PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Essential Hypertension”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1992

[24-hour blood pressure changes in elderly people with isolated systolic hypertension, essential hypertension and normotension].

In order to evaluate circadian blood-pressure (BP) profile characteristics typical of old age, we compared circadian BP profile in elderly subjects with isolated systolic hypertension (ISH; greater than 160/less than 90 mmHg), essential hypertension (EH; diastolic BP greater than or equal to 95 mmHg), and normotension (N; less than 140/less than 90 mmHg). Each group consisted of 18 subjects, approximately matched in age and sex, (age range 60-82 years; mean age 67.5 years). Ambulatory 24-h BP-monitoring was carried out using a SpaceLabs 90202 with measurements made every 30 min. In ISH, causal systolic BP is higher and circadian systolic BP is lower than in EH (n.s.). Circadian diastolic BP is lower than in EH and higher than in N; both are statistically highly significant (p less than 0.001, u-test, Wilcoxon). The decrease during the resting period is 6 mmHg in EH and 17 mmHg in ISH. In ISH there is a considerable difference of 39 mmHg between casual BP and circadian 24-h BP, in contrast to N and to EH, and this is due to a particular hyperreactivity. This discrepancy is typical of old age and holds the danger of over-treatment, if only causal BP is taken into consideration.

Aged↗
PubMedDate not supplied

The pathogenesis of essential hypertension.

Essential hypertension is a quantitative abnormality, the pathological effects and risks increasing with the blood pressure level. In Western countries blood pressure rises with age in most individuals, so essential hypertension is more frequent in middle and older age groups. It is likely that an individual's blood pressure level is determined by many interacting factors. These include heredity, which probably acts multifactorially, and many environment influences, including psychological stress and obesity. Specific factors may be of varying importance in different individuals and in different populations. Several physiological mechanisms control the blood pressure level and may be altered in essential hypertension. In early hypertension sympathetic nervous activity is sometimes increased, although in long-standing hypertension this is less marked. Cardiac output may be increased in borderline hypertension but is normal in established hypertension, when total peripheral resistance is increased. Total exchangeable sodium is normal, while the renal pressure-natriuresis balance is altered, so that for a given pressure the hypertension kidney excretes less sodium. In some patients, plasma renin is low, probably as a result of renal adaption to prolonged hypertension. The pathogenic sequence in essential hypertension is uncertain. Increased autonomic activity may cause vasoconstriction in renal and other arterioles and increase cardiac output, leading to a rise in blood pressure. Elevated pressure itself produces structural changes in the resistance vessels, including those of the kidney, which eventually maintain the hypertension even when the initiating stimulus is removed. The way in which heredity and environment influence pathogenic mechanism is also uncertain. Heredity might, for example, influence the autonomic response to stress or the liability to irreversible changes in the resistance vessels or in the kidney. Environmental factors may also increase autonomic activity, enhance vascular reactivity or alter renal function.

Blood Pressure↗
PubMed1991

Association and linkage analyses of restriction fragment length polymorphisms for the human renin and antithrombin III genes in essential hypertension.

Essential hypertension is a highly hereditable disorder in which genetic influences predominate over environmental factors. The molecular genetic profiles which predispose to essential hypertension are not known. In rats with genetic hypertension, there is some recent evidence pointing to linkage of renin gene alleles with blood pressure. The genes for renin and antithrombin III belong to a conserved synteny group which, in humans, spans the q21.3-32.3 region of chromosome I and, in rats, is linkage group X on chromosome 13. The present study examined the association of particular human renin gene (REN) and antithrombin III gene (AT3) polymorphisms with essential hypertension by comparing the frequency of specific alleles for each of these genes in 50 hypertensive offspring of hypertensive parents and 91 normotensive offspring of normotensive parents. In addition, linkage relationships were examined in hypertensive pedigrees with multiple affected individuals. Alleles of a REN HindIII restriction fragment length polymorphism (RFLP) were detected using a genomic clone, lambda HR5, to probe Southern blots of HindIII-cut leucocyte DNA, and those for an AT3 PstI RFLP were detected by phATIII 113 complementary DNA probe. The frequencies of each REN allele in the hypertensive group were 0.76 and 0.24 compared with 0.74 and 0.26 in the normotensive group. For AT3, hypertensive allele frequencies were 0.49 and 0.51 compared with normotensive values of 0.54 and 0.46. These differences were not significant by chi 2 analysis (P greater than 0.2).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
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↗
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↗
PubMed1977

Catecholamines, cyclic AMP and renin in two contrasting forms of essential hypertension.

Essential hypertension (EH) can be subdivided according to the sympathetic and renin activity into two contrasting forms: (1) borderline beta-hyperadrenergic renin hyperresponsive and (2) stable beta-hypoadrenergic renin hyporesponsive EH. These two forms probably represent two expreme poles in the spectrum of EH in which sympathetic and renin hyper- or hyporeactivity cannot be accounted for by catecholamine determinations solely. beta-Adrenergic responsiveness monitored by plasma cyclic AMP determinations revealed plasma cyclic AMP, renin and circulatory hyperresponsiveness to isoproterenol in borderline hyperadrenergic EH while the opposite, cyclic AMP and renin hyporesponsiveness to insulin-induced hypoglycemia have been described in low renin stable EH. The kidney is in the center of the adrenergic abnormality in the two forms of EH with the borderline one excreting into the urine catecholamines not accounted for by their glomerular filtration. Catecholamines solely, however, do not account for the differences in both forms of EH which can probably be attributed to their different beta-adrenergic responsiveness.

Adrenergic beta-Antagonists↗
PubMed1988

[Comparison of renal hemodynamics in 2 types of arterial hypertension, essential and renovascular, in man. Physiopathological implications].

Split renal function tests were studied in 41 patients with unilateral stenosis of the main renal artery in comparison with 36 subjects with essential hypertension. The two populations were matched for sex, age (39 +/- 10 vs 37 +/- 11 years (+/- 1 standard deviation) and systemic arterial pressure (193/114 +/- 29/15 vs 205/110 +/- 30/17 mmHg). The PAH clearance (CPAH) was decreased in essential hypertensives. The decrease was similar in the right (160.3 +/- 56.9 ml/min/m2) and left kidneys (158.7 +/- 45 ml/min/m2). The inulin clearance (Cin) was similar in both kidneys (35.2 +/- 12.5 vs 33.6 +/- 11.6 ml/min/m2). In addition, in essential hypertensive, CPAH was negatively correlated with blood pressure (p less than 0.01). In patients with renal artery stenosis, CPAH of the "stenotic" kidney was reduced (91.5 +/- 47.8 ml/min/m2) as well as Cin (22.9 +/- 9.3 ml/min/m2). In contrast, a significant increase in CPAH (194.1 +/- 63.8 ml/min/m2) and Cin (47.6 +/- 12.6 ml/min/m2) was observed in the contralateral kidney. Kidney function (CPAH and Cin) was not correlated with blood pressure in the "stenotic" kidney. CPAH and Cin of the non stenotic kidney were positively and significantly correlated with systemic arterial pressure (p less than 0.01). Cin was positively correlated with CPAH (p less than 0.001) in all kidneys in renovascular or in sustained essential hypertensives. However, in the contralateral kidney of renovascular hypertensives, a significant upward resetting of the correlation was observed. The Cin/CPAH was increased in the stenotic kidney (25.7 +/- 7.6%), as well as in the contralateral kidney (25.6 +/- 6.2%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Captopril and kidney function in renovascular and essential hypertension.

In the present study 25 patients with various forms of severe hypertension (essential hypertension: n = 12; renovascular hypertension: n = 11; unilateral small kidney: n = 2), which were treated with captopril for a mean control period of 34.9 months, were investigated. Reduction of mean blood pressure under captopril was comparable in all subgroups. However, patients with renovascular hypertension showed a significant increase in serum creatinine from 117 to 162 mumol/l (p less than 0.05) after 34.9 months, whereas in essential hypertensives even a slight decrease could be observed (113 vs. 111 mumol/l). Serum creatinine of the 2 patients with unilateral small kidney remained within the normal range. Changes in creatinine were markedly higher in cases with bilateral renal artery stenosis and/or in those with a very high initial plasma renin activity (greater than 15 ng/ml X 3 h). Our findings underline the necessity of cautious application of captopril in patients with renovascular hypertension.

Adult↗
PubMed1992

Increased norepinephrine spillover into the jugular veins in essential hypertension.

In essential hypertension sympathetic nerve firing is commonly increased. A central nervous system origin has been presumed but not tested directly. To estimate cerebral norepinephrine release in essential hypertension, spillover of norepinephrine into the cerebrovascular circulation was measured by isotope dilution, with high internal jugular venous sampling. Norepinephrine was released into the cerebrovascular circulation in both hypertensive patients and healthy volunteers and was present after administration of the ganglion blocker trimethaphan and in patients with sympathetic nervous failure, indicating that brain neurons and not cerebrovascular sympathetic nerves were the probable source. Although differing among hypertensive patients, norepinephrine spillover on average was higher in the hypertensive patients (153 +/- 41 pmol/min) than in healthy subjects (59 +/- 12 pmol/min; p less than 0.05), and was elevated in six of 17 patients, in whom the accompanying whole body norepinephrine spillover rate was higher than in the remaining 11 patients (p less than 0.01). To test for a possible link between brain norepinephrine release and human sympathetic nervous function, the effect of the tricyclic antidepressant desipramine (0.3 mg/kg i.v.) on both brain and whole body norepinephrine spillover was measured in healthy volunteers. Desipramine lowered the cerebrovascular spillover of norepinephrine, its precursor dihydroxyphenylalanine, and its metabolite dihydroxyphenylglycol by 50-80% and produced a mean fall of 35% in whole body norepinephrine spillover. One interpretation of these results is that human sympathetic nerve firing is dependent on norepinephrine release within the brain and that increased cerebral norepinephrine release may possibly be present in some patients with essential hypertension, underlying their higher sympathetic nerve firing rates.

Cerebrovascular Circulation↗
PubMed1991

Aspirin test for differentiation of unilateral renovascular hypertension from hyperreninemic essential hypertension.

Responses of renin release and blood pressure to aspirin DL-lysine (ASP) were examined to find out if the responses could help in the differentiation between unilateral renovascular hypertension (RVH) and hyperreninemic essential hypertension (EHT). The two studies involved ten patients with unilateral RVH, eight with hyperreninemic EHT, and five with hyporeninemic EHT. In a radiological study, before and 30 min after an intravenous injection of ASP (18 mg/kg), renal venous and abdominal aortic plasma was sampled and assayed for prostaglandin (PG) E2 and plasma renin activity (PRA). Systemic blood pressure was measured serially. The reproducibility of the responses to ASP was confirmed in a bedside study. In unilateral RVH, ASP suppressed renin release from the stenotic kidney and reduced the renal vein PRA ratio to less than 1.5 via the inhibition of PG synthesis, which is accelerated in that kidney. The mean suppression of aortic PRA at this dose of ASP was 35% in these patients, and their blood pressure decreased in proportion to the suppression of PRA. However, in the two EHT groups, ASP elevated the mean blood pressure. The renal synthesis of PGE2 was inhibited by ASP in all patients, but the suppression of PRA, while small, was significant (19% in the aorta) in the patients with hyperreninemic EHT, and not significant in patients with hyporeninemic EHT. The different responses of blood pressure and PRA to ASP between RVH and EHT were reproducible in the bedside study.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Cytoplasmic free [Ca2+] is increased in the platelets of spontaneously hypertensive rats and essential hypertensive patients.

The cytoplasmic free calcium concentration [( Ca2+]i) was assessed with the fluorescent dye Quin 2 in platelets and lymphocytes of spontaneously hypertensive rats (SHR), normotensive Wistar-Kyoto rats (WKY), essential hypertensive patients (EHP) and normotensive human control subjects (NCS). [Ca2+]i was significantly higher in the platelets of 8- and 20-week-old SHR in comparison with WKY. However, no difference was evident after weaning. Changes of cellular calcium in hypertensive rats apparently evolved simultaneously with the development of high arterial pressure. [Ca2+]i was significantly higher in platelets of EHP than in NCS. In lymphocytes of SHR, [Ca2+]i was not different from WKY at 4 and 8 weeks, but was increased at 14 weeks and at older ages. In EHP, intralymphocytic [Ca2+] was only modestly higher than in controls. On the whole, the results suggest that control of cytoplasmic calcium in these blood cells is similarly affected in human and animal models of primary hypertension.

Adult↗
PubMed1987

Diltiazem maintains renal vasodilation without hyperfiltration in hypertension: studies in essential hypertension man and the spontaneously hypertensive rat.

The systemic and renal hemodynamic effects of diltiazem were determined in patients with mild to moderately severe essential hypertension and in rats with spontaneous hypertension (SHR). Seven patients were treated for one full year (300 mg/day, average dose) and 10 SHR and 10 normotensive Wistar-Kyoto (WKY) rats received 1 and 2 mg/kg, intravenously. In both man and rat with genetic hypertension, arterial pressure was reduced through a fall in total peripheral resistance without associated reflexive increases in heart rate and cardiac index; and the patients demonstrated no change in plasma volume. In both man and the SHR: renal blood flow increased (in SHR not statistically significant) as arterial pressure and renal vascular resistance fell; glomerular filtration rate (GFR) remained unchanged and the filtration fraction (FF) significantly fell; and calculated intrarenal hemodynamic indices (using the Gomez formulae) demonstrated falls in afferent and efferent glomerular arteriolar pressures and resistances and in intraglomerular pressures, thereby explaining the unchanged GFRs and the decline in FF. These findings in both hypertensive man and rat are in contrast with those of the normotensive WKY that only demonstrated a fall in afferent glomerular arteriolar resistance. Thus, these data demonstrate that diltiazem controlled arterial pressure in both forms of genetic hypertension associated with falls in systemic and renal arteriolar resistances and with improved intrarenal hemodynamics without glomerular hyperfiltration.

Adult↗
PubMed1988

[Intracellular free calcium and plasma calcium in patients with essential hypertension. Is there a correlation between extracellular and intracellular disorders of calcium regulation in essential hypertension?].

Alterations in intracellular free calcium regulation as well as disturbances of extracellular calcium homeostasis have been observed in patients with essential hypertension. It has been hypothesized that a generalized defect of calcium regulation might be of importance in the pathogenesis of essential hypertension. In one hypothesis a primary calcium-deficiency in essential hypertension has been linked to subsequent membrane instability and altered intracellular free calcium concentrations. We therefore investigated the relationship between intracellular free calcium concentrations in platelets and ionized as well as total plasma calcium in patients (n = 38) with essential hypertension and in age-matched normotensive subjects (n = 35). Intracellular free calcium in hypertensive patients was elevated by 13% (p less than 0.05) although there was a wide overlap between the values of the two groups. However, no difference with regard to the ionized or total plasma calcium concentrations could be observed. Total plasma calcium concentration, ionized plasma levels as well as intracellular free calcium were positively correlated (p less than 0.05) with mean arterial blood pressure. No correlation however was found between the extracellular and intracellular calcium compartments. We therefore could not observe a generalized defect of calcium regulation in essential hypertension, and extracellular calcium concentrations do not seem to be related to intracellular calcium derangement in this disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Systemic and renal effects of a new angiotensin converting enzyme inhibitor, benazepril, in essential hypertension.

Seventeen essential hypertensive patients with normal renal function were treated with a new non-sulphydryl orally active angiotensin converting enzyme (ACE) inhibitor, benazepril, 10 mg given once or twice daily, according to diastolic blood pressure levels, for 6 weeks. In all patients, changes in blood pressure, systemic and renal hemodynamics, plasma renin activity and urinary aldosterone and albumin excretions were assessed at the end of a 2-week placebo run-in period and at the end of the study. Benazepril monotherapy controlled blood pressure well. No changes in cardiac output, heart rate or stroke volume were observed, while peripheral vascular resistance was significantly decreased (-11%, P less than 0.05). Plasma volume was unaltered. The glomerular filtration rate was stable, but effective renal plasma flow was increased because of the marked reduction in renal vascular resistance (-35%) and, therefore, the filtration fraction was decreased. Urinary albumin excretion remained unchanged. A significant increase in plasma renin activity (P less than 0.001) and a decrease in urinary aldosterone excretion were seen. No side effects were observed during the treatment period. In conclusion, our results suggest that benazepril alone is an effective antihypertensive agent in patients with essential hypertension. The blood pressure lowering effect is due mainly to systemic vasodilation and is observed up to 24 h after administration of the drug. The vasodilation appears to be more consistent in the renal than in the systemic circulation.

Adult↗
PubMed1992

Sib pair linkage analysis of renin gene haplotypes in human essential hypertension.

Although essential arterial hypertension is believed to have a strong genetic predisposition, the gene(s) responsible are unknown. The mechanisms underlying the regulation of blood pressure and experimental studies place the renin gene among the main candidate genes that need to be tested in humans. We tested the hypothesis of a linkage between the renin gene and essential hypertension using the affected sib pair method. Siblings (133 subjects, 52.1 +/- 10.9 years) from 57 families were selected for sustained hypertension (160.7 +/- 22.9/99.5 +/- 12.8 mmHg with 80% of patients under antihypertensive treatment), of early onset (40.7 +/- 12.0 years), in the absence of obesity, diabetes mellitus, and secondary hypertension. Eight renin haplotypes were generated from three diallelic renin restriction fragment length polymorphisms (RFLPs) (TaqI, HinfI, HindIII) located throughout the renin gene. The allelic concordance between the sib pairs was analyzed by identity by state relationships for 98 sib pairs (41 for 41 couples, 39 for 13 trios, 18 for 3 quartets). Allelic frequencies in the 57 hypertensive probands were similar to those observed among 102 hypertensive subjects studied previously. Six of eight possible haplotypes were observed, the informativity of the marker corresponded to 70% of heterozygosity. Allelic concordance for all sib pairs according to sibship size was not significantly different from that expected under the hypothesis of no linkage (t = 0.52, P = 0.15) reflecting only a small excess of renin alleles shared by the hypertensive sibs (1.44 +/- 0.6 vs 1.36 +/- 0.6). Likewise the linkage hypothesis was unsupported by weighted estimates to correct for possible bias due to large sibship size. Thus, the sib pair analysis suggests that the renin gene does not have a frequent role in the pathogenesis of essential hypertension; further more powerful linkage studies or other approaches will be needed to detect contributions at the renin locus to the heritability of essential hypertension.

Alleles↗