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

The angiotensinogen gene locus (1q42-43) has been linked to hypertension in affected relative-pair studies (including a previous UK study), but the role of the Met-->Thr polymorphism at position 235 remains controversial. Using this marker, we investigated the relationship between angiotensinogen genotype and blood pressure in two data sets from the East Anglia region of the United Kingdom. Two hundred twenty-three untreated hypertensive and 187 normotensive control subjects were recruited through local general practices. Blood pressure (including pretreatment measurements in the hypertensive group), age, sex, body mass index, alcohol consumption, cholesterol level, and angiotensinogen genotype were recorded for all subjects. The influence of angiotensinogen genotype on blood pressure was assessed with a general linear model ANOVA with adjustment for age, sex, body mass index, and alcohol consumption. There was no evidence for an association between angiotensinogen genotype and blood pressure level in either the hypertensive or normotensive data set. Angiotensinogen genotype did not influence blood pressure in subjects aged < 50 years, women, or those with a body mass index < 26 kg/m2. We conclude that the angiotensinogen Met-->Thr polymorphism is not a marker for blood pressure level in these East Anglian subjects. Further studies are required to confirm the involvement of the 1q locus in the development of hypertension in UK subjects and to delineate the functional variant(s) in this chromosomal region that influences blood pressure.
Hypertension 1996 Nov
PMID:Blood pressure and the M235T polymorphism of the angiotensinogen gene. 890 43

Severe post-transplant obesity has previously been shown to have a negative impact on graft survival following kidney transplantation. It also contributes to late patient mortality and is associated with hypertension, diabetes and hyperlipidemia. We undertook Roux-en-Y gastric bypass (GBP) in three morbidly obese (200-260% ideal body weight) (IBW) patients 6-8 yr following kidney transplantation. Roux-en-Y gastrojejunostomy to a 30 ml stapled gastric pouch was created with the jejunojejunostomy (both loops) 80-120 cm from the ligament of Treitz. By 12 months post-GBP, weight loss plateaued at 100-150% IBW. Both patients that had developed post-transplant diabetes mellitus (PTDM) had complete resolution within 9 months following GBP. On average the patients required 3 less hypertension (HTN) medications after GBP; 2 of the 3 patients are now normotensive off medication. Improvements in hyperlipidemia were also shown. The absolute cyclosporine (CsA) requirement (mg/d) increased by approximately 33% (p = NS), and there was also a significant increase in the weight adjusted CsA requirement from 1.8 to 3.5 mg/kg/d (p = 0.02, ANOVA) following GBP in order to maintain similar TDX trough CsA levels. GBP offers significant reduction in weight, HTN, PTDM and hyperlipidemia in morbidly obese kidney transplant recipients. However, CsA dose requirements may increase after GBP as a consequence of the defunctionalized intestine.
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PMID:Gastric bypass in morbidly obese kidney transplant recipients. 893 Apr 54

The effects of chronic treatment with the specific AT1 angiotensin receptor antagonist, irbesartan, or the angiotensin converting enzyme inhibitor, enalapril, were assessed in uninephrectomized fawn-hooded hypertensive rats (FHH) and compared with vehicle treatment. Three days after uninephrectomy, irbesartan (240 mg/liter), enalapril (80 mg/liter) or vehicle were administered via the drinking water. Systolic blood pressure (SBP) and protein excretion rates (UprotV) were determined monthly. In rats receiving irbesartan (N = 7) and enalapril (N = 6) SBP (132 +/- 3 mm Hg and 133 +/- 6, respectively) was essentially normalized at 12 weeks when compared with vehicle (169 +/- 6 mm Hg (N = 6); all comparisons were P < 0.05 by ANOVA). Similarly, proteinuria was lower in irbesartan (44 +/- 12 mg/day) and enalapril (19 +/- 2) groups versus vehicle (123 +/- 10 mg/day). Treatment with both drugs was associated with marked reduction in glomerulosclerosis at 12 weeks (both < 5% vs. vehicle, 43 +/- 9%) without effect on glomerular volume. In identically prepared rats, glomerular capillary hydraulic pressure (PGC, estimated from stop-flow pressure, Psf) was lower in FHH receiving irbesartan (58 +/- 1 mm Hg, N = 6) or enalapril (54 +/- 2, N = 6) than in vehicle-treated rats, in whom PGC was greatly elevated (68 +/- 2 mm Hg; N = 7). Despite this, GFR and single nephron GFR were well maintained. These data support a critical role for AT1 receptor-mediated, angiotensin-dependent processes in the pathogenesis of hypertension in FHH, and further implicate elevated PGC as a major determinant of glomerular injury in this model.
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PMID:The angiotensin receptor antagonist, irbesartan, reduces renal injury in experimental chronic renal failure. 894 34

Similar to endothelial modulation of vascular tone, nitric oxide (NO) released from the coronary and endocardial endothelium may modulated LV performance with an improvement of LV diastolic distensibility. The aim of the present study was to assess a potential relationship between endothelial function and LV performance in essential hypertension. Thirty-nine normotensive subjects (NT) and 46 never treated hypertensive patients (HT) were grouped according to the renal vasodilatatory response to infusion of L-arginine (30 g within 60 min). HT patients responders to L-arginine (n = 19) were defined by an increased > or = 5% of renal plasma flow (RPF) estimated by the clearance of I-Hippuran. LV mass index and afterload-corrected fractional shortening were determined by echocardiography. Mitral peak early (E) and late (A) diastolic flow velocity were assessed by Doppler. Results of ANOVA were (means +/- SD): [table: see text] In HT patients E/A was positively correlated with %RPF (r = 0.27; p < 0.01) and negatively correlated with age (r = -0.52 p < 0.01) and systolic BP (r = -0.36 p < 0.01). In multiple regression analysis the relation between E/A and %RPF was dependent of age. This results confirm that aging and hypertension are the main determinants of the alteration of LV diastolic function. The link between these factors may be the endothelium which abnormal regulatory function secondary to aging and HT may be associated to an impairment of NO dependent LV relaxation.
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PMID:[Endothelial dysfunction and cardiac performance in untreated hypertension]. 894 63

To detect genetic loci responsible for stroke susceptibility, we produced 107 male F2 progenies crossed between stroke-prone spontaneously hypertensive rats (SHRSP/Izm) and normotensive Wistar Kyoto rats (WKY/Izm) and followed them up until they developed cerebral stroke. One hundred and twenty-five simple sequence repeat (SSR) markers were analyzed in these F2 rats. Nine of 107 F2 rats suffered from macroscopically overt stroke. In these 9 rats, the segregation ratio of 3 genotypes at 6 SSR marker loci on chromosomes 2, 4, 9, and 10 was highly distorted from the expected value (the observed sp/sp:sp/wky:wky/ wky ratio was either 6:3:0 or 6:2:1, while the expected was 1:2:1, p < 0.01 by chi 2 test). Further, the brain weight was significantly heavier (p < 0.001) in the F2 rats suffering from stroke, suggesting that the brain weight was a parameter for stroke. The brain weight of F2 rats cosegregated with D4Mit19, D4Mgh7, and D4Mgh8 (p = 0.0015, 0.0014, and 0.0040 by ANOVA, respectively) on chromosome 4 supporting genetic effects of this genetic loci on the pathogenesis of cerebral stroke. Blood pressure did not cosegregate with these markers on chromosome 4. These results suggest that a region on chromosome 4, independently of hypertension, determines genetic susceptibility to cerebral stroke.
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PMID:The region responsible for stroke on chromosome 4 in the stroke-prone spontaneously hypertensive rat. 895 54

A gene designated S(A) has been implicated in hypertension (HT) in rat genetic models and Japanese HT patients. However, a linkage study in whites was negative. Because of the limitations of genetic analyses, confirmation in different settings is imperative. Therefore, we conducted a cross-sectional case-control study involving 106 HT and 96 normotensive (NT) white subjects. A polymerase chain reaction technique was developed for PstI restriction fragment length polymorphism (RFLP) determination. We could find no association of this RFLP with HT (frequency of minor allele, A2 = 0.11 in HTs v 0.07 in NTs). However, A2 displayed an association with increase in body mass index in HTs: for a body mass index mean of 26 kg/m2 or more, A2 = 0.17 compared to 0.06 for body mass index of less than 26 kg/m2 (chi2 = 6.4, P = .01; odd ratio 3.4, 95% confidence interval 1.2 to 10.0); for a body mass index of 28 kg/m2 or more, A2 = 0.20 (chi2 = 10.4, P = .001; odds ratio 4.0, 95% confidence interval 1.5 to 10.5). Furthermore, A2 tracked significantly with elevation in body mass index in the HTs (F = 4.8, P = .01 by one-way ANOVA). In conclusion, we could find no association of S(A) genotype with HT, but obtained preliminary evidence for a possible association with variation in body mass index in a severely affected HT group with a strong family history of HT.
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PMID:Association analyses of S(A) gene variant in essential hypertensives. 905 79

1. An association between hyperinsulinaemia, insulin resistance and hypertension was previously described in spontaneously hypertensive rats (SHR). We therefore tested whether chronic exogenous hyperinsulinaemia, which did not affect blood pressure of normotensive rats, may aggravate hypertension in young SHR. 2. Insulin was administered for 4 weeks by a graded increase of a sustained release insulin implant, without carbohydrate supplementation. 3. Initial bodyweight of seven SHR and five sham-implanted control SHR, aged 6-8 weeks, was not different between the groups or by week 4. 4. Glucose levels decreased in the treated rats [2-way ANOVA F(1:10) = 18.7. P < 0.005] and were 7.3 +/- 0.1 mmol/L in the controls and 4.4 +/- 0.7 mmol/L in the treated SHR, respectively. Insulin levels were comparable at baseline and increased to 1002 +/- 978 pmol/L in treated rats at week 4 while remaining 270 +/- 78 pmol/L in the controls [F(1:10) = 6.1, P < 0.05]. The systolic blood pressure (tail-cuff) was significantly increased in insulin treated SHR in weeks 1-3[F(1:10) = 5.1, P < 0.05] though it was comparable at baseline and week 4. 5. In the presence of a hypertensive predisposition, chronic exogenous hyperinsulinaemia accelerates the time course of the development of hypertension without affecting its severity.
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PMID:Chronic exogenous hyperinsulinaemia accelerates the development of hypertension in spontaneously hypertensive rats. 907 91

103 patients who received a cyclosporine-treated primary cadaver kidney transplant (TX) at our center between 1985 and 1989, whose graft survived for more than 1 year and who accepted to undergo voiding cystography after TX were analyzed and grouped according to the highest grade (regardless to whether active or passive) of vesicourteral reflux (VUR): group 0, absent (n = 14); group 1-2, grade I or II (n = 62); group 3, grade III (n = 27). Patient follow-up ranged from 5 to 10 (median 7) years. Patient and graft survivals and prevalence of hypertension (defined as the persistent need of antihypertensive therapy), did not differ significantly between groups (Mantel-Cox test p: n.s. in all cases). GFR (Cockroft and Gault) and proteinuria were evaluated with ANOVA for repeated measures at 1, 2, 3, 4 and 5 years in the 96 patients (group 0: 13, group 1-2: 56, group 3: 27) whose grafts lasted for 5 years or more. Neither GFR values (p: n.s.) nor GFR behaviour over time (p: n.s.) differed between groups, although a progressive decline of GFR was noted in all groups (p < 0.002). Proteinuria neither showed any significant differences between groups in values (p: n.s.) or behaviour over time (p: n.s.), nor any trend in behaviour over time in all groups as a whole (p: n.s.). Finally, in the first 5 years after TX the 3 groups did not differ for number of urinary tract infections (UTIs) (mean value for all patients: 2.5, range 0-22, episodes/pt/5 years) (p: n.s.), or for number of UTIs with leukocyturia (mean 0.6, range 0-6, episodes/pt/5 years) (p: n.s.), or for number of febrile UTIs (mean 0.3, range 0-5, episodes/pt/5 years) (p: n.s.), or for number of UTIs with sepsis (mean 0.1, range 0-2, episodes/pt/5 years) (p: n.s.). The same results were obtained when, instead of episodes/ pt/5 years, percentages of patients without or with 1 or more of such episodes in the same period were considered. In conclusion, VUR does not seem to be hazardous for the transplanted kidney in the medium to long-term.
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PMID:Vesicoureteral reflux after kidney transplantation: clinical significance in the medium to long-term. 920 64

Endothelin-1 (ET-1) is a potent vasoconstrictor peptide derived from endothelial cells and may be important in the control of systemic blood pressure (BP) and local blood flow. Immunoreactive ET-1 plasma levels may be normal or elevated in human arterial hypertension, although the exact pathophysiological role of ET-1 remains to be established. The aim of our study was to determine the relationship between the components of the renin-angiotensin-aldosterone system and plasma ET-1 levels in patients with low, normal or high-renin essential hypertension. The study groups included 13 patients with low-renin essential hypertension (average age 43.5 +/- 16.2 years), 16 patients with normal-renin essential hypertension (46.5 +/- 13.4 years), 11 patients with high-renin essential hypertension (40.7 +/- 13.8 years) and 12 healthy subjects (43.1 +/- 11.4 years). Our results demonstrated that the mean ET-1 values of all patients with essential hypertension were 10.4 +/- 3.4 pg/ml; there was not a statistical correlation between plasma renin activity (PRA) and the ET-1 levels of hypertensives; instead there was a statistically significant correlation between plasma ET-1 and plasma aldosterone (PA) (r = 0.393; P < 0.026). In particular mean plasma ET-1 values in patients with low-renin essential hypertension (12.6 +/- 2.1 pg/ml) were significantly higher (ANOVA = 0.000, P < 0.05) than those of normotensive subjects (7.7 +/- 1.7 pg/ml), patients with normal-renin essential hypertension (8.5 +/- 2.8 pg/ml), and patients with high-renin essential hypertension (9.9 +/- 3.8 pg/ml), respectively. There was a statistical correlation between PA and ET-1 levels in patients with low-renin essential hypertension (r = 0.619, P < 0.024). Our study demonstrated that there was an increase of circulating ET-1 levels in patients with low-renin essential hypertension and ET-1 plasma levels correlated with PA. The results suggest that ET-1 may play an important role in this particular form of human essential hypertension.
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PMID:High plasma endothelin-1 levels in hypertensive patients with low-renin essential hypertension. 928 62

Cigarette smoking is a major risk factor for coronary heart disease. To further investigate the relationship of nicotine with other cardiac risk factors, we studied the impact of nicotine on blood pressure and glucose tolerance. Adult male Sprague-Dawley rats were randomly assigned to receive nicotine or placebo pellets implanted subcutaneously. Weight gain was controlled by pair-feeding, and was not significantly different between nicotine- and placebo-treated animals. Blood pressure (in mm Hg) increased throughout a 3-week treatment period in nicotine-treated animals and was significantly higher [P < .05 by two-way ANOVA] than in placebo-treated rats. Blood pressure returned to normal within 1 week following exhaustion of the pellets. Oral glucose tolerance tests performed 2.5 weeks after pellet placement showed similar glucose, insulin, and free fatty acid (FFA) profiles by two-way ANOVA. In summary, smokeless nicotine exposure leads to sustained but reversible hypertension without deterioration in glucose tolerance or insulin action when weight gain is controlled. We conclude that in rats smokeless nicotine adversely affects the coronary risk profile by increasing blood pressure.
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PMID:Smokeless nicotine administration is associated with hypertension but not with a deterioration in glucose tolerance in rats. 928 88


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