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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. There is evidence to suggest that essential hypertension is a polygenic disorder and that it arises from yet-to-be-identified predisposing variants of certain genes that influence blood pressure. The cloning of various hormone, enzyme, adrenoceptor and hormone receptor genes whose products are involved in blood pressure control and the identification of polymorphisms of these has permitted us to test their genetic association with hypertension. 2. Cross-sectional analyses of a number of candidate gene markers were performed in hypertensive and normotensive subjects who were selected on the basis of both parents being either hypertensive or normotensive, respectively, and the difference in total alleles on all chromosomes for each polymorphism between the hypertensive and normotensive groups was tested by chi 2 analysis with one degree of freedom. 3. A marked association was observed between hypertension and insertion alleles of polymorphisms of the insulin receptor gene (INSR) (P < 0.0040) and the dipeptidyl carboxypeptidase-1 (angiotensin I-converting enzyme; kininase II) gene (DCP1) (P < 0.0018). No association with hypertension was evident, however, for polymorphisms of the growth hormone, low-density lipoprotein receptor, renal kallikrein, alpha 2- and beta 1-adrenoreceptor, atrial natriuretic factor and insulin genes. 4. All but one of the hypertensive subjects had at least one of the hypertension-associated alleles, and although subjects homozygous for both were three times more frequent in the hypertensive group, examination of the nine possible genotypes suggested that the INSR and DCP1 alleles are independent markers for hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Independent, marked associations of alleles of the insulin receptor and dipeptidyl carboxypeptidase-I genes with essential hypertension. 810 54

The mechanisms responsible for the increase in blood pressure response to high salt intake in salt-sensitive patients with essential hypertension are complex and only partially understood. A complex interaction between neuroendocrine factors and the kidney may underlie the propensity for such patients to retain salt and develop salt-dependent hypertension. The possible role of vasodilator and natriuretic agents, such as the prostaglandins, endothelium-derived relaxing factor, atrial natriuretic factor, and kinin-kallikrein system, requires further investigation. An association between salt sensitivity and a greater propensity to develop renal failure has been described in certain groups of hypertensive patients, such as blacks, the elderly, and those with diabetes mellitus. Salt-sensitive patients with essential hypertension manifest a deranged renal hemodynamic adaptation to a high dietary salt intake. During a low salt diet, salt-sensitive and salt-resistant patients have similar mean arterial pressure, glomerular filtration rate, effective renal plasma flow, and filtration fraction. On the other hand, during a high salt intake glomerular filtration rate does not change in either group, and effective renal blood flow increases in salt-resistant but decreases in salt-sensitive patients; filtration fraction and glomerular capillary pressure decrease in salt-resistant but increase in salt-sensitive patients. Salt-sensitive patients are also more likely than salt-resistant patients to manifest left ventricular hypertrophy, microalbuminuria, and metabolic abnormalities that may predispose them to cardiovascular diseases. In conclusion, salt sensitivity in hypertension is associated with substantial renal, hemodynamic, and metabolic abnormalities that may enhance the risk of cardiovascular and renal morbidity.
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PMID:Salt sensitivity in hypertension. Renal and cardiovascular implications. 814 22

Plasma concentrations of atrial natriuretic factor (ANF) have been reported to be unchanged or increased in patients with essential hypertension. Head out of water immersion (HOI) in a thermoneutral bath induces diuresis and natriuresis, an increase in plasma ANF, and reductions in plasma renin activity and aldosterone concentrations. HOI was used in this study to stimulate the secretion of ANF, and compare its release in patients with essential hypertension (EH) (n = 14) and normotensive subjects (n = 13). Renal function changes induced by HOI were also monitored. HOI that lasted 2 h was compared with a control-seated period in each subject. Blood pressure was significantly reduced (P < .05) in normotensive controls from 112 +/- 3/74 +/- 2 to 100 +/- 3/61 +/- 2 mm Hg, and in patients with EH from 137 +/- 4/93 +/- 3 to 123 +/- 3/78 +/- 2 mm Hg. Plasma levels of ANF increased significantly (P < .05) in both groups from 5.9 +/- 1.3 to 16.3 +/- 3 pmol/L in normotensive controls and from 6.0 +/- 0.9 to 13.2 +/- 2.5 pmol/L in patients with EH. Plasma cyclic guanosine monophosphate concentrations increased more (P < .05) in the patients with EH (3.9 +/- 0.4 to 6.1 +/- 0.5 nmol/L) than in controls (3.4 +/- 0.3 to 4.8 +/- 0.4 nmol/L), whereas plasma renin activity levels decreased in controls (2.29 +/- 0.58 to 1.63 +/- 0.55 ng/mL/h) and to a greater degree in patients with EH (1.62 +/- 0.52 to 0.77 +/- 0.19 ng/mL/h, P < .05) by HOI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal effects of immersion in essential hypertension. Carvedilol Study Group. 817 47

This study aimed to assess and compare the effects of urapidil and clonidine on right ventricular volumes and function in 20 physical status ASA III patients, with a borderline untreated essential hypertension and with or without chronic coronary artery disease. The patients were randomly assigned to two equal groups to receive either urapidil (0.4 mg.kg-1) or clonidine (2.5 micrograms.kg-1). Neither patient had congestive heart failure, valvular heart disease, previous myocardial infarction, nor was any being treated with beta-blocking agents or with amiodarone. Usual anti-anginal medication (nifedipine and isosorbide) was maintained up to the time of the procedure. Monitoring was obtained from ECG, Swan-Ganz catheter fitted out with a fast response-thermistor, and radial artery cannula. Blood samples were withdrawn for plasma atrial natriuretic factor determination. Thirty minutes after catheter insertion, baseline data were collected in supine and 45 degrees head-up tilt positions. Following urapidil or clonidine i.v. injection, three series of measurements (3, 8 and 13 min) were made in supine and tilt positions according to a randomized sequence. The two groups were similar with regard to age, weight, height, coronary artery disease and treatment. Urapidil and clonidine elicited a similar decrease in mean arterial pressure of 14% in supine position and 20% in head-up tilt position, combined with an exclusive decrease in systolic index i.e. not associated with a change in peripheral vascular resistances. Despite the decrease in arterial pressure, heart rate remained unchanged. Right ventricular ejection fraction was maintained after both urapidil and clonidine, however end-diastolic and end-systolic volumes decreased, with no modification by tilting.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Is urapidil a venodilator?]. 831 50

Atrial natriuretic peptide (ANP) is a hormone produced, stored and secreted by atrial muscle cells. By its natriuretic, diuretic and blood pressure lowering activities ANP is possibly an endogenic antagonist for the sodium-retaining, vasopressor renin-angiotensin-aldosterone system (RAAS). In diseases associated with increased intravascular volume ANP plasma concentrations have been found elevated, in those associated with decreased volume ANP has been found decreased. In essential hypertension and chronic heart or renal failure diagnostic conclusions may be drawn from the ANP plasma concentration. This review summarizes the present knowledge about physiology and pathophysiology of ANP and values in addition the diagnostic power of ANP measurements for clinical routine in hypertension, heart and renal failure.
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PMID:[Is there a clinical indication for the determination of atrial natriuretic peptide?]. 834 82

Cardiac function and plasma levels of atrial natriuretic factor (ANF) were studied in a group of 38 patients with untreated essential hypertension and in a group of 31 well matched normotensive controls. ANF was slightly but significantly higher in hypertensives and was directly correlated with mean arterial pressure and inversely with plasma renin activity (PRA). Hypertensives showed normal systolic function and higher cardiac mass compared to controls. ANF was inversely correlated to echocardiographic indexes of left ventricular performance in the former group. At Doppler echocardiographic evaluation, hypertensives showed an impairment in diastolic function which was correlated to the increase in ANF levels. Stepwise multiple regression analysis performed with ANF as the dependent variable and several biohumoral and echocardiographic parameters as the independent variables showed that only cardiac diastolic function and PRA significantly affect ANF levels in hypertensives. In conclusion, an impairment in cardiac diastolic function may be responsible together with other factors for the increased ANF levels encountered in essential hypertension.
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PMID:Cardiac diastolic abnormalities and atrial natriuretic factor in essential hypertension. 837 14

The detailed integrated renal, hormonal, and hemodynamic effects of acute (first dose) and established (4 days) inhibition of endopeptidase 24.11 by SCH 42495 (200 mg, every 12 hours) were documented in eight patients with essential hypertension in a double-blind, balanced random-order, crossover study. SCH 42495 suppressed plasma endopeptidase activity (> 90%, P < .001) for the duration of the dosing period. Initially, plasma atrial natriuretic factor levels increased markedly (+123%, P < .01) and remained elevated, although to a lesser extent (+34%, P < .01), with established enzyme inhibition. Cyclic guanosine monophosphate in both plasma and urine remained elevated throughout the treatment period. Significant augmentation of sodium excretion in excess of placebo values (96 +/- 27 mmol sodium, P < .001) was established in the initial 24 hours of dosing but later became attenuated, with a mild antinatriuresis (P < .01) in the latter 3 days of treatment. Blood pressure, heart rate, the renin-angiotensin-aldosterone system, and plasma norepinephrine levels were all initially (first dose) unchanged. With established enzyme inhibition (day 4), however, blood pressure was significantly lower (mean 24-hour values, 9.3 +/- 3/-3.8 +/- 1 mm Hg, P < .05 for both systolic and diastolic pressures) than matched placebo values, whereas heart rate was higher (2.7 +/- 1 beats per minute, P < .01). Mean 24-hour values of plasma renin activity (+33%, P < .05), aldosterone (+36%, P < .05), and norepinephrine (+40%, P < .001) were all clearly increased above placebo values with established enzyme inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endopeptidase 24.11 inhibition by SCH 42495 in essential hypertension. 839 13

Investigations in genetic forms of experimental hypertensions revealed certain haemodynamic, metabolic and humoral abnormalities in experimental animals already during the prehypertensive period. With regard to the obvious ratio of hereditary factors in the pathogenesis of human essential hypertension (EH), the objective of the present study was to test whether also in healthy normotensive subjects with a positive family history of EH some metabolic and humoral deviations can be detected, as compared with offspring from normotensive families. The authors compared therefore selected biochemical and humoral parameters in 20 sons of hypertensive parents (SH) with the findings in 20 sons from normotensive pa families (SN). SH had, as compared with SN, a significantly higher systolic BP (119 +/- 2.59 > 111.0 +/- +/- 2.04 mmHg). The trend of higher basal blood sugar levels 5.03 +/- 0.15 > 4.70 +/- 0.41 mmol/l) and the higher concentration of immunoreactive insulin (81.4 +/- 9.54 > 70.4 +/- after a glucose load +/- 7.78 microU/l) did not reach statistical significance. In SH plasma concentrations of adrenaline, noradrenaline and dopamine were significantly higher as well as the atrial natriuretic factor (11.7 +/- 0.77 > 8.4 +/- 0.40 fmol/ml) and of endothelin (18.2 +/- 1.70 > 12.7 +/- 0.87 fmol/ml). A load of 75 g glucose raised, as expected, the blood sugar level, IRI and C-peptide, but reduced unexpectedly the endothelin concentration in both groups. As to other biochemical parameters (fibrinogen, sodium, potassium, urea, creatinine, uric acid, cholesterol, HDL- and LDL-fractions, triacylglycerols), no significant differences were found between SH and SN. The finding of a raised mass of the left ventricle and certain differences in the diastolic and systolic left ventricular function are discussed in another paper. The results indicate that in young men with a positive family-history of EH already certain haemodynamic, metabolic and humoral deviations exist before clinical manifestation of hypertension which could contribute to later development of EH and its organ complications.
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PMID:[Metabolic and humoral characteristics of normotensive offspring in a family with a history of essential hypertension]. 851 40

Out of all until now discovered natriuretic factors it is still the atrial natriuretic factor (ANF) which is the most significant with its diuretic, natriuretic and vasodilatory effects. Its effect is antagonistic to sodium retention factors. The increase of its levels in arterial hypertension is more of secondary character, but according to some authors the functional deficit of ANF secretion can be applied also primarily in the development and maintenance of high blood pressure. ANF levels represent a good marker of the clinical severeness and are of prognostic value. Increased levels were detected also in cases of renal failure and partially in hepatic cirrhosis. Natriuretic hormone, in comparison to ANF, is a natriuretic and vasoconstrictive substance, the effect of which is based on the mechanism of sodium pump inhibition. Chemically the main candidate is represented by endogenous ouabain, or a digitalis-like activity. It increases physiologically due to the expansion of extracellular fluid during gravidity and in newborn. Its pathological increase is brought about by some forms of essential hypertension and in the diseases associated with fluid retention and edema development. Cirrhosis of the liver can reflect both the degree of sodium retention and haemodilution, as well as the severeness of hepatic lesion. (Tab. 2, Ref. 30.).
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PMID:[The clinical significance of natriuretic hormones]. 862 37

In essential hypertension, cardiovascular structure is believed to be influenced by hormonal and by hemodynamic factors. The objective of the present study was, in essential hypertensives, to investigate the relationship between blood pressure (BP) level as well as circulating hormones on the one hand and cardiovascular structure on the other. Seventy-nine untreated essential hypertensives were examined by 24-h ambulatory BP monitoring, echocardiography, microscopy of subcutaneous resistance vessels and analyzes of plasma for angiotensin II (P-Ang II), aldosterone, atrial natriuretic factor and 24-h urinary excretion of catecholamines. Multiple regression analysis showed a statistically significant correlation between P-Ang II and the end diastolic interventricular septal diameter (IVSDd) (R = 0.32, P = .005) and a weak correlation between P-Ang II and the left ventricular posterior wall diameter (R = 0.22, P = .049). These correlations were closer in the subgroup of patients (N = 54) who had never received antihypertensive treatment (R = 0.42/0.32, respectively). A weak, though statistically significant, correlation was found between the catecholamine excretion and systolic BP (R = 0.26, P = .03). A statistically negative correlation existed between catecholamines and end-diastolic left ventricular internal diameter index (R = -0.36, P = .001). No significant relationship was found between hormonal levels and the tunica media structure of the resistance arteries. In conclusion, P-Ang II was in this study significantly correlated to IVSDd, but not to resistance artery structure. In essential hypertension a complex relationship exists between humoral and hemodynamic factors and cardiovascular remodeling.
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PMID:Influence of humoral and neurohormonal factors on cardiovascular hypertrophy in untreated essential hypertensives. 869 18


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