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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Sib pair linkage analysis of renin gene haplotypes in human essential hypertension. 134 86

A total of 530 patients with Takayasu arteritis were studied. Among 346 patients who were diagnosed by aortography, the female to male ratio was 2.9 to 1, and the age of onset ranged from 5 to 45 years. Three hundred and eighteen (60%) patients with secondary hypertension, including renovascular hypertension in 281, and 197 (37.2%) with pulseless extremities were found in the series. All the patients were treated with medical or surgical procedures. Surgical treatment is preferred if clinical status of the patient permits. The patients were followed for 1-29 years (average 7.8 years). There were 55 deaths (10.4%) in this series. Cerebral hemorrhage was found as a common cause of death. Five-year and ten-year survival rates were 93.1% and 91.1%, respectively.
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PMID:Takayasu arteritis in China: a report of 530 cases. 136 Sep 68

Primarily hypervolaemic, high output forms of hypertension, with features indicating or strongly suggesting fluid overload as the cause of elevated cardiac output, resulting from renal disease with reduced glomerular filtration rate causing sodium retention, renal tubular causes of sodium retention, greatly excessive sodium intake and low renin hypertension, can be treated by reduction of sodium intake and potentiation of its excretion by diuretic therapy, removal of the cause (e.g. aldosteronoma), and calcium antagonists. Excessive vasoconstriction resulting from noradrenaline (norepinephrine) in neurogenic hypertension, phaeochromocytoma, orthostatic hypertension and alpha-adrenergic drug administration; angiotensin excess due to renal ischaemia brought about by aortic coarctation, renal arterial and arteriolar stenosis, intraluminal obstruction, external renal compression, renin-producing tumours, intrinsic kidney diseases and excessive renin substrate; and vascular structural disorders such as atherosclerosis, arteriolitides and fibrosis with or without calcification of major arteries may also induce hypertension. Secondary hypertension of uncertain mechanism may occur in hyperparathyroidism, hyper-or hypothyroidism, or acromegaly. All are best treated by appropriate correction of the endocrine excess or deficiency. It may also occur in pregnancy, where the mechanism may involve prostaglandin-thromboxane imbalance or calcium deficiency; calcium deficiency with some evidence of benefit from calcium supplements; and the recumbent hypertension paradoxically associated with autonomic failure. Excellent responses to specific correction of the underlying cause or pathogenetic mechanism is usual in young individuals but less frequent in older patients.
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PMID:Secondary hypertension. An overview of its causes and management. 137 54

Several studies have demonstrated that patients with hypertension have greater plasma insulin levels than normotensive subjects. The aim of the present study was to clarify if hyperinsulinemia in hypertension is a consequence of either increased pancreatic secretion or decreased hepatic clearance, and to determine whether abnormalities of glucose metabolism are equally present in essential and secondary hypertension. In an observational cross-sectional study, fasting blood glucose, plasma insulin, and plasma C-peptide levels were measured in five patient groups: 34 lean normotensive, 19 overweight normotensive, 25 lean essential hypertensive, 27 overweight essential hypertensive, and 20 secondary hypertensive subjects. The blood glucose/plasma insulin and plasma insulin/plasma C-peptide ratios were calculated as indexes of insulin sensitivity and hepatic insulin clearance, respectively. Subjects with essential hypertension and, to a greater extent, those who were overweight, exhibited significantly higher fasting insulin and C-peptide levels and significantly lower glucose/insulin ratios as compared with lean normotensive subjects. In contrast, no differences were observed between secondary hypertensive and control subjects. Mean blood pressure was significantly and independently correlated to body mass index, plasma insulin and plasma C-peptide levels, and the glucose/insulin ratio. In lean essential hypertensive and secondary hypertensive subjects, the insulin/C-peptide ratios were comparable to controls, indicating normal hepatic insulin clearance. In both overweight groups, a trend to increased insulin/C-peptide ratios was observed. This study shows that in essential hypertensive subjects, hyperinsulinemia is caused by insulin hypersecretion, whereas in overweight subjects, both increased insulin secretion and decreased hepatic insulin clearance might be involved.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin hypersecretion: a distinctive feature between essential and secondary hypertension. 143

The incidence of hypertension is increased in obesity, a state associated with an insulin resistance syndrome. By using an euglycemic clamp method, Ferrannini et al. demonstrated the existence of an insulin resistance state in patients with essential hypertension. However, the body mass index of the subjects studied appeared to be slightly excessive. This abnormality has not been observed in patients with secondary hypertension. Insulin resistance is probably localized to peripheral tissues such as muscles and may be associated with other cellular abnormalities. Can insulin resistance, characterized by a raised circulating insulin concentration in the presence of normal blood glucose, be responsible for certain "modifications" associated with essential hypertension? Insulin induces sodium retention and increases the aldosterone-secreting effect of angiotensin II. These effects are likely to promote a rise in blood pressure and an increase in the sensitivity of vessels to endogenous substances. Moreover, insulin is a known growth factor and is involved in lipoprotein metabolism. If insulin resistance plays an important role in the maintenance of complications of essential hypertension, it is important that the treatments used tend to correct this anomaly. Thiazide diuretics and beta-blockers aggravate insulin resistance while angiotensin converting-enzyme inhibitors correct this condition.
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PMID:[Arterial hypertension, hyperinsulinism and insulin resistance]. 143

1. The purpose of the present study was to examine changes in membrane fluidity in hypertension by means of an electron spin resonance (ESR) and a spin labelling methods. 2. Erythrocytes from spontaneously hypertensive rats (SHR) and from patients with essential hypertension were examined and compared with those from age-matched normotensive controls. ESR spectra were obtained for a fatty acid spin label agent (5-nitroxide stearate) in the membranes. The values of outer hyperfine splitting (2T' parallel) and of order parameter (S) of the ESR spectra were significantly higher in erythrocytes from SHR and patients with essential hypertension than in those from normotensive controls. Similar results were obtained in cultured vascular smooth muscle cells of SHR. This finding shows that the membrane fluidity might be lower in SHR and in essential hypertension. 3. When Ca was loaded to erythrocytes with a Ca-ionophore (A23187), the parameters of the ESR spectra showed a greater increase (membrane fluidity was decreased) in SHR and in patients with essential hypertension than that in the normotensive controls. The Ca-induced alterations in membrane fluidity were not definitely observed in secondary hypertension. 4. These results suggest that the lower membrane fluidity might be a genetically determined abnormality of hypertension. The marked reduction of the membrane fluidity by Ca-loading in SHR and in essential hypertension might support the hypothesis that an abnormality of the Ca-handling at cellular levels could affect physical properties of the biomembranes in genetic hypertension.
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PMID:Membrane fluidity as a genetic marker of hypertension. 144 3

In many different clinical situations, including some cases of secondary hypertension, nighttime blood pressure (BP) is abnormally increased in the majority of patients, with consequent flattening of the 24-hour BP profile, but the clinical importance of this finding in such conditions is unknown. In patients with essential hypertension, ambulatory BP has been shown to decrease by 10-20% from day to night, but in severe or malignant hypertension this diurnal BP rhythm may be blunted or even abolished. One of the reasons why the noninvasive monitoring of BP may be a reliable tool in assessing the day-night BP changes is the demonstration that frequent cuff inflations do not interfere to a significant extent with the haemodynamic effects of sleep. Part of the differences between the studies in the reported day-night BP drop may be artifactual, owing to the very different time intervals defining the daytime and nighttime subperiods in the single studies. In unselected patients with essential hypertension, a sizable proportion of subjects (17 to 40%) shows abnormally high nighttime BP, with consequent flattening of the 24-hour BP profile (the so called "non dippers", as opposed to the "dippers" who show a maintained diurnal BP rhythm). Several clinical studies carried out in independent laboratories show that the target organ damage induced by hypertension (left ventricular hypertrophy, cerebrovascular lesions) is more severe in hypertensive "non dippers" than in "dippers", possibly because of the different duration of exposure to high BP levels over the 24 hours.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The day-night changes in ambulatory blood pressure: another risk indicator in hypertension?]. 147 64

Both primary hypothyroidism and secondary hypertension are thought to be relatively uncommon in most parts of the tropics. A Nigerian hypothyroid patient with thyroxine-responsive hypertension is reported, and this syndrome (secondary hypothyroid hypertension) is examined with respect to its possible aetiopathogenesis.
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PMID:Primary hypothyroidism with secondary hypertension: a case report. 150 8

Patients (pts) with essential hypertension normally exhibit a typical diurnal variation with a nocturnal blood-pressure (BP) decreased. A lack of this periodicity is often reported in pts with secondary hypertension. 24-h BP measurement was therefore performed in 308 pts with essential hypertension, and in 172 pts with secondary hypertension, in order to evaluate the diagnostic value of nocturnal BP decrease. Diagnoses of the secondary hypertensives were: renoparenchymatous hypertension (n = 29), diabetic nephropathy (n = 24), morbus Conn (n = 6), renal artery stenosis (n = 32), pheochromocytoma (n = 5), hemodialysis pts (n = 30), and kidney transplantation (n = 44). Pts with essential hypertension showed a mean systolic and diastolic BP decrease during the nighttime period of 22 +/- 7 mmHg and 17 +/- 5 mmHg, respectively. In contrast, the corresponding values in secondary hypertension were 5.7 +/- 9.2 mmHg (systolic decrease) and 5.2 +/- 5.9 (diastolic decrease). Pts with pheochromocytoma who had a nighttime increase in BP demonstrated the greatest difference from the essential hypertensives, followed by pts with either diabetic nephropathy or after kidney transplantation. A lack of nocturnal BP decline (less than 10% of the daytime values) was detected in 69.8% of pts with secondary hypertension, but only in 5.2% of pts with essential hypertension. In summary, these results suggest that the absence of a nighttime decline in BP during 24-h ambulatory monitoring is an indication of secondary hypertension and should lead to further investigations. Furthermore, a nightly hypertension is associated with a higher risk of complications.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diagnostic significance of absent nocturnal blood pressure decrease in 24-hour long-term blood pressure measurement]. 151 20

Noninvasive 24-h blood pressure (BP) monitoring has demonstrated a diurnal blood pressure profile in most individuals that is characterized by higher arterial pressures during wakefulness and lower pressures at night during sleep. Recently, reports suggest that this typical diurnal variation is absent in syndromes of autonomic dysfunction and in some forms of secondary hypertension. We investigated the 24-h BP, BP variability, and adrenal steroid concentrations in a patient with deoxycorticosterone (DOC)-secreting adrenal adenoma prior to and following adrenalectomy. Preoperatively, when the patient had a ten-fold increase in serum concentrations of DOC, there was no fall in nocturnal BP despite a marked reduction in heart rate during sleep. Postoperatively, when the concentrations of DOC and other adrenal steroids returned to normal values, the 24-h BP profile normalized with restoration of the nocturnal reduction in pressure. These findings document the effects of mineralocorticoid overproduction on diurnal BP regulation. Intensive investigation of individuals with a well-defined etiology of hypertension and the absence of diurnal variation of BP may lead to further hypotheses that will define the role of both autonomic and nonautonomic factors in BP control.
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PMID:Diurnal blood pressure variability in mineralocorticoid excess syndrome. 152 69


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