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)

1. Increased urinary albumin excretion is common in patients with essential hypertension and is at least to some extent correlated with prevailing blood pressure levels. However, the generalized vascular dysfunction present in advanced atherosclerotic disease may independently influence this parameter. 2. To evaluate this possibility, we assessed blood pressure, ultrasonographic carotid thickness, cardiac mass, minimum forearm vascular resistances, metabolic parameters and the angiotensin-converting enzyme genotype in patients with untreated essential hypertension and atherosclerotic peripheral vascular disease (n = 11). The results were compared with similar data obtained in matched groups of patients with uncomplicated hypertension and with normotensive control subjects (n = 11 per group). 3. Urinary albumin excretion was higher in hypertensive patients with atherosclerosis than in those without complications; carotid thickness was higher in atherosclerotic patients and a positive, statistically significant correlation existed between this parameter and urinary albumin excretion. In the same patient group, systolic blood pressure, fasting insulin and triacylglycerol levels were elevated and correlated with urinary albumin levels. However, differences in urinary albumin excretion persisted after taking into account the influence of those parameters by analysis of covariance. The distribution of angiotensin-converting enzyme genotype patterns and values of cardiac mass and minimum forearm vascular resistances did not differ significantly among the experimental groups. 4. The data suggest that vascular status may influence urinary albumin excretion in patients with essential hypertension, while confirming the importance of systolic blood pressure levels as a determinant of the raised urinary albumin excretion.
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PMID:Urinary albumin excretion and atherosclerosis in essential hypertension. 903 90

Insertion/deletion (I/D) polymorphism of angiotensin-I-converting enzyme (ACE) gene was studied by use of the polymerase chain reaction in 168 normal subjects living in Moscow region and in 70 patients: 38 with essential hypertension (EH), 9 of which survived myocardial infarction at young age, 13 with hypertrophic cardiomyopathy (HCMP) and 19 with myocardial infarction (MI). Left ventricular hypertrophy (LVH) was detected in 24 of 38 EH patients. There was a highly significant increase in the frequency of the ID genotype in EH patients compared to the controls (62.4% versus 32.7%, P < 0.01). There was a relevant decrease in the frequency of the DD genotype in EH patients in comparison with the control (20.8% versus 47.6%, P < 0.05). These results strongly suggest that the ACE gene is associated with EH. No significant differences in both allele and genotype frequencies of the ACE gene were revealed in two groups of patients with MI and with HCMP compared to the controls. Thus, no relations between the ACE gene and these disorders were observed. In hypertensives with MI the II genotype was not detected and the frequency of both D allele and DD genotype was sufficiently increased compared to normotensive patients with MI. Thus, the DD genotype in hypertensives may be a risk factor for MI. The frequency of the DD genotype was significantly increased in hypertensive patients with LVH compared to the uncomplicated hypertension (37.5% versus 7.1%, P < 0.05). Therefore, this genotype is associated with LVH in hypertensive subjects.
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PMID:[The polymorphism of the angiotensin-converting enzyme gene in patients with hypertension, left ventricular hypertrophy and the development of a myocardial infarct at a young age. Preliminary report]. 941 19

The aim of this study was to evaluate whether salt-sensitivity in essential hypertension produces a significant comparative difference in diastolic function and ventricular mass when compared with sodium-resistance. Recent epidemiological data have demonstrated a positive correlation between sodium intake and arterial pressure. Furthermore, a positive correlation has been detected between sodium intake and left ventricular hypertrophy (LVH) independently of arterial pressure. Thirty-one patients who had never been treated before for uncomplicated hypertension were studied. Each subject received a 30 mmol/per day sodium diet for 14 days, supplemented with a further 190 mmol of sodium in the first study week (220 mmol for the first 7 days and 30 mmol for the second 7 days). Throughout the study compliance was assessed by measuring daily urinary sodium excretion. Sodium sensitivity of blood pressure was defined as the difference (5% or more) between blood pressure at the end of the low and high sodium intake periods. On this basis 16 patients were defined as salt-sensitive (SS) and 15 patients as salt-resistant (SR). The two groups were homogeneous for age, sex and race. Baseline mean arterial pressure (MAP) was comparable between SS (108 +/- 1.8 mm Hg) and SR (107 +/- 2.1 mm Hg, P = NS). Each patient was submitted to M-MODE and two-dimensional echocardiogram studies in order to estimate left ventricular mass using the Penn conventional formula and parameters of left ventricular diastolic function. The left ventricular mass measurement showed higher values in the SS group although this did not reach statistical significance (118.4 +/- 4.4 vs 112.0 +/- 4.2 gr/mq, P = NS). Both interventricular septal and posterior wall thickness did not demonstrate significant differences between the two groups. The salt-sensitive group showed impaired left ventricular diastolic function; in particular, the first diastolic peak representing the early maximum of diastolic filling velocity (E) was lower in SS subjects than in SR subjects (71.6 +/- 2.9 vs83.1 +/- 3.3 cm/sec, P < 0.02). No significant difference was detected in the second peak representing the atrial maximum of filling velocity (A) (69.0 +/- 2.3 vs 66.0 +/- 2.0 cm/sec, P = NS). As a consequence the E/A ratio was significantly different (0.73 +/- 0.2 in the SR vs 1.2 +/- 0.04 in the SS group, P < 0.05). Moreover, the peak E integral was lower in SS than in SR subjects (8. 7 +/- 0.6 vs11.2 +/- 0.5 cm, P < 0.005; no difference for the peak A integral (6.0 +/- 0.3 vs 5.7 +/- 0.4 cm, P = NS). The E peak deceleration time was significantly reduced in the SS group (400.3 +/- 13.5 vs 500.9 +/- 12.8 cm/sec, P < 0.001). No significant difference was found for the isovolumetric relaxation time (IVRT) (95.7 +/- 4.3 vs 92.2 +/- 4.0, P = NS). Our data show an impaired diastolic function expressed by a reduced early diastolic filling velocity (peak E) and a significantly abnormal E/A ratio in SS in comparison with SR subjects. Therefore abnormalities in diastolic function are detectable earlier in SS hypertensive subjects than in SR irrespective of actual MAP.
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PMID:Early abnormalities in left ventricular diastolic function of sodium-sensitive hypertensive patients. 1051 43

We examined the effects of the vasodilator peptide adrenomedullin (AM) infused intravenously into subjects with essential hypertension. Eight men 39 to 58 years old with uncomplicated hypertension (147/96+/-5/3 mm Hg at baseline) were studied in a placebo-controlled, crossover design. Each subject received intravenous AM in a low and a high dose (2.9 and 5.8 pmol. kg(-1). min(-1) for 2 hours each) or vehicle-control (Hemaccel) infusion in a random order on day 4 of a controlled metabolic diet (80 mmol/d Na(+), 100 mmol/d K(+)). Plasma AM reached pathophysiological levels during infusion (18+/-4 pmol/L in low dose, 34+/-9 pmol/L in high dose) with a concurrent rise in plasma cAMP (+8.4+/-1.2 pmol/L, P:<0. 05 compared with control). Compared with control, high-dose AM increased peak heart rate (+17.8+/-2.3 bpm, P<0.01), lowered systolic (-24.6+/-0.9 mm Hg; P<0.01) and diastolic (-21.9+/-1.4 mm Hg; P<0.01) blood pressure, and increased cardiac output (+1.0+/-0. 1 L/min in low dose, +2.9+/-0.2 L/min in high dose; P<0.01 for both). Despite a rise in plasma renin activity during high dose (P<0.05), aldosterone levels did not alter. Plasma norepinephrine levels increased 1295+/-222 pmol/L (P<0.001) and epinephrine increased 74+/-15 pmol/L (P<0.05) with high-dose AM compared with control. AM had no significant effect on urine volume and sodium excretion. In subjects with essential hypertension, the intravenous infusion of AM to achieve pathophysiological levels produced significant falls in arterial pressure, increased heart rate and cardiac output, and stimulated the sympathetic system and renin release without concurrent increase in aldosterone. Urinary parameters were unaltered. Although AM has potent hemodynamic and neurohumoral effects in subjects with essential hypertension, the threshold for urinary actions is set higher.
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PMID:Hemodynamic, hormone, and urinary effects of adrenomedullin infusion in essential hypertension. 1104 Feb 40

More than 50% of patients with mild uncomplicated hypertension will need combination therapy to reach target blood pressure, as defined by the Joint National Committee. This percentage is even higher in hypertensive patients with diabetes, renal impairment and congestive heart failure in whom target blood pressures are lower. Combination therapy of angiotensin converting enzyme inhibitor and low dose diuretic offers distinct advantages in the treatment of essential hypertension. The two drug classes may have a synergistic effect on hypertensive target organ disease and blood pressure. Triple therapy with a calcium antagonist may be needed to achieve blood pressure control in more severely hypertensive patients.
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PMID:The choice of first-line therapy: rationale for low-dose combinations of an angiotensin converting enzyme inhibitor and a diuretic. 1171 46

The aim of the study was to examine whether the circulating cell adhesion molecules, von Willebrand factor (vWf) and endothelin-1, are elevated in patients with essential hypertension with no other risk factors for atherosclerosis and thus may serve as a markers of endothelial dysfunction in uncomplicated hypertension. Furthermore, the effect of treatment with the ACE inhibitor, quinapril, on levels of endothelial dysfunction markers were studied. The levels of adhesion molecules (intercellular cell adhesion molecule-1 [ICAM-1], E-selectin, P-selectin), von Willebrand factor (vWf) and endothelin-1 were measured in patients with hypertension without any other risk factors of atherosclerosis before and after treatment with quinapril (n = 22) and in normotensive controls (n = 22). Compared with normotensive subjects, the hypertensive patients had significantly higher levels of ICAM-1 (238 vs 208 ng/ml, P = 0.02), vWf (119 vs 105 IU/dl, P < 0.05) and endothelin-1 (5.76 vs 5.14 fmol/ml, P < 0.05). Three-month treatment of hypertensive patients with quinapril led to a significant decrease in the levels of endothelin-1 (5.76 vs 5.28 fmol/ml, P < 0.01). We did not observe significant changes in the levels of adhesion molecules and vWf after ACE inhibitor treatment, although a trend toward a decrease was apparent with all these parameters. Patients with uncomplicated hypertension with no other risk factors of atherosclerosis had significantly elevated levels of ICAM-1, vWf, and endothelin-1. Our data suggest that these factors may serve as markers of endothelial damage even in uncomplicated hypertension. In hypertensive patients, treatment with the ACE inhibitor quinapril resulted in a significant decrease in endothelin-1 levels. These findings indicate a beneficial effect of ACE inhibitors on endothelial dysfunction in hypertensive patients.
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PMID:Circulating intercellular cell adhesion molecule-1, endothelin-1 and von Willebrand factor-markers of endothelial dysfunction in uncomplicated essential hypertension: the effect of treatment with ACE inhibitors. 1214 57

Current clinical guidelines state that only beta-blockers, diuretics, calcium channel antagonists and ACE inhibitors should be used for initial pharmacotherapy for uncomplicated hypertension. On basis of experience, efficacy and costs beta-blockers and diuretics are first choice. However, the importance of the renin-angiotensin-aldosterone-system in the pathophysiology of hypertensive end-organ damage is increasingly recognised nowadays, and modulation of this system may therefore exert favourable effects on cardiovascular and cerebrovascular complications. In the LIFE study, a recently published double-blinded, randomised trial, the angiotensin-II receptor (A-II) antagonist losartan was compared with the beta-blocker atenolol in patients with essential hypertension and left ventricular hypertrophy (LVH). Patients randomised to the A-II antagonist suffered statistically significantly fewer clinical end-points, specifically fewer cerebrovascular accidents, whereas both treatments resulted in a similar decrease in blood pressure. In the subset of diabetic patients, the use of the A-II antagonist yielded an even more favourable outcome. In our opinion, it should now also be permitted to prescribe A-II antagonists as initial pharmacotherapy for patients with uncomplicated essential hypertension. It might be considered to prescribe A-II antagonists as preferred treatment for patients with essential hypertension and known LVH, especially in diabetic patients.
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PMID:[Treatment of hypertension: angiotensin-II antagonists potentially better than beta-blockers in the occurrence of cardiovascular and cerebrovascular damage; the LIFE study in perspective]. 1267 53

This study was designed to determine whether the levels of soluble intercellular adhesion molecule-1 (sICAM-1) and tumor necrosis factor-alpha (TNF-alpha) were elevated in subjects with uncomplicated hypertension who presented with no other risk factors or evidence of athero-sclerosis. The effects of administration of an angiotensin type-1 antagonist (losartan) on the serum concentrations of these molecules were also examined. Twenty hypertensive (HT) subjects (12 men and 8 women, mean age 49.1 +/-7.2 years) without other risk factors or cardiovascular disease received placebo for 4 weeks. The patients were then treated with losartan (50 mg/day) for 24 weeks. After 4, 12, and 24 weeks of losartan treatment, sICAM-1 and TNF-alpha levels were measured. The same parameters were measured in 20 normotensive control subjects (C), matched for sex and age. HT had sICAM-1 and TNF-alpha basal values higher than C (respectively 351.7 +/-97.4 vs 201.6 +/-32.3 ng/mL, p<0.001 and 31.8 +/-2.4 vs 15.3 +/-2.2 pg/mL, p<0.001). There was a positive correlation between sICAM-1 and TNF-alpha levels, but no correlation in HT between the average diastolic and systolic blood pressure (clinic and ambulatory monitoring) and the sICAM-1 or TNF-alpha levels was observed. Losartan treatment caused a significant decrease of sICAM-1 levels at the end of the first month of treatment (300.2 +/-64.4 ng/mL, p<0.05), but the values reverted to the basal levels at the following time points. No variation of TNF-alpha levels during losartan treatment was observed. These results show that patients with uncomplicated mild essential hypertension presented with high plasma ICAM-1 and TNF-alpha concentrations. Although all the patients were responsive to the antihypertensive treatment with losartan, their plasma concentrations of TNF-alpha were not modified, and sICAM-1 concentrations decreased only for a short period of time. This suggests that in uncomplicated hypertension other factors besides the blood pressure modulate the endothelial inflammation.
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PMID:Effects of AT1 receptor antagonist losartan on sICAM-1 and TNF-alpha levels in uncomplicated hypertensive patients. 1502 75

Structural and functional changes in large and small arteries in hypertension, even at early stages, may affect one or several end organs such as the brain, heart, and kidneys, contributing to cardiovascular morbidity and mortality. Therefore, modern treatment strategies should not only target blood pressure (BP) reduction but also normalize vascular structure and function. The purpose of this article is to review the large body of evidence, from randomized double-blind clinical trials, that has been gathered in regard to the angiotensin-converting enzyme (ACE) inhibitor perindopril, demonstrating its efficacy in reducing BP, reversing abnormalities of vascular structure and function in patients with essential hypertension, and ultimately preventing cardiovascular events. At the site of small resistance arteries, long-term treatment with perindopril, but not atenolol, reduced arterial wall hypertrophy for a given BP reduction. The improvement in small artery function in response to structural changes is exemplified at the site of the coronary circulation. Perindopril increased coronary blood flow and coronary reserve, in parallel with the regression of periarteriolar and interstitial collagen of coronary arterioles. At the site of large arteries, long-term treatment with perindopril reduced carotid and radial artery wall hypertrophy, and reduced carotid artery internal diameter. In response to these structural changes, large artery function improved at the site of the carotid and brachial arteries, showing a higher arterial distensibility, and at the site of the coronary circulation, showing a normalized arterial dilation in response to a cold pressor test or an increase in blood flow. Moreover, in patients with end-stage renal disease, perindopril decreased pulse wave velocity independently of BP changes, resulting in a highly significant relative risk reduction in all-cause and cardiovascular mortality. The multifactorial antiatherosclerotic profile of perindopril suggests a beneficial effect not only in patients with uncomplicated hypertension but also in patients with established coronary heart disease or previous stroke, as exemplified by the EUropean trial on Reduction Of coronary events with Perindopril in stable coronary Artery disease (EUROPA) and the Perindopril pROtection aGainst REcurrent Stroke Study (PROGRESS).
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PMID:Evidence for benefits of perindopril in hypertension and its complications. 1612 52

Limited evidence is available about the relationship between ambulatory heart rate (HR) and target organ damage (TOD) in uncomplicated hypertension. We sought to investigate the association between ambulatory HR and subclinical cardiac, vascular and renal markers of TOD in never-treated essential hypertensives. A total of 580 subjects with recently diagnosed (<or= 1 year) grade 1 and 2 hypertension, categorized by tertiles of HR levels, assessed by two 24-h ambulatory blood pressure monitoring at 1- to 4-week interval, sex and the presence or absence of TOD were considered for this analysis. All subjects also underwent laboratory and ultrasonographic investigations searching for microalbuminuria (MA), left ventricular hypertrophy (LVH) and carotid atherosclerosis (carotid thickening/plaque). In the whole population, as well as in both genders, LVH, carotid atherosclerosis and MA prevalence rates did not significantly increase with 48-h HR tertiles. When patients were categorized according to the presence or absence of TOD (that is, LVH, carotid atherosclerosis or MA) no significant intergroup differences in 48-h HR were found. Furthermore, average 48-h HR was similar in patients without organ involvement as in those with one, two or three TOD signs. Finally, in a multivariate analysis age, 48-h systolic blood pressure and metabolic syndrome assessed by ATP III criteria, but not HR were independently associated with TOD. Our findings showing that 48-h ambulatory HR is not associated with markers of TOD do not support the view that a faster HR may have an additive value in predicting organ damage in the early phases of essential hypertension.
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PMID:Ambulatory heart rate and target organ damage in never-treated essential hypertensives. 1782 95


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