than in NBP, 39.5 +/- 29.1 vs 30.8 +/- 23.2 mmol, P less than 0.01. Of those children with FH-, the 4-hour Na excretion in HBP was higher than in NBP, 39.8 +/- 29.4 vs 29.3 +/- 21.5 mmol, P less than 0.001, but no significant difference was found between HBP and NBP in children with FH+. We believed that the above changes in electrolytes in the children with their BP at higher-level percentiles represent an abnormal relation between potassium and arterial BP in the early stage of hypertension, as well as the early compensatory natriuresis of the kidneys.
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PMID:[Sodium and potassium in children with hypertension]. 279 85

Na+ interaction with unsealed human red cell ghosts has been studied by 23Na-NMR relaxation rate (R1) measurements. Data on a total of nine subjects including seven volunteer normotensives (NBP) and two untreated hypertensives (HBP) are presented. Qualitative treatment of the data gives information on the dynamic behavior of Na+ undergoing fast exchange between the free and bound states. The excess longitudinal relaxation rate (delta R)-1 plotted against total [Na+], known as the James-Noggle plot, exhibits different behavior for NBP and HBP ghosts, with a relatively low binding constant of approx. 100 M-1 for HBP (p less than 0.025) compared to a high constant of 500-1000 M-1 for NBP. To associate our NMR data with membrane-bound (Na+ + K+)-ATPase, 23Na relaxation rates were measured in the presence of 5 mM ouabain. James-Noggle plots constructed for ouabain-sensitive excess relaxation rates show the binding for NBP to be even high affinity (greater than 10(3) M-1) but low capacity. These data may suggest that for a given amount of intracellular Na+, the binding affinity could determine the distribution of Na+ between the membrane and cytoplasm, and that the (Na+ + K+)-ATPase which is primarily responsible for the Na+ affinity might assume an abnormal transport mechanism in HBP membranes.
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PMID:23Na-NMR studies of Na+ interaction with human red cell membranes from normotensives and hypertensives. 370

We investigated the renin-angiotensin system in the genetically hypertensive (HBP), normotensive (NBP) and low blood pressure (LBP) mice developed by G. Schlager, one of the authors. Renin in the plasma, kidney and submaxillary gland was determined by enzymatic assay and by direct radioimmunoassay (DRIA). Trypsinization of mouse plasma was also investigated. PRA and plasma renin content were not significantly different in the different lines, sexes and generations. Trypsinization of the plasma revealed the presence of inactive renin, as has also been found in humans, hogs, dogs and rats. The proportion of active renin against trypsinized total renin was about 54-77% and was not significant in the different lines, sexes and generations. There was also no significant difference in renal renin content in the various lines, sexes and generations. However, in the submaxillary gland, renin content and activity were high in male mice, in every line. These data suggest that the renin-angiotensin system may not contribute to the established phase of blood pressure.
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PMID:Renin-angiotensin system in genetically hypertensive mice. 638 22

We studied the glomerular hemodynamics and activity of the tubuloglomerular feedback system (TGFS) in Wistar rats with persistent hypertension 60 days after removal of the clipped kidney in the Goldblatt (two-kidney, one clip) hypertension model. Ten hypertensive rats (HBP) were compared with 12 normotensive ones (NBP). Micropuncture studies revealed that values for the single nephron glomerular filtration rate (SNGFR), glomerular plasma flow (QA), and afferent oncotic pressure (PAR.A) were similar in both groups, whereas glomerular capillary pressure (PGC) and effective filtration pressure (EFP) were higher in the HBP group (p less than 0.05). A slight but insignificant increase in afferent resistance was present in the HBP group. A positive correlation was found between mean arterial pressure and stop flow pressure (SFP) (r = 0.64, p less than 0.05) but not with SNGFR, suggesting a reduction in the ultrafiltration coefficient in hypertensive rats. This was further supported by studies of the activity of the TGFS, which demonstrated that interrupting flow to the macula densa was followed by a smaller increment in SNGFR in HBP, in spite of a similar rise in SFP. The mechanism responsible for decreasing glomerular permeability is unknown but could be related to structural changes in glomerular capillary or to an increase in intrarenal angiotensin II, as has been demonstrated previously in this model. It is suggested that these adaptations occurring in the kidney exposed to hypertension can contribute to the maintenance of elevated arterial pressure after removing the stenotic kidney.
Hypertension
PMID:Glomerular hemodynamics in persistent renovascular hypertension in the rat. 665 58

Effects of NBP on liability of stroke, life span and neurological deficits following stroke were studied in stroke prone spontaneously hypertensive rats (SHRsp). The SHRsp rat was kept on 1% NaCl solution as drinking water and was fed 15 g soft food containing 0.6-0.8 g NaCl per day. Total NaCl intake for one rat was 1.1-1.3 g per day. After the onset of stroke, tap water and normal food was given instead of that containing NaCl. The neurological deficits were evaluated by a specially designed scoring system. These symptoms were divided into 4 degrees (1-4). Grade 1. stress (mild). Grade 2. forelimb or head twitch or with stress (severe). Grade 3. hemiparalysis, body inclined or disabled. Grade 4. paralysis, tremor or convulsion. Blood pressure, heart rate and body weight were measured once every 2 weeks. The weights of heart, brain and kidneys were also measured. The results show that NBP pre-treatment at the dose of 100 mg.kg-1.d-1 po delayed the onset of stroke. So, like nimodipine, NBP showed a stroke preventive action in SHRsp rats. In addition, treatment with NBP 100 mg.kg-1.d-1 po after the onset of stroke, the life span was prolonged and the score of neurological deficit decreased significantly. Because high blood pressure can not be lowered by NBP treatment, therefore, the protective effect against stroke can not be explained by the effect of hypotension. No change was found in BP, HR and the organ weight. The results indicate that NBP is expected to be useful in the treatment of stroke.
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PMID:[Effect of dl-3-n-butylphthalide (NBP) on life span and neurological deficit in SHRsp rats]. 876 59

The objective of the study was to assess the evolution of renin, angiotensin II, atrial natriuretic factor (ANF) and blood pressure (BP) in the first trimester following renal transplantation in man Thirty-two recipients were investigated for 3 months post-transplantation. Twenty had a history of hypertension with moderate cardiac hypertrophy. Thirty-one retained their native kidneys. Five kidney donors had a history of mild hypertension. The recipients were perioperatively volume-expanded with 0.9% saline and diuresis was maintained for 48 h with furosemide and dopamine. The sodium intake was 25 mEq/24 hours. Prophylactic immunosuppressive therapy was antilymphocyteglobulins (25 cases), or anti-LFA1 (7 cases) and maintenance therapy was cyclosporine-prednisone (8 cases), or cyclosporine-prednisone-azathioprine (24 cases). Mean BP, serum creatinine, urinary sodium excretion (UNA) and hormonal (renin, angiotensin II and ANF) parameters were collected every other day for the first week after transplantation and then twice monthly. Twenty (62.5%) patients developed hypertension and hypertension was more frequent in patients with a delayed graft function, than in patients with immediate good graft function (10/20 vs. 4/12, p < 0.05%). Both hypertensive (group HBP) and normotensive (group NBP) patients had similar very low renin and angiotensin II plasma levels, after an initial early peak. Analysis of covariance with multiple regression analysis showed that in the HBP patients, BP was negatively correlated with UNA (p = 0.02) and positively with plasma ANF (p < 0.01). The normal BP patients also showed a correlation between BP and UNA, although it was limit of statistical significance (p = 0.05); there was no correlation between ANF and BP. We conclude that the RAS is rapidly depressed after renal transplantation and does not interfere with BP regulation. The hypertension in the early stage of post-transplantation varies inversely with the urinary sodium excretion. The defective sodium excretion, which dominates the effect of the low sodium diet, results in volume overload, increased ANF and volume-dependent hypertension.
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PMID:Relationship between blood pressure and renin, angiotensin II and atrial natriuretic factor after renal transplantation. 928 46

The aim of the present study was to assess the long-term results of adrenalectomy and to evaluate potential risk factors for the persistence or recurrence of hypertension. Forty-five patients with Cushing's syndrome caused by benign cortisol-producing adrenocortical adenomas were evaluated before and for a period of 1 year after surgical cure. When the patients were classified into two groups according to whether their preoperative BP was more (HBP group) or less (NBP group) than 140/90 mmHg, the BP level was found to be continuously higher in the HBP group than in the NBP group during the year after surgery. This finding suggests that the preoperative BP level in Cushing's syndrome may be a determinant factor for persistent hypertension after surgery (P<0.05). In addition, a correlation was found between postoperative BP level and duration of hypertension (P<0.05), but no relationships were found between postoperative BP levels and other factors, including age, BMI, tumor size, serum cortisol, aldosterone, potassium, total cholesterol, or glucose levels. The above findings indicate that intensive control of preoperative BP to maintain it below 140/90 mmHg with antihypertensive medication is a very important means of improving prognosis for postoperative BP. Immediate diagnosis and surgical treatment to reduce the duration of hypertension are also crucial for the long-term BP prognosis.
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PMID:Risk factors associated with persistent postoperative hypertension in Cushing's syndrome. 1119 56

The purpose of the study is to establish a model of cold-induced stroke in hypertensive rats, and to study the preventive effect of dl-3n-butylphthalide ( NBP ) on stroke. Stroke-prone renovascular hypertension(RHRSP) was created in Sprague-Dawley rats. The animals were assigned randomly to NBP, aspirin treated and vehicle control group, with administration of the medications for 7 days, and then subjected to cold treatment in an environmentally controlled chamber for 3 days to induce the occurrence of stroke. The incidence of stroke, the volume of the brain lesion, patency of the microvessels by FITC-dextran perfusion and the number of microvessels by immunohisochemical detection of vwF were investigated. Cold induced different types of stroke in RHRSP. The incidence of ischemic stroke and the volume of the infarct were decreased, and the perfused microvessels were increased with NBP pretreatment. Our data suggest that NBP prevents cold-induced ischemic stroke via improvement of cerebral microvessels.
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PMID:dl-3n-butylphthalide prevents stroke via improvement of cerebral microvessels in RHRSP. 1755 27


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