Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The present study was designed to evaluate the possible beneficial effects of biofeedback-assisted relaxation to pharmacotherapy on blood pressure and heart rate in patients with essential hypertension. Twenty patients with essential hypertension and without any complications or end-organ damage participated in the study. All the patients were using anti-hypertensive drugs. The study protocol consisted of an interview, 10 days baseline, 10 biofeedback-assisted relaxation sessions and a 10-day post-treatment period. Interview blood pressure (BP) and heart rate (HR) measurements, baseline mean values of systolic blood pressure (SBP), diastolic blood pressure (DBP) and HR recorded during the 1st, 10th and 20th minutes of each session and the post-treatment mean values were evaluated. Significant differences were found between the mean values of SBP, DBP and HR after the whole treatment protocol (Wilcoxon signed-ranks test). The mean values of SBP, DBP and HR measurements recorded during the 1st, 10th and 20th minutes of the biofeedback-assisted relaxation sessions, which were evaluated by repeated measures of ANOVA on ranks test, showed a significant decrease only for the 10th minute values at the end of the whole treatment program. Despite a short follow-up, it was suggested that these results were encouraging considering the fact that once the patients are thoroughly instructed in home practice of relaxation and encouraged to develop their own strategies for relaxation, the long term outcome may also be promising.
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PMID:Biofeedback assisted relaxation in essential hypertension: short-term follow-up of contributing effects of pharmacotherapy on blood pressure and heart rate. "Brief communication". 917 85

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

Insulin resistance and hyperinsulinemia are associated with essential hypertension. There is also evidence of hyperinsulinemia in women who developed hypertension in pregnancy (P). The present study examines whether chronic hyperinsulinemia in pregnant rats plays a role in the development of hypertension in pregnancy. A sustained-release insulin pellet was implanted subcutaneously in 15 Wistar rats (P-INS) 1 wk before and on day 7 of pregnancy; 14 control rats were sham-implanted (P-SHAM). Tail-cuff systolic BP (SBP), serum triglycerides, glucose, insulin, renal function, and urinary excretion of Na+ and of metabolites of nitric oxide were determined throughout pregnancy. Data were analyzed by ANOVA with basal body weight as covariate analysis of covariance. Results are expressed as the mean +/- SD. Body weight; water and food intake; urine volume; creatinine clearance; and level of proteinuria at the end of pregnancy were similar in both groups. The number of fetuses was 9 +/- 2.3 in P-INS versus 11 +/- 2.4 in pregnant control rats (P < 0.05). Before mating, SBP was similar, but at the end of pregnancy SBP was 110 +/- 18 mmHg in P-INS versus 85 +/- 12 mmHg in pregnant rats (P < 0.05). Serum triglycerides and Na+ were also higher in P-INS rats. The fractional excretion of Na+ was 3.1 +/- 1.0 versus 4.4 +/- 1.5, respectively (P < 0.01). The percent increase in nitric oxide metabolite excretion was 233 +/- 14 versus 370 +/- 17%, respectively (P < 0.01). Chronic hyperinsulinemia, without sugar supplementation, and hypertriglyceridemia may cause a decrease in the synthesis of nitric oxide in P-INS rats. The development of hypertension in these rats may be associated with an impaired vasodilatation, together with an increased renal sodium reabsorption.
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PMID:Chronic exogenous hyperinsulinemia in pregnancy: a rat model of pregnancy-induced hypertension. 944 81

The aim of our study was to evaluate the relationships between endothelial function, small resistance artery structure, and blood pressure in patients with primary or secondary hypertension. Sixty subjects were included in the study: 9 patients with pheochromocytoma, 10 with primary aldosteronism, 17 with renovascular hypertension, and 13 with essential hypertension with 11 normotensive subjects who served as controls. Clinic and 24-hour ambulatory blood pressure (ABPM) were evaluated. All subjects were submitted to a biopsy of subcutaneous fat. Small resistance arteries were dissected and mounted on a micromyograph and the media/lumen ratio was calculated. A dose-response curve to acetylcholine was performed at cumulative concentrations from 10(-9) to 10(-5) mol/L. The vasodilator response to acetylcholine was similarly impaired in the four groups of hypertensive patients (ANOVA P<.05 versus normotensive controls), without any significant difference among them. In subcutaneous small arteries of patients with either primary aldosteronism or renovascular hypertension, a marked increase in media:lumen ratio was observed, while in patients with pheochromocytoma, the extent of vascular structural alterations was similar to that observed in essential hypertension. No significant correlation between media-lumen ratio or clinic blood pressure and maximum acetylcholine-induced vasodilatation was observed. On the contrary, a significant, albeit not very close, correlation between ABPM values and maximum acetylcholine-induced vasodilatation was observed (r=34, P<.05 with 24-hour systolic blood pressure, r=0.36, P<.05 with 24-hour diastolic blood pressure). In conclusion, endothelial dysfunction seems to be independent from the degree of vascular structural alterations and from the etiology of hypertension, and it is probably more linked to the hemodynamic load.
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PMID:Endothelial dysfunction in hypertension is independent from the etiology and from vascular structure. 945 25

To determine the effects of an oral glucose challenge on cellular Na+/H+ exchange in vivo we measured plasma glucose concentrations, plasma insulin concentrations, plasma C-peptide concentrations, arterial blood pressure, cytosolic pH (pHi) and cellular Na+/H+ exchange in 24 patients with essential hypertension (HT) and 41 age-matched healthy normotensive control subjects (NT) during a standardized oral glucose tolerance test. Under resting conditions, the plasma glucose concentrations, plasma insulin concentrations, plasma C-peptide concentrations and Na+/H+ exchange activity were significantly higher in HT compared with NT (P < 0.05 in each case). A significant increase in lymphocytic Na+/H+ exchange activity was only seen in NT (resting 0 h: (4.23 +/- 0.2) x 10(-3) pHi/s; mean +/- S.E.M.; 1 h after glucose administration: (6.00 +/- 0.56) x 10(-3) pHi/s; 2 h after glucose administration: (6.65 +/- 0.64) x 10(-3) pHi/s; P = 0.0003 by Friedman's two-way ANOVA), but not in HT (resting 0 h: (6.07 +/- 0.36) x 10(-3) pHi/s; 1 h after glucose administration: (6.72 +/- 1.02) x 10(-3) pHi/s; 2 h after glucose administration: (6.71 +/- 0.62) x 10(-3) pHi/s; P = 0.7470). During an oral glucose challenge the systolic (P < 0.0001) and diastolic (P < 0.0001) blood pressure significantly decreased in HT but not in NT. Essential hypertension shows abnormal in vivo regulation of Na+/H+ exchange and blood pressure following oral glucose intake.
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PMID:Na+/H+ exchange during an oral glucose challenge in patients with essential hypertension. 948 89

Angiotensin II type 1 receptor (AT1) mediates the vasoconstrictive and growth-promoting effect of angiotensin II in humans. It has been reported that a polymorphism of the AT1 gene (an A/C transversion at position 1166: A-C1166) occurs more frequently in resistant hypertensives taking two or more antihypertensive drugs. On the contrary, a recent study of the influence of the A-C1166 polymorphism on aortic stiffness demonstrated that the distribution of the genotypes did not differ between normotensive and hypertensive subjects. In addition, a recent population-based survey of Caucasian hypertensives reported lower blood pressure values in CC homozygotes than in heterozygotes and AA homozygotes. Because of these controversial results and the lack of a sufficient amount of data the present study was designed to assess the contribution of the AT, gene A-C1166 polymorphism to resistant essential hypertension. Forty-eight subjects with resistant essential hypertension (HT) and 48 normotensive (NT), age and sex-adjusted controls (from a population of 300 healthy blood donors) were selected. All subjects were genotyped for the A-C1166 polymorphism in the 3'-UTR of the AT1 gene using PCR-based techniques. The influence of genotype on blood pressure (BP) was investigated using ANOVA Randomized Complete Block (ANOVA RCB) design according to sex, age and BMI. There were no significant differences in allele or genotype frequencies between HT and NT subjects (X2 = 0.61; P = NS). In HT subjects higher values of systolic blood pressure were associated with the C allele of the AT1 gene only in older and overweight patients (P < 0.001 and P < 0.001, respectively). Also in HT patients an association between the presence of the C allele of the AT1 gene and higher values of diastolic blood pressure was present in overweight patients (P = 0.001). These results suggest that in resistant hypertensive subjects the AT1 A-C1166 polymorphism is potentially involved in the regulation of blood pressure. As the effects of genotypes on blood pressure are pronounced in older and overweight subjects this polymorphism may amplify the effects of age and BMI on resistant essential hypertension.
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PMID:Association of angiotensin II type 1 receptor polymorphism with resistant essential hypertension. 949 6

Felodipine is a second-generation dihydropyridine calcium antagonist used to treat mild to moderate arterial hypertension. The authors used venous occlusion plethysmography to study the effect of this drug on lower limb arterial inflow and venous outflow in 10 at rest patients with mild essential hypertension. They also sought correlations between changes in district blood flow and blood pressure. Plethysmography was carried out at 8 AM and 4, 8, and 24 hours later at baseline (after washout), on the first day of treatment with a single daily administration of 10 mg felodipine ER, and after 7 and 30 days of treatment. The drug was given after the 8 AM evaluation. The authors determined rest flow, maximal venous incremental volume (MVIV) at 40 mmHg and 60 mmHg, and gradient of venous volume between 60 and 40 mmHg divided by the pressure difference (DV/DP) as index of venous distensibility. On the days of plethysmographic evaluation, arterial blood pressure and heart rate were measured continuously over 24 hours by the ABPM (Ambulatory Blood Pressure Monitoring). The results were analyzed by ANOVA. Rest flow, MVIV, and DV/DP were stable at the baseline evaluation. On days 1, 7, and 30 of treatment the rest flow after 4 and 8 hours was significantly greater than at 8 AM but had always returned to normal after 24 hours. No other plethysmographic parameters changed significantly; in particular venous outflow remained unchanged. Mean arterial, systolic, and diastolic blood pressure were significantly reduced, compared with baseline, following treatment on the first day and after 7 and 30 days' treatment. There was no effect on heart rate. The authors conclude that felodipine is useful for the treatment of mild essential hypertension, since it reduces arterial resistance without altering venous capacitance or distensibility.
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PMID:Effect of felodipine on arterial blood flow and venous function at rest in patients with mild essential hypertension. 959 29

-Essential hypertensives display enhanced signal transduction through pertussis toxin-sensitive G proteins. The T allele of a C825T variant in exon 10 of the G protein beta3 subunit gene (GNB3) induces formation of a splice variant (Gbeta3-s) with enhanced activity. The T allele of GNB3 was shown recently to be associated with hypertension in unselected German patients (frequency=0.31 versus 0.25 in control). To confirm and extend this finding in a different setting, we performed an association study in Australian white hypertensives. This involved an extensively examined cohort of 110 hypertensives, each of whom were the offspring of 2 hypertensive parents, and 189 normotensives whose parents were both normotensive beyond age 50 years. Genotyping was performed by polymerase chain reaction and digestion with BseDI, which either cut (C allele) or did not cut (T allele) the 268-bp polymerase chain reaction product. T allele frequency in the hypertensive group was 0.43 compared with 0.25 in the normotensive group (chi2=22; P=0.00002; odds ratio=2.3; 95% CI=1.7 to 3.3). The T allele tracked with higher pretreatment blood pressure: diastolic=105+/-7, 109+/-16, and 128+/-28 mm Hg (mean+/-SD) for CC, CT, and TT, respectively (P=0.001 by 1-way ANOVA). Blood pressures were higher in female hypertensives with a T allele (P=0.006 for systolic and 0.0003 for diastolic by ANOVA) than they were in male hypertensives. In conclusion, the present study of a group with strong family history supports a role for a genetically determined, physiologically active splice variant of the G protein beta3 subunit gene in the causation of essential hypertension.
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PMID:G-protein beta3 subunit gene (GNB3) variant in causation of essential hypertension. 985 80

A locus for essential hypertension has been found recently on chromosome 17 in the general vicinity of the inducible nitric oxide synthase (iNOS) gene (NOS2A at 17cen-q11.2). We therefore tested NOS2A markers for association and linkage with hypertension in affected Australian Anglo-Caucasians. Patients for the association study (n=112) were from our cohort of hypertensives (systolic/diastolic=175+/-25 SD/112+/-19 mm Hg) who were the offspring of 2 hypertensive parents; control subjects (n=164) were normotensives whose parents were both normotensive. The linkage study involved 156 hypertensive sib-pairs. Genotypes for an 8-allele pentameric repeat located 2.6 kb upstream of NOS2A and of a biallelic tetranucleotide repeat 0.7 kb upstream were determined by polymerase chain reaction and automated gene scan analysis. In the association study, the frequency of the minor allele of the biallelic marker was 0.18 in the hypertensives and 0.14 in the normotensives (chi21 df=1.1, P=0.3). Allele frequencies for the multiallelic marker were also similar in each group (chi2 7 df=9.8, P=0.2). Furthermore, no genotypic differences in blood pressure were apparent. In the sib-pair study, SPLINK APM, and MAPMAKERS/SIBS did not indicate excess allele sharing. We also examined genotype as a function of age. In the younger (< 60 years) hypertensives as well as younger or older normotensives, genotype and allele frequency of the biallelic marker was similar (0.12 to 0.14). However, in hypertensives >/=60 years of age, frequency of the minor allele was 0.28 (chi2=7.4, P=0.006). Homozygotes for this allele were rare. Frequency of heterozygotes was 0.19 for normotensives but 0.39 for the older hypertensives (chi2=8.0, P=0.018) and was 0.40 for hypertensive sibs >/=60 years of age with a diastolic pressure >/=100 mm Hg. Furthermore, homozygotes for the major allele were 7 years younger than heterozygotes (P=0.05 by ANOVA). In conclusion, the present study shows (1) no evidence for a role of NOS2A in hypertension and (2) a genotypic difference in frequency of a NOS2A promoter variant in older hypertensives, seen in 2 different cohorts. A possible interpretation of the latter observation is that NOS2A genotype could affect longevity, at least in patients at high risk by having moderate to severe hypertension.
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PMID:Different frequencies of inducible nitric oxide synthase genotypes in older hypertensives. 1020 25


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