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PubMed2004

The methylentetrahydrofolate reductase gene variant (C677T) as a risk factor for essential hypertension in Caucasians.

Essential hypertension (EH) is a common, multifactorial disorder likely to be influenced by multiple genes of modest effect. The methylenetetrahydrofolate reductase (MTHFR) gene C677T mutation is functionally important, being strongly associated with reduced enzyme activity and increased plasma levels of homocysteine. Mild hyperhomocysteinemia is a known risk factor for cardiovascular disease (CVD) and hypothesised also to be involved in hypertension pathophysiology. The present study was performed to determine the prevalence of the 677T mutation in Australian Caucasian patients diagnosed with EH and to test whether the C677T variant is associated with the disorder. A case-control cohort, consisting of 250 EH patients and 250 age, sex and racially matched normotensive controls, were used for the association study. Comparison of C677T allele frequencies revealed a higher proportion of the mutant allele (T) in the EH group (40%) compared to unaffected controls (34%) (p=0.07). Furthermore, genotypic results indicated that the prevalence of the homozygous mutant genotype (T/T) in the affected group was higher than that of controls (14%:10%) (p=0.17). Interestingly, conditional logistic regression showed that the MTHFR C677T mutation conferred a mild, yet significant increase in risk of essential hypertension after adjusting for body mass index (odds ratio=1.57, 95% confidence interval: 1.04-2.37, p=0.03). These findings require further investigation in large independent samples, but suggest that essential hypertension, like CVD, may be mildly influenced by the MTHFR C677T variant.

Adult↗
PubMed2000

Dynamic renal function testing by compartmental analysis: assessment of renal functional reserve in essential hypertension.

BACKGROUND: In essential hypertension, acute haemodynamic changes due to dietary protein load cause patterns of acute changes in renal function that are fundamentally different from changes in normal controls. METHODS: Renal clearances of sinistrin, an inulin-like polyfructosan, and p-aminohippurate were determined before and after protein ingestion. These tests were performed in healthy controls and in patients with essential hypertension (mean arterial pressure of 112+/-2 mmHg, age, 52+/-2 years; mean+/-SEM) within a washout period, and after long-term treatment with carvedilol and fosinopril, respectively. RESULTS: In 15 healthy volunteers, protein ingestion increased glomerular filtration rate (GFR) from 110.3+/-3.6 to 120. 6+/-4.4 ml/min (P=0.0006; two-tailed pairwise t-test). In contrast, it led to an acute decrease in GFR in 16 hypertensive patients, from 111.8+/-2.9 to 103.6+/-3.3 ml/min (P=0.0010). The eight patients who were randomized to receive carvedilol improved in their renal response to protein (GFR increased from 101.4+/-6.4 to 107.1+/-5.4 ml/min; P=0.04), whereas the eight other patients randomized to receive fosinopril exhibited no change in GFR (final value 105+/-4.9 ml/min). In the patients, the acute shifts in renal plasma flows were not significant. Mean arterial blood pressure of the patients decreased from 112+/-2 to 100+/-3 mmHg (P=0.0015). CONCLUSIONS: In essential hypertension an acute protein load induces a decrease in GFR that may normalize under antihypertensive treatment. The acute changes in GFR can be reliably monitored by the here-described compartmental analysis method of renal functional reserve.

Adult↗
PubMed1975

Central neurohormonal mechanisms in spontaneously hypertensive rats compared with human essential hypertension.

Consideration of the results obtained in studies of spontaneously hypertensive rats indicates that these animals can serve as useful models for perhaps the most common type of essential hypertension of man. Other variants of essential hypertension probably occur where the relative balance between the genetic elements predisposing to high blood pressure may be somewhat different.

Animals↗
PubMed1996

Left ventricular structural and functional characteristics in patients with renovascular hypertension, primary aldosteronism and essential hypertension.

To investigate the effect of different etiologies of hypertension on left ventricular structure and function, we compared echocardiographic findings in 10 patients with renovascular hypertension (35 +/- 9 years), 10 patients with primary aldosteronism (42 +/- 9 years), and 14 patients with essential hypertension (41 +/- 6 years). There were no significant differences among the three groups in age, sex, body surface area, blood pressure, interventricular septal thickness, posterior wall thickness, left ventricular end-diastolic dimension or end-systolic dimension, relative wall thickness, left ventricular mass index, or spectrum of left ventricular adaptation (concentric remodeling, concentric hypertrophy, or eccentric hypertrophy). There were no differences in systolic function or diastolic function, which was assessed in terms of the peak rate of increase in dimension normalized for left ventricular end-diastolic dimension (dD/dt/D), the relaxation time, and the relaxation time to peak velocity of lengthening among groups. Multiple regression analysis showed that the systolic blood pressure was the most important determinant of left ventricular mass index (r = 0.56, P < .01), and that left ventricular mass index was the most important determinant of relaxation time and the relaxation time to peak velocity of lengthening (r = 0.48, P < .01 and r = 0.59, P < .01, respectively). The dD/dt/D was correlated only with left ventricular end-systolic dimension (r = 0.59, P < .01). Our results suggest that blood pressure may be a strong determinant of left ventricular hypertrophy, irrespective of the etiology of hypertension, and that the degree of hypertrophy may be related to left ventricular diastolic dysfunction in hypertensive patients with normal systolic function.

Adult↗
PubMed2005

Endothelial progenitor cell senescence is accelerated in both experimental hypertensive rats and patients with essential hypertension.

OBJECTIVES: Recent studies have revealed an association between coronary risk factors and both the number and function of bone marrow-derived endothelial progenitor cells (EPCs). Although hypertension is an important coronary risk factor, the influence to the EPCs is not fully understood. We investigated the effect of hypertension on EPC senescence. METHODS: Experimental study We investigated the number and senescence of EPCs in spontaneously hypertensive rats (SHR/Izm) and deoxycorticosterone acetate (DOCA)-salt hypertensive rats. EPCs were isolated from peripheral blood of rats and were characterized. EPC senescence was detected by acidic beta-galactosidase staining. In addition, we measured the telomerase activity using polymerase chain reaction-enzyme-linked immunosorbent assay. CLINICAL STUDY: EPCs were isolated from peripheral blood samples in 37 patients with essential hypertension. After ex-vivo cultivation, we detected senescence and measured the telomerase activity. The total severity index of hypertension-induced organ damage was calculated by the summation of each severity index in the classification of hypertension severity by Tokyo University (1984). RESULTS: Experimental study The EPC senescence in SHR/Izm and DOCA-salt hypertensive rats was significantly increased compared with that of control rats. The telomerase activities in SHR/Izm and DOCA-salt hypertensive sensitive rats were also significantly lowered compared with those of control rats. Clinical study Compared with the control group, EPCs from hypertensive patients showed accelerated senescence and also showed reduced telomerase activity. In hypertensive patients, the degree of hypertension-induced organ damage was negatively correlated with telomerase activity, and was positively correlated with EPC senescence. CONCLUSIONS: EPC senescence is accelerated in both experimental hypertensive rats and patients with essential hypertension, which may be related to telomerase inactivation. The hypertension-induced EPC senescence may affect the process of vascular remodeling.

Aged↗
PubMed1985

Effects of converting enzyme inhibition on blood pressure, plasma renin activity (PRA) and plasma aldosterone in hypertensive diabetics compared to patients with essential hypertension.

Hypertension with diabetes mellitus has been associated with suppression of the renin-angiotensin-aldosterone system. We have studied the effects of the converting enzyme inhibitor, captopril, on blood pressure, plasma renin activity (PRA) and plasma aldosterone in 10 stable hypertensive diabetic subjects and 10 age-matched patients with essential hypertension. There was no clinical evidence of complication in the diabetic subjects and their diabetic treatment remained unchanged throughout the study. Mean captopril doses used were similar in both groups. In the diabetics and the essential hypertensives, treatment resulted in a significant and similar decrease in blood pressure. Pre-treatment basal and stimulated PRA and the change of PRA with captopril were also similar. Pre-treatment stimulated plasma aldosterone and the response of aldosterone to postural stress was significantly lower in the diabetic group, suggesting an impaired adrenal responsiveness to stress. Despite this, our findings indicate that the hypotensive action of captopril is at least as effective in hypertension associated with otherwise uncomplicated diabetes mellitus as in essential hypertension.

Aldosterone↗
PubMed1980

Captopril affects blood pressure equally in renovascular and essential hypertension and in the fluid-depleted anephric state.

1. The haemodynamic effects of 100 mg of captopril in renovascular hypertension (n = 11), essential hypertension (n = 12) and the anephric state (n = 7) were compared. Brachial artery pressure was measured in all patients, and changes in right atrial pressure, pulmonary artery pressure, pulmonary capillary wedge pressure and cardiac output were followed in renovascular and essential hypertension. Nephrectomized patients were studied before and after fluid withdrawal by ultrafiltration. 2. The pretreatment concentration of active renin in plasma was 100 +/- 24 mu-units/ml (mean +/- SEM) in renovascular hypertension, and 24 +/- 4 mu-units/ml in essential hypertension. In nephrectomized patients pretreatment renin was 1.7 +/- 0.3 mu-units/ml, and renin was unresponsive to withdrawal of 1.8 +/- 0.21 of body fluid. 3. The effects of captopril were maximal after 60-90 min. Mean arterial pressure after 90 min was lowered by 19 +/- 4% in renovascular hypertension, by 17 +/- 4% in essential hypertension and by 16 +/- 3% in fluid-depleted nephrectomized patients. These changes were not significantly different despite the marked differences in renin. Captopril had no effect on arterial pressure in the fluid-replete anephric state. 4. The effects of captopril on cardiac filling pressures and cardiac output in renovascular and essential hypertension were also not different. 5. It is concluded that the antihypertensive action of captopril may be largely independent of circulating renin.

Adult↗
PubMed1992

Urinary calcium excretion in essential hypertension.

Patients with essential hypertension have been reported to have higher levels of urinary calcium excretion (UCaV) than normotensive persons. We tested the hypothesis that the calciuria of hypertension is due to dietary factors and evaluated several alternate mechanisms. UCaV was studied in 15 patients with essential hypertension compared with 16 age- and gender-matched normotensive control subjects. For subjects taking self-selected, free-living diets, the difference in UCaV between normotensive (130 +/- 14 mg/day) and hypertensive subjects (201 +/- 37 mg/day) was not significant (p = 0.1). However, in a controlled diet with moderately restricted sodium intake (88 mEq), urinary calcium excretion was significantly higher (p = 0.02) in the hypertensive than in the normotensive group receiving 400 mg calcium (204 +/- 25 vs 132 +/- 13 mg/day) and 1400 mg calcium (272 +/- 31 vs 187 +/- 25 mg/day). Twenty-four-hour UCaV was directly and significantly correlated with blood pressure (r = 0.63 for standing systolic blood pressure; p < 0.001). A 1000 mg oral calcium load caused similar changes in UCaV (0.12 +/- 0.11 vs 0.12 +/- 0.07 mg per 100 ml glomerular filtration) and serum ionized calcium level (0.06 +/- 0.08 vs 0.06 +/- 0.02 mmol/L) in normotensive and hypertensive subjects, respectively, suggesting that there was no difference in intestinal calcium absorption between the groups. Fasting UCaV did not differ between the hypertensive (8.9 +/- 4.5 mg per 2 hours) and normotensive groups (10.9 +/- 11.5 mg per 2 hours).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Plasma levels of atrial natriuretic peptide in patients with borderline and essential hypertension.

Plasma levels of atrial natriuretic peptide (ANP) were measured in outpatients with borderline hypertension (n = 15) and essential hypertension (n = 13) and in normotensive subject (n = 11). There were no significant differences among the three groups in age, serum protein, albumin, or electrolyte levels, plasma renin activity (PRA), or plasma concentrations of aldosterone and cortisol. The plasma ANP levels in the normotensive, borderline hypertensive, and essential hypertensive subjects were 36 +/- 6 pg/ml (mean +/- S.E.), 64 +/- 11 pg/ml, and 82 +/- 14 pg/ml, respectively. The levels in the essential hypertensive subjects were significantly (p less than 0.05) higher than those in the normotensives. In both borderline and essential hypertensives (n = 28), the plasma ANP levels were significantly correlated positively with systolic blood pressure (r = +0.385, p less than 0.05), and negatively with PRA (r = -0.484, p less than 0.05) and serum total calcium (r = -0.516, p less than 0.01). These results suggest that the elevation of circulating ANP in hypertensives is involved in the pathogenesis of hypertension.

Adult↗
PubMed2001

Effect of calcium antagonist or beta blockade treatment on nitric oxide-dependent vasodilation and oxidative stress in essential hypertensive patients.

OBJECTIVES: Essential hypertension is associated with impaired endothelium-dependent vasodilation caused by oxygen free radical-induced nitric oxide (NO) breakdown. Since calcium antagonists can improve endothelial function in hypertensive patients, we tested whether this beneficial effect could be related to restoration of NO availability by antioxidant activity. METHODS: In 10 healthy subjects and 20 essential hypertensive patients, we studied forearm blood flow (strain-gauge plethysmography) modifications induced by intrabrachial acetylcholine (from 0.15-15 microg/100 ml per min), bradykinin (0.005-0.05 microg/100 ml per min), two endothelium-dependent vasodilators, and sodium nitroprusside (1-4 microg/100 ml forearm tissue per min), an endothelium independent vasodilator, in the absence and presence of NG-monomethyl-L-arginine (L-NMMA) (100 microg/100 ml forearm tissue per min), an NO synthase inhibitor. RESULTS: In controls, vasodilation to acetylcholine and bradykinin was inhibited by L-NMMA. In hypertensive patients, vasodilation to acetylcholine and bradykinin, but not to sodium nitroprusside, was blunted and resistant to L-NMMA. Hypertensive patients were randomized to a 12-week treatment with lacidipine (4-6 mg/daily) or atenolol (50-100 mg/daily) (n = 10 each group). Lacidipine but not atenolol increased the vasodilation to acetylcholine and bradykinin and restored the inhibiting effect of L-NMMA on endothelium-dependent vasodilation, without affecting the response to sodium nitroprusside. Moreover, lacidipine reduced circulating markers of oxidative stress including plasma and low-density lipoprotein (LDL) hydroperoxides, the susceptibility of LDL to Cu2+-induced oxidation and the reactive oxygen species generated from human umbilical vein endothelial cells after incubation with LDL derived from plasma of the patients. CONCLUSIONS: Lacidipine increases endothelium-dependent vasodilation by restoring NO availability, and this effect possibly is related to antioxidant activity.

Adrenergic beta-Antagonists↗
PubMed2003

Short-term blood pressure variability in renovascular hypertension and in severe and mild essential hypertension.

This study was designed to examine short-term blood pressure variability (BPV) in patients with different severity and forms of chronic medically treated hypertension. Power spectral analysis of BPV was performed from continuous finger blood pressure (Finapres) recordings. Ten patients with renovascular hypertension (RVHT), 34 with severe essential hypertension (SEHT) and 29 with mild essential hypertension (MEHT) as well as healthy age- and sex-matched control subjects were studied. The RVHT group was characterized by reduced low frequency (LF) power of both systolic and diastolic BPV (P =0.004 and P =0.003 respectively) when compared with the control group. There was also a tendency to lower total power of diastolic BPV (P =0.094). On the contrary, the SEHT group had increased total power of diastolic BPV (P =0.044). However, in the SEHT group, we found no differences in the LF and high frequency power of systolic and diastolic BPV when compared with controls. The MEHT group presented with lower LF power of systolic and diastolic BPV (P =0.028 and P =0.003 respectively) and, in addition, high frequency power of diastolic BPV was lower than in the control group (P =0.020). When the hypertensive groups were compared with each other, total power and LF power of diastolic BPV (P =0.043 and P =0.039 respectively) were lower in the RVHT group than in the SEHT group. In addition, total power of diastolic BPV was lower (P =0.030) in the MEHT group than in the SEHT group. No differences were observed in BPV between the RVHT and MEHT groups. The results show that BPV in hypertensive patients groups behaved differently. This suggests that both the aetiology and severity of hypertension have a significant influence on short-term BPV measured in laboratory conditions and that different control mechanisms are operating in these clinically distinctly different hypertension groups.

Adrenergic beta-Antagonists↗
PubMed1989

A program for oriented treatment of essential hypertension.

Treatment of essential hypertension is often a complex task and needs appropriate methodology. A newly developed computer program can help physicians to choose the best pharmacological approach to the treatment of essential hypertension. Based on an oriented clinical history, the program asks the user to give the physiological, pathological and pharmacological antecedents of the patient to be treated. Taking into account these characteristics, 19 antihypertensive drugs are ordered according to their indications and contraindications in the patient. Diet advice based on body weight and the patient's habits are considered as well. The program is designed to explain why decisions are made, so it can be useful in teaching medical students or postgraduates.

Antihypertensive Agents↗
PubMed1982

The relation of genetics to essential hypertension: a review.

Essential hypertension is fundamentally a genetic disease which emerges because of environmental impact. The genetic factors involve intracellular abnormalities which affect calcium metabolism within smooth muscle cells and possibly within the heart and sympathetic nervous system. These abnormalities are influenced by one or more proteins of which calmodulin is a candidate. Sodium pump abnormalities may be primary but may be secondary feedback effects. Homeostasis keeps the blood pressure and cardiac function normal, but eventually becomes less effective. Such homeostasis is produced by negative feedback, but positive external factors also influence the eventual results. Gross homeostasis is provided by the baroreceptors, the renin-angiotensin-aldosterone system, etc. The malfunction of any one or any combination of these systems may produce or accelerate hypertension. Hyperplasia and hypertrophy of arteriolar smooth muscle play their role but also multiply the genetic cellular defects. It is possible that in the early history of man essential hypertension had an advantage which now has become obsolete because normotensive man's potential lifespan has been increased by modern civilization.

Animals↗
PubMed2002

Short- and long-term neuroadrenergic effects of moderate dietary sodium restriction in essential hypertension.

BACKGROUND: In essential hypertension, marked restrictions in dietary sodium intake cause in the short-term period an increase in muscle sympathetic nerve traffic (MSNA) and a baroreflex impairment. The present study was set out to assess on a long-term basis the neuroadrenergic and reflex effects of moderate sodium restriction. METHODS AND RESULTS: In 11 untreated mild to moderate essential hypertensive patients (age 42.0+/-2.6 years, mean+/-SEM), we measured beat-to-beat blood pressure (Finapres), heart rate (ECG), and MSNA (microneurography) at rest and during stepwise intravenous infusions of phenylephrine and nitroprusside. Measurements were performed at regular sodium intake, after 1 and 8 weeks of low-sodium diet (80 mmol NaCl/d), and repeated again at regular sodium intake. After 1 week, urinary sodium excretion was markedly reduced. This was accompanied by a slight blood pressure reduction, no heart rate change, and a significant increase in plasma renin activity, aldosterone, and MSNA (+23.0+/-4.6% P<0.05). Whereas baroreflex heart-rate control was unchanged, baroreflex modulation of MSNA was reduced by 46.8+/-5.1% (P<0.01). At the end of the 8-week low-sodium diet, the neurohumoral and baroreflex responses were similar to the ones observed after 1 week of the dietary intervention. All changes disappeared when regular sodium diet was restored. CONCLUSIONS: Thus, a moderate dietary sodium restriction triggers a sympathetic activation and a baroreflex impairment. Maintenance of low-sodium diet for several weeks does not attenuate these adverse adrenergic and reflex effects.

Adult↗
PubMed1992

Sympathomoderating influence of benazepril in essential hypertension.

OBJECTIVE: In essential hypertension, captopril attenuates forearm vasoconstriction reflexly induced by deactivation of cardiopulmonary and arterial baroreceptors, thus exerting a sympathomoderating effect. We investigated whether this is a common effect of angiotensin converting enzyme (ACE) inhibitors. METHODS AND DESIGN: Cardiopulmonary and arterial baroreceptors were deactivated by progressively reducing central venous pressure (CVP) through progressively greater lower body negative pressures in eight untreated mild essential hypertensives on a moderately low-sodium diet (50 mmol/l per day). This deactivation was performed after oral administration of the non-sulphidrylic ACE inhibitor benazepril (10 mg) and placebo according to a double-blind randomized crossover experimental design. RESULTS: After placebo, the reduction in CVP increased forearm vascular resistance (FVR; mean arterial pressure: plethysmographic forearm blood flow ratio). After benazepril, baseline blood pressure (beat-to-beat finger pressure) and FVR were significantly reduced whilst plasma angiotensin II was suppressed and PRA increased (both measured by radioimmunoassay). The FVR increases induced by progressive CVP reduction were less than after placebo administration, and the overall difference was statistically significant. Benazepril did not affect the reflex FVR reduction observed by increasing CVP through leg raising, nor the reflex changes in plasma norepinephrine measured by high-performance liquid chromatography accompanying the changes in FVR. CONCLUSIONS: Benazepril attenuates sympathetic vasoconstriction as does captopril. This effect (which is mainly operative during an increased sympathetic drive and exerted through a reduction of adrenoceptor responsiveness) is thus likely to be a class- rather than a compound-related feature.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1987

Altered calcium metabolism in red blood cells of hypertensives: persistent marker or sequel of essential hypertension?

The characteristics of the increased calcium (Ca) influx observed in metabolically depleted red blood cells (RBCs) of hypertensive patients were investigated. Twenty-four normotensives, 16 untreated essential hypertensives, and 10 essential hypertensives under sufficient blood pressure control by 50-100 mg/day atenolol were studied. Free intracellular concentrations of Ca, sodium (Na), and potassium (K) were assessed using ion-selective electrodes in freeze-thawed RBCs, which were metabolically depleted by 30 mM desoxy-glucose at 37 degrees C for 48 h. In the treated hypertensives values for Ca and K at 24 and 48 h were not different from values for the normotensives, whereas elevated Ca was found in RBCs of untreated hypertensives. Na in treated hypertensives was significantly increased at 0 and 48 h, thus, being similar to values for untreated hypertensives. Additionally, RBCs of six normals were stressed in a glass/teflon potter. Before metabolic depletion electrolytes were not affected by this procedure, while Ca at 24 and 48 h of metabolic depletion increased to significantly higher values for the hypertensive patients as compared to the controls. These results suggest that the altered Ca metabolism in the RBCs of hypertensives may reflect a secondary phenomenon due to the mechanical damage to RBCs by the elevated blood pressure.

Atenolol↗