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PubMed1999

Identification of a polymorphic glutamic acid stretch in the alpha2B-adrenergic receptor and lack of linkage with essential hypertension.

Essential hypertension, a clinically significant elevation in blood pressure with no recognizable cause, is believed to be attributable to the collective effect of genetic predisposing factors in combination with specific environmental factors, such as diet and stress. Of the genetic causes, genes coding for proteins involved in blood pressure regulation, such as the alpha- and beta-adrenergic receptors, are obvious candidates. The alpha2-adrenergic receptor plays a key role in the sympathetic nervous system by mediating the effects of epinephrine and norepinephrine. To evaluate the potential role between the alpha2B receptor and essential hypertension, we scanned the alpha2B-receptor gene for genetic variation in 108 affected sibling pairs. The screening revealed two major forms of the receptor. They differ by the presence of either 9 or 12 glutamic acid residues in the acidic domain of the third cytoplasmic loop of the protein. Investigation of the pattern of this variation in hypertensive sibling pairs suggests that the alpha2B receptor locus does not contribute substantially to genetic susceptibility for essential hypertension.

Alleles↗

PubMed2001

Chromosome 17 and the inducible nitric oxide synthase gene in human essential hypertension.

Essential hypertension is a common multifactorial trait that results in a significantly increased risk for heart attack and stroke. The condition has a genetic basis, although at present the number of genes is unknown. In order to identify such genes, we are utilising a linkage scanning approach using microsatellite markers and affected sibships. Here we provide evidence for the location of at least one hypertension susceptibility locus on chromosome 17. Analysis of 177 affected sibpairs gave evidence for significant excess allele sharing to D17S949 (SPLINK: P=0.0029; MAPMAKER SIBS: P=0.0033; ASPEX: P=0.0061; GENEHUNTER: P=0.0096; ANALYZE (SIBPAIR): P=0.0025) on 17q22-24, with significant allele sharing also indicated for an additional marker, D17S799 (SPLINK: P=0.025; MAPMAKER SIBS: P=0.025) located close to the centromere. Since these two genomic regions are well separated, our results indicate that there may be more than one chromosome 17 locus affecting human blood pressure. Moreover, further investigation of this chromosome, utilizing a polymorphism within the promoter of the iNOS candidate gene, NOS2A, revealed both increased allele sharing among sibpairs (SPLINK: P=0.02; ASPEX: P=0.00004) and positive association (P=0.034) of NOS2A to essential hypertension. Hence these results indicate that chromosome 17 and, more specifically, the NOS2A gene may play a role in human essential hypertension.

Alleles↗

PubMed2003

Calcium antagonist treatment by lercanidipine prevents hyperpolarization in essential hypertension.

Essential hypertension is associated with impaired endothelium-dependent vasodilation caused by oxidative stress-induced nitric oxide (NO) breakdown and compensatory production of a hyperpolarizing factor. To test whether calcium antagonist treatment can restore NO availability and prevent hyperpolarization through antioxidant properties, in 15 healthy subjects and 15 patients with essential hypertension, we studied forearm blood flow (strain-gauge plethysmography) modifications induced by intrabrachial bradykinin (5, 15, 50 ng/100 mL per minute), an endothelium-dependent vasodilator, in basal conditions, during infusion of NG-monomethyl-l-arginine (L-NMMA, 100 microg/100 mL per minute), an NO-synthase inhibitor, and ouabain (0.72 microg/100 mL per minute), an Na+-K+ ATPase inhibitor to prevent hyperpolarization. These infusions were repeated in the presence of the antioxidant vitamin C (8 mg/100 mL/min). The response to sodium nitroprusside was also evaluated. In controls, vasodilation to bradykinin was inhibited by L-NMMA and remained unchanged by ouabain or vitamin C. In hypertensive patients, vasodilation to bradykinin was blunted and resistant to L-NMMA but sensitive to ouabain. Vitamin C increased the response to bradykinin and restored the inhibiting effect of L-NMMA while preventing the effect of ouabain. In hypertensive patients, infusions were repeated after 3-month treatment with lercanidipine (10 to 20 mg daily). Lercanidipine decreased plasma lipoperoxides, isoprostanes, and malondialdehyde and increased plasma antioxidant capacity. Moreover, lercanidipine increased the vasodilation to bradykinin and restored the inhibiting effect of L-NMMA on bradykinin-induced vasodilation while preventing the effect of ouabain. Finally, vitamin C no longer exerted its facilitating activity. These results indicate that in essential hypertension, lercanidipine increases endothelium-dependent vasodilation by restoring NO availability and preventing hyperpolarization, an effect probably determined by antioxidant activity.

Antioxidants↗

PubMed2002

[The effect of aspirin on rheological properties of erythrocytes in essential hypertension].

Essential hypertension is one of the most important risk factors for cardiovascular diseases. Its pathophysiological mechanism is unknown. Recent data suggests that deformability and aggregation of red blood cells may play an important role in the regulation of blood rheology in hypertension. Simultaneously there are reports suggesting that antihypertensive effects of angiotensin converting enzyme inhibitors (ACEI) could be counteracted by high doses of aspirin. We postulate that these effects could be related to the changes in blood rheology. Accordingly we designed a study to evaluate the effect of low or high dose of aspirin on deformability and aggregability of red blood cells from patients with essential hypertension. Deformability and aggregability of red blood cells were measured by laser diffractometer (Rheodyn SSD, Myrenne GmbH) and computerized automatic aggregometer (MA1 Myrenne GmbH, Germany), respectively. The effects of aspirin on deformability and aggregation of red blood cells were studied ex vivo in whole blood from three groups of patients with essential hypertension (group I: 10 patients receiving placebo, group II: 23 patients receiving 75 mg/day p.o. aspirin for 3 days, and group III: 23 patients receiving 300 mg/day p.o. aspirin for 3 days). Subjects in all groups received the same combination of antihypertensive agents consisting of: one of ACEI (enalapril or perindopril), one of beta-antagonists (metoprolol or bisoprolol), and diuretic agent (indapamid). In patients receiving high dose of aspirin (300 mg/day) we observed that erythrocyte aggregability was 25% higher than in the placebo group (MEA = 25.8 +/- 6 SD, vs MEA = 20.6 +/- 3 SD, p < 0.05). Aspirin had no effects on deformability of erythrocytes or on arterial blood pressure. High doses of aspirin or possibly also other nonsteroidal anti-inflammatory drugs (NSAID) in patients receiving antihypertensive therapy can directly affect rheological properties of the blood due to the activation of red blood cell aggregation. Increased aggregation of red blood cells during antihypertensive therapy may be an important indicator of the worsening of organ perfusion.

Adrenergic beta-Antagonists↗

PubMed1986

Spectrum of deranged sodium homeostasis in essential hypertension.

Essential hypertension is thought to produce a uniform exaggerated natriuresis and diuresis. Because validation of this formulation in humans is incomplete, the natriuretic and diuretic responses to acute volume expansion were characterized by using water immersion to the neck. This method provides a volume stimulus identical to that induced by 2 L of saline without plasma compositional change. Twenty-seven subjects with essential hypertension were studied on three occasions in the seated posture while in balance on a 10 mEq Na, 100 mEq K diet: during the seated control study, during 4 hours of head-out immersion, and during saline infusion (2 L/2 hours). Four subjects had exaggerated urinary Na excretion in response to neck immersion (Group 3), and 16 had a normal response (Group 2) indistinguishable from that of 15 previously studied normal subjects. The remaining seven subjects (Group 1) had blunted or absent natriuretic responses compared with that in normal subjects (p less than 0.005). Similar results were obtained with saline administration; cumulative Na excretion in Group 1 was markedly less than that in Group 2 and the normal subjects. The heterogeneity in Na excretion indicates that an exaggerated natriuresis is not a uniform concomitant of essential hypertension. The significant inverse correlation between basal plasma aldosterone level and peak urinary as well as cumulative Na excretion suggests that plasma aldosterone constitutes a determinant of the differing natriuretic responses. In contrast to findings with urinary Na excretion, the diuretic responses of Groups 1 and 2 were identical. The striking dissociation between renal Na and water handling underscores the specificity of the derangement in renal Na handling.

Adult↗

PubMed1991

The aetiology of essential hypertension.

Essential hypertension is primarily hereditary. The property inherited is present in all cells but because of adaptation and differentiation it is particularly prominent in systemic vascular smooth muscle. This inherited property is manifested functionally as increased reactivity to vasoactive substances, such as (-)noradrenaline and angiotensin II. This abnormal function is present before the onset of hypertension. Vascular hypertrophy and hyperplasia are not only caused by hyperactivity of the smooth muscle and by the hypertension itself but are also trophic effect of the agonists, especially noradrenaline. The only two proteins in vascular smooth muscle which can produce both contractile and trophic effects are the guanosine triphosphate binding protein (Gs) and phospholipase C. Phospholipase C has already been demonstrated to be abnormally active in response to agonists in the spontaneously hypertensive rat and in human essential hypertension. The Gs protein is less likely to be critically abnormal since it is active in the vascular smooth muscle relaxation cascade as well as in contraction. None of the other proteins involved in vascular smooth muscle contraction or relaxation affect both contractile reactivity and cellular growth. There are many secondary effects dependent upon the phospholipase C abnormality such as calcium (Ca2+) cellular content, Ca2+ Mg2+ ATPase pump effects and possibly Ca2+ Na+ exchange. There are also many secondary effects impinging on the phospholipase C abnormality including changes in noradrenaline and angiotensin II metabolism. Present antihypertensive therapy is directed largely at secondary factors dependent upon or influencing the primary phospholipase C cascade. The path is now open for a more direct and basic diagnostic and therapeutic attack.

Humans↗

PubMed2006

Decreased pituitary response to insulin-induced hypoglycaemia in young lean male patients with essential hypertension.

Essential hypertension is associated with changes in central catecholaminergic pathways which might also be reflected in the pituitary response to stress stimuli. The aim of this study was to determine whether the response of pituitary hormones, cortisol, plasma renin activity, aldosterone and catecholamines to insulin-induced hypoglycaemia is changed in hypertension. We studied 22 young lean male patients with newly diagnosed untreated essential hypertension and 19 healthy normotensive, age- and body mass index (BMI)-matched controls. All subjects underwent an insulin tolerance test (0.1 IU insulin/kg body weight intravenously) with blood sampling before and 15, 30, 45, 60 and 90 min after insulin administration. Increased baseline levels of norepinephrine (P<0.05), increased response of norepinephrine (P<0.001) and decreased response of growth hormone (P<0.001), prolactin (P<0.001), adrenocorticotropic hormone (P<0.05) and cortisol (P<0.001) were found in hypertensive patients when compared to normotensive controls. Increased norepinephrine levels and a decreased pituitary response to metabolic stress stimuli may represent another manifestation of chronically increased sympathetic tone in early hypertension.

Adult↗

PubMed1998

Effects of isolated systolic hypertension and essential hypertension on large and middle-sized artery compliance.

BACKGROUND: Systolic hypertension of the elderly is characterized by a reduction in arterial compliance. Whether and to what extent this involves arteries of various structure and size is not well known. OBJECTIVE: To study carotid and radial artery compliance in systolic hypertension of the elderly, compared to essential hypertension and normotension. METHODS: We investigated 28 elderly patients with systolic hypertension (age 68.6 +/- 1.4 years, mean +/- SE; systolic blood pressure > 160 mmHg and diastolic blood pressure < 90 mmHg) plus 17 age-matched patients with essential hypertension and 15 age-matched healthy normotensive subjects. Radial and carotid artery compliance were evaluated using echotracking techniques. In both arteries compliance was assessed statistically and dynamically, i.e. as compliance values throughout the diasto-systolic pressure range. Measurements included intima-media wall thickness of the radial artery. RESULTS: Compared to normotensive subjects, carotid artery compliance was reduced in essential hypertension and more so in systolic hypertension. However, although in both groups radial artery wall thickness was markedly greater than in the normotensive group, radial artery compliance was markedly reduced in systolic hypertension, but unchanged in essential hypertension. CONCLUSIONS: In systolic hypertension of the elderly the reduction of arterial compliance is marked in both muscular and large elastic arteries, while in elderly essential hypertensives changes in arterial compliance are more heterogeneous, i.e. only carotid artery compliance is reduced. The different effects of these two types of hypertension on arterial mechanics are visible throughout the physiological range of blood pressure and probably accounted for by different alterations in vessel wall structure.

Aged↗

PubMed2003

[Genetic aspect of essential hypertension].

Essential hypertension affects up to 30% of the adult population; its pathogenesis involves interactions between genetic and environmental factors. Improved understanding of the molecular basis of essential hypertension may facilitate the development of new targeted forms of pharmacological therapy that can be tailored to the needs of individual patients and thereby minimize the risk of morbidity and mortality from cardiovascular diseases. The genetic analysis of complex traits and diseases such as blood pressure and hypertension is difficult because of their polygenic origin, genetic heterogeneity, variable penetrance, unknown modes of inheritance, and variable effects of environmental factors. Molecular variants of the angiotensinogen (AGT) gene, a key component of the renin-angiotensin system, are considered a genetic risk for primary hypertension. Some of the genotypes can be used to identify individual patients who would benefit from a specific anti-hypertensive treatment as well as from a specific life style modification.

Angiotensinogen↗

PubMed1981

Histocompatibility antigens in black patients with essential hypertension.

Essential hypertension is a common disorder with potentially life-threatening sequelae. Hypertension among black persons may have characteristics different from hypertension among white persons. It has been estimated that up to 60% of population variance in blood pressure may be attributable to genetic differences. We studied the distribution of HLA antigens in 100 black hypertensives and 100 normotensive controls. Hypertension was not significantly associated with any of the 25 HLA antigens identified. We conclude that HLA-A and HLA-B locus antigens are not associated with essential hypertension in the black patient.

Adult↗

PubMed2001

Restoration of nitric oxide availability after calcium antagonist treatment in essential hypertension.

Essential hypertension is associated with impaired endothelium-dependent vasodilation caused by oxygen free radical-induced nitric oxide (NO) breakdown. Because calcium antagonists can improve endothelial function in patients with essential hypertension, in this study we tested the hypothesis that this beneficial effect could be related to restoration of NO availability by antioxidant properties. In 15 healthy subjects and 15 hypertensive patients, we studied forearm blood flow (strain-gauge plethysmography) modifications induced by intrabrachial acetylcholine (ACh; 0.15, 0.45, 1.5, 4.5, and 15 microg/100 mL per minute), an endothelium-dependent vasodilator in basal conditions, during infusion of N:(G)-monomethyl-L-arginine (L-NMMA, 100 microg/100 mL forearm tissue per minute), an NO-synthase inhibitor, vitamin C (8 mg/100 mL forearm tissue per minute), and finally, simultaneous infusion of L-NMMA and vitamin C. The response to sodium nitroprusside (SNP; 1, 2, and 4 microg/100 mL forearm tissue per minute) was also evaluated. In control subjects, vasodilation to ACh was inhibited by L-NMMA and not changed by vitamin C. In hypertensive patients, vasodilation to ACh was blunted as compared with control subjects and resistant to L-NMMA. Vitamin C, which decreased plasma isoprostanes and increased plasma antioxidant capacity, increased the response to ACh and restored the inhibiting effect of L-NMMA. In hypertensive patients, the study was repeated after 3-month treatment with nifedipine gastrointestinal therapeutic system (30 to 60 mg/daily). Nifedipine treatment decreased circulating plasma lipoperoxides and isoprostanes and increased plasma antioxidant capacity. Moreover, nifedipine increased the vasodilation to ACh but not to SNP and restored the inhibiting effect of L-NMMA on ACh-induced vasodilation, whereas vitamin C no longer exerted its facilitating activity. These results indicate that nifedipine increases endothelium-dependent vasodilation by restoring NO availability, an effect probably determined by antioxidant activity.

Acetylcholine↗

PubMed1998

G-protein beta3 subunit gene (GNB3) variant in causation of essential hypertension.

-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.

Age of Onset↗

PubMed1993

Effects of doxazosin, a selective alpha 1-inhibitor, on plasma insulin and blood glucose response to a glucose tolerance test in essential hypertension.

Essential hypertension is characterized by an insulin-resistance state that may be responsible for the increased atherogenesis typical of this disease. To investigate the effect on glucose and insulin metabolism of doxazosin, an antihypertensive drug whose favorable impact on lipid metabolism is well known, 10 newly diagnosed essential hypertensive patients of the same age and body mass index (BMI) were selected for our study. They underwent an oral glucose tolerance test (OGTT) with measurement of plasma insulin levels before and after a 6-month treatment period with doxazosin. In this period of time, they took no other drugs and followed no diets, nor did their weights vary. The daily dose of doxazosin was increased (maximum, 8 mg) to achieve a normotensive blood pressure (< 140/90). At the end of treatment, total and low-density lipoprotein (LDL) cholesterol levels (225 +/- 18 v 200 +/- 16 and 177 +/- 8 v 150 +/- 7 mg/dL, respectively; P < .05) were decreased, confirming the lipid-lowering effect of the drug. The OGTT showed a significant decrease of plasma insulin (16.04 +/- 1.8 v 10.99 +/- 0.9 mU/mL.min, P < .05) and blood glucose (22.54 +/- 1.6 v 20.83 +/- 1.6 g/dL.min, P < .05) areas. The glucose to insulin ratio, also known as the insulin sensitivity index, increased (1.56 +/- 0.15 v 1.95 +/- 0.12, P < .05). These findings seem to provide evidence of a favorable effect of doxazosin on insulin action.

Blood Glucose↗

PubMed2006

Chronic treatment with long-acting nifedipine reduces vasoconstriction to endothelin-1 in essential hypertension.

Essential hypertension is associated with enhanced biological activity of endothelin-1 (ET-1) and impaired endothelium-dependent vasodilatation. Dihydropyridine calcium antagonists have antioxidant activity in vitro, and they improve endothelial function in vivo. We tested whether calcium antagonists also influence the biological activity of ET-1 in essential hypertensive (EH) patients in the presence and absence of hypercholesterolemia. In 9 healthy subjects (normotensive [NT] subjects, age: 48.3+/-7.6 years; blood pressure: 118+/-8.6/69+/-5.4 mm Hg) and 21 EH subjects (age: 50.0+/-7.8 years; blood pressure: 164.4+/-5.4/103.8+/-4.4 mm Hg), we studied forearm blood flow and its modification induced by intrabrachial administration of ET-1, phenylephrine, acetylcholine, and sodium nitroprusside at baseline and after 24 weeks of treatment with a nifedipine gastrointestinal therapeutic system (30 to 60 mg per day). At baseline, the first dose of ET-1 (0.5 microg/100 mL of forearm tissue per minute) caused a slight vasodilatation in NT but not in EH subjects, whereas the following higher doses caused a comparable dose-dependent vasoconstriction in EH and NT subjects. The effect of acetylcholine was significantly reduced in EH as compared with NT subjects. In contrast, sodium nitroprusside and phenylephrine had similar effects in NT and EH subjects. After chronic treatment with the nifedipine gastrointestinal therapeutic system, the vasoconstrictor effect induced by both ET-1 and phenylephrine was significantly blunted, whereas the response to acetylcholine was significantly increased and the vasodilation to sodium nitroprusside unchanged. Hypercholesterolemic EH subjects showed a further reduced response to acetylcholine compared with normocholesterolemic EH subjects, and the nifedipine gastrointestinal therapeutic system restored the vasodilation to acetylcholine in this subgroup. In conclusion, in EH subjects, chronic treatment with a long-acting dihydropyridine calcium antagonist not only exhibits a blood pressure-lowering effect but also reduces ET-1-induced vasoconstriction and improves endothelium-dependent vasodilation. Those vasculoprotective effects may importantly contribute to a reduction in major clinical events seen during treatment with these compounds.

Acetylcholine↗

PubMedDate not supplied

Effects of ramipril therapy on some components of insulin resistance syndrome in patients with essential hypertension.

Essential hypertension presents a component of insulin resistance syndrome. Insulin resistance exists whenever normal concentration of hormone produces less than normal biologic response. This prospective clinical study included 15 patients (7 male and 8 female), with normal glucose tolerance, aged 53.24 +/- 6.60 years, BMI 26.97 +/- 1.24 kg/m2, with mild-to-moderate essential hypertension before and after ramipril treatment lasting 12 weeks. For assessment of peripheral insulin sensitivity and glucose effectiveness we used a reduced samples Bergman's Minimal Model method. At week 12, we noted a 50% elevation of mean insulin sensitivity index, but without achieving normal reference values (Si = 1.22 +/- 0.66 vs 1.78 +/- 0.8 x 10(-4) min/microU/ml). Glucose effectiveness, plasma lipids and electrolytes were relatively unchanged. Haemoglobin and platelet count were significantly decreased. Being metabolically neutral, with antithrombotic activity, ramipril can be recommended for treatment of patients with hypertension and insulin resistance, especially for patients with accompanied diabetes mellitus.

Adult↗

PubMed2001

Telomeres: the time factor in essential hypertension.

Essential hypertension, particularly systolic hypertension, can be characterized as a disorder of aging. The diverse expressions of this disorder represent the interactions of a genetic script, the environment, chance, and a temporal factor. The temporal factor, namely the telomeres, is biological, intrinsic, and dynamic. Telomere length is heritable, is inversely related to pulse pressure, and can be modified by reactive oxygen species. The incorporation of a temporal factor into models of essential hypertension may provide a heretofore missing link explaining variations in age-dependent increase in pulse pressure.

Humans↗

PubMed1980

Relaxation therapy as an adjunct treatment for essential hypertension.

Essential hypertension is one of the leading problems seen by a family physician, and it is not easily treated. In some instances, a behavioral therapy may serve as a useful adjunct to the pharmacological treatment of this disease. Evidence indicates that relaxation therapy in combination with medical treatment results in significantly greater reductions in systolic and diastolic blood pressure than the use of medical treatment alone. Progressive muscle relaxation, Benson's "relaxation response," hypnosis, and blood pressure biofeedback are the four most common behavioral treatments for essential hypertension. The first two of these are both effective and well suited to use in a family practice.

Antihypertensive Agents↗

PubMed1991

The microcirculation and essential hypertension.

Essential hypertension is characterized by a progressive increase of the mean arterial pressure paralleled by a concomitant increase in the total peripheral resistance. This elevated resistance is the consequence of (a) a decreased internal diameter, (b) an increased wall-to-lumen ratio or (c) a decreased number of small arteries or arterioles. A considerable part of the elevated vascular resistance is determined at the microcirculatory level. This paper reviews the studies performed to unravel the resistance-elevating mechanisms in the microvasculature of different tissues. Furthermore the possible role of the microcirculation in the pathogenesis of essential hypertension is discussed.

Animals↗