UMLS:C0085580 - FACTA Search

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

The time course of structural and functional parameters using echocardiography and the level of atrial natriuretic factor (ANF) employing immunoradiometric assay were examined in 37 patients with essential hypertension taking a 3-week therapy with nifedipine (corinfar) in doses individually chosen. The changes in the structural and functional parameters of the hypertensive heart were found to be associated with its endocrine function. A course therapy of patients with essential hypertension with nifedipine in individually based doses caused a significant rise in plasma ANF levels, a normalization of cardiac compensatory mechanism function. The findings may be a basis for studying the new mechanisms of calcium antagonist action.
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PMID:[Structural-functional state of the hypertensive heart and atrial natriuretic factor during treatment with nifedipine]. 182 74

Plasma levels of atrial natriuretic factor were measured in 71 patients with essential hypertension and 13 with borderline arterial hypertension by using radioimmunoassay. Higher concentrations of plasma atrial natriuretic factor were found to be dependent on hemodynamic changes in patients with Stage II hypertensive disease. There was a weaker atrial natriuretic factor-natriuresis relationship in patients with early essential hypertension. Left ventricular myocardial hypertrophy was shown to greatly affect plasma atrial natriuretic factor concentrations. There was an inverse correlation between the level of atrial natriuretic factor and the concentration of plasma aldosterone, which suggests that they might act antagonistically, affecting fluid-and-electrolyte homeostasis. The angiotensin-converting enzyme blocker enalapril maleate used as an antihypertensive agent caused a significant reduction in plasma atrial natriuretic factor concentrations.
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PMID:[Atrial natriuretic factor in patients with hypertension]. 183 18

130 cases of patients with essential hypertension (EH) and 70 cases of normal subjects were researched for correlation between TCM differential types and plasma levels of renin, angiotension II, aldosterone, atrial natriuretic factor (ANF) in patients with EH. Results indicated that: (1) basic level of renin was lower in patients with EH than that in normal subject. There were significant differences of plasma levels of renin between different TCM types. Plasma renin level of excessive Yang patients was higher than that in normal subject group and groups of deficiency of Yin essence combined with excessive Yang as well as deficiency of both Yin and Yang (P less than 0.01-0.001). Plasma level of angiotension II was significantly higher in group of excessive Yang than that in normal subject and other two groups (P less than 0.01-0.001). It was indicated that there were correlation between plasma basic level of renin, angiotension II and TCM types. (2) Plasma ANF level in patients with EH was significantly lower than that in group of normal subject (P less than 0.01). There were significant differences between groups of three different TCM types (P greater than 0.05). The result suggested that lower plasma ANF level was general character in three groups with EH. The prognosis of these patients was discussed.
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PMID:[Relation between traditional Chinese medicine differential types and plasma levels of renin, angiotension II, aldosterone, atrial natriuretic factor in patients with essential hypertension]. 183 35

Plasma levels of immuno-reactive atrial natriuretic factor (ANF) and ambulatory blood pressure were studied in 42 male subjects, aged 18 to 31 y, including 24 subjects with normal BP and 18 with borderline essential hypertension. ANF was measured in the morning (9 a.m.-12 a.m.), with the subjects in the supine and in the upright positions. Ambulatory BP was determined in all subjects every 15 minutes, for a whole 24 hour period. A scatter plot of office SBP or DBP versus upright or supine ANF suggested negative relationships (not significant). In contrast, the plasma ANF level was significantly correlated to ambulatory BP, especially to daytime BP (r = -0.52, p less than 0.001, between daytime SBP and upright ANF; r = -0.50, p less than 0.001, between daytime DBP and upright ANF). The data suggested that ANF is decreased in borderline hypertension, but the decrease can be evidenced only when BP is repeatedly determined to afford reliable data. An inhibition of the atrial release of ANF might be one possible mechanism contributing to the genesis of borderline essential hypertension.
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PMID:Atrial natriuretic factor and ambulatory blood pressure in young male subjects with normal or borderline office blood pressure. 183 73

Atrial natriuretic factor (ANF) is a recently discovered, volume responsive hormone with multiple potent antihypertensive actions. This article reviews data supporting hypothetical associations between ANF and essential hypertension, examines reports of plasma ANF concentrations in hypertension, discusses the efficacy of ANF and its analogs in the treatment of hypertension, and reviews future issues in ANF research. ANF has been shown to elicit vasodilatation, suppress plasma renin activity, inhibit the synthesis and release of aldosterone, antagonize sympathetically-mediated release of norepinephrine, and promote diuresis and natriuresis. A metaanalysis of plasma ANF concentrations reported in normal and hypertensive subjects reveals a 5 +/- 19 pg/mL (pooled, weighted mean and standard deviation) higher ANF level in age-matched, untreated hypertensives without evidence of end-organ damage. This difference may be inappropriately low given the increase in atrial filling pressures found in hypertension. Low doses of ANF elicit greater reductions in blood pressure in hypertensive subjects than in normals. Recently, inhibitors of the ANF-degrading enzyme, neutral endopeptidase, and of the ANF "clearance" receptor have enhanced the antihypertensive actions of endogenous or exogenously administered ANF. Human studies are currently in progress testing the antihypertensive efficacy of orally administered neutral endopeptidase inhibitors. The discovery of ANF has led to the elucidation of a family of natriuretic peptides from brain, heart, and kidney, and promises to enlarge our understanding of volume regulation in normal and pathophysiological states. The possibility that essential hypertension is associated with inappropriately low plasma ANF levels or altered responsiveness to ANF may offer new insights into the pathogenesis and treatment of hypertension.
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PMID:Atrial natriuretic factor and hypertension. A review and metaanalysis. 145 90

Changes of humoral factors related to the regulation of fluid volume were investigated in exercise training for hypertensives. Twelve patients with essential hypertension were treated with an aerobic exercise for 10 weeks. A significant reduction in blood pressure from 161 +/- 3/100 +/- 2 mmHg at week 0 to 142 +/- 5/94 +/- 3 mmHg at week 4 was observed which continued until week 10. Urine dopamine was increased significantly at the 4th week from 386 +/- 29.4 micrograms/day at week 0 to 524 +/- 46.3 micrograms/day and plasma atrial natriuretic factor (ANF) was significantly reduced at the 4th week, from 41.5 +/- 2.7 pg/ml at week 0 to 32.6 +/- 3.7 pg/ml. Plasma volume was found reduced significantly from 2,531 +/- 166 ml/m2 at week 0 to 2,221 +/- 165 ml/m2 at week 10. These results suggest that the increase of dopamine and reduction of plasma ANF which took place at the early stage might be related to, at least in part, the depletion of plasma volume and the reduction of blood pressure in mild exercise for hypertensives.
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PMID:Changes of dopamine and atrial natriuretic factor by mild exercise for hypertensives. 183 83

Plasma immunoreactive atrial natriuretic factor (ANF) and urinary sodium excretion were measured in elderly patients with isolated systolic hypertension (ISH) (n = 11), age-matched essential hypertensive patients (EHT; n = 16) and normotensive subjects (NT; n = 9) before and during a 60 min infusion of hypertonic saline (120 mEq of Na+). An exaggerated natriuresis during the sodium load was observed only in ISH. Baseline plasma ANF levels in ISH were significantly lower (P less than 0.05) than those of EHT and NT. There was no significant change in plasma ANF in EHT and NT subjects after the saline load. In contrast, there was a significant increase in plasma ANF (P less than 0.05) after the saline load in ISH. The change in urinary sodium excretion was significantly correlated with the change in plasma ANF (r = 0.75, P less than 0.01) in ISH. We conclude that an exaggerated natriuresis during a hypertonic saline infusion may be linked to an increase in plasma ANF in elderly ISH patients.
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PMID:Plasma atrial natriuretic factor in isolated systolic hypertension in the elderly: response to hypertonic saline infusion. 183 65

In an attempt to explore pathophysiological mechanisms relevant for the development for future primary hypertension, we investigated young normotensive men with positive family histories of hypertension (PFH) regarding blood pressure, body weight, systemic and renal haemodynamics as well as cardiovascular hormones and sodium homeostasis. Sixteen subjects with PFH and thirteen controls with negative family histories (NFH), matched for age and body weight were investigated at age 31 and after five years. Blood pressure and heart rate did not differ between the two groups at the first or follow-up examination. At follow-up body weight had increased and a positive correlation between blood pressure and body mass index was found in subjects with PFH, while subjects with NFH had unchanged blood pressure and body weight. Initially, intraerythrocyte sodium content was increased in subjects with PFH, however, at follow-up intraerythrocyte sodium content did not differ between the two groups. At follow-up systemic and renal haemodynamics and sodium homeostasis were investigated in fifteen subjects with PFH and in twenty-nine controls matched for age (36 +/- 5 year) and with NFH. The control group was divided into one group matched for body mass index (n = 15) and one group with normal body mass index (n = 14). Blood pressure and central venous pressure were measured during bolus injections of phenylephrine and during an acute saline/fluid load (1000ml 0.9% NaCl within 10 min). Renal haemodynamics and blood pressure were measured during low doses (0.1 and 0.5 ng/min/kg) continuous infusions of angiotensin II (AII). At baseline blood pressure, body weight and sodium excretion were higher in subjects with PFH and matched controls as compared with lean controls. Calf and forearm haemodynamics (pletysmography), plasma catecholamines, plasma renin activity, angiotensin II, aldosterone, blood volume and erythrocyte sodium efflux rate constant did not differ between the three groups. Circulating atrial natriuretic peptide was higher in subjects with PFH than in the two control groups. In subjects with PFH there was a negative correlation between renal sodium excretion at baseline and the ouabain-sensitive sodium efflux rate constant. During the acute saline/fluid load central venous pressure and systolic blood pressure increased more and venous vascular compliance (ml/mmHg/kg) was reduced in PFH. Atrial natriuretic peptide release and renal sodium excretion were blunted during saline/fluid load in subjects with PFH as compared with the two control groups. Renal blood flow and renal vascular resistance did not differ at baseline. Glomerular filtration rate was somewhat higher in PFH.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Family history and pathophysiological mechanisms of primary hypertension. Studies in non-hypertensive young men with positive and negative family histories of hypertension. 188 13

Vasoactive hormones acting as endocrine, neuroendocrine, or local hormonal systems (intracrine, autocrine, and paracrine) are an important component of the many factors that regulate blood pressure. Hypertension may be the result of an alteration in the balance between vasodepressor and vasopressor hormonal systems. Changes in this balance could be due to genetic factors such as mutations in one of the genes of the vasoactive system or environmental factors that alter the synthesis and release of one or more vasoactive hormones. Endocrine and neuroendocrine vasopressor hormonal systems, such as the renin-angiotensin system and catecholamines, play a well-established and important role in the regulation of blood pressure and the pathogenesis of some secondary forms of hypertension. The blockade of such systems has already resulted in effective antihypertensive treatment. The role of local hormonal systems is less well established; however, recent evidence suggests they also play an important role in the regulation of blood pressure and the pathogenesis of hypertension. Some vasopressor hormonal systems, such as the renin-angiotensin system, can act as both endocrine or local hormonal systems. Work using transgenic rats harboring the mouse Ren-2 gene has conclusively demonstrated that the renin-angiotensin system, acting as a local hormonal system, has the capability to cause severe hypertension. Whether this model of experimental hypertension mimics any type of human hypertension is not known. Vasodepressor hormones such as kinins, prostaglandins, and endothelium-derived relaxing factor (EDRF) act mainly as local hormonal systems, with the notable exception of atrial natriuretic factor, which may act as both an endocrine and a local hormone. The tissue kallikrein-kinin system, acting either directly or via paracrine eicosanoids or EDRF, participates in local regulation of the circulation, renal function, and the acute antihypertensive effect of angiotensin converting enzyme inhibitors. A restriction fragment length polymorphism (RFLP) that distinguishes the kallikrein gene family of a strain of spontaneously hypertensive rats (SHR) from normotensive Brown Norway rats has been identified. In a set of 32 recombinant inbred strains derived from these SHR and Brown Norway strains, the RFLP marking the kallikrein gene family of SHR cosegregated with an increase in blood pressure. Also, in a study of Utah families it was found that a dominant-allele kallikrein gene expressed as high urinary kallikrein excretion was associated with a decreased risk of essential hypertension. In conclusion, vasopressor and vasodepressor hormones, acting not only as endocrine but also as local hormones, play an important role in the regulation of blood pressure and the pathogenesis of hypertension.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Local hormonal factors (intracrine, autocrine, and paracrine) in hypertension. 188 59

Clonidine, an agonist of central alpha-2-adrenergic receptors, reduced the peripheral sympathetic activity. With regard to the mutual pathophysiological relationship of blood pressure regulating mechanisms, the authors wanted to find out whether after clonidine administration, in addition to the known suppression of catecholamine levels (CA), also changes in the concentration of other pressor and depressor humoral substances will occur. They investigated therefore in 15 patients with essential hypertension (EH) and in three patients with pheochromocytoma the urinary excretion of free noradrenaline (NA), adrenaline (A) and dopamine (DA), the plasma renin activity (PRA), the aldosterone concentration (PAC) and atrial natriuretic factor (ANF) in plasma, using radioimmunoanalysis, always before and 24 hours after clonidine administration (Haemiton retardR) by the oral route. Its administration led in patients with EH to a decline of NA and DA. On the other hand, in pheochromocytoma their urinary excretion did not change in an unequivocal way, and when it declined, never normal NA and DA levels were reached. A excretion remained unaltered in both groups of patients. The drop of PRA after clonidine as a result of the drop of peripheral adrenergic activity was not associated with an expected parallel drop of PAC but by its rise. This effect can be explained by a reduction of the tonic inhibition of PAC output when the DA level declines. The rise of ANF after clonidine administration will be the subject of subsequent investigations. It cannot be ruled out that this effect is due to the direct action of clonidine on alpha receptors in the heart.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The effect of clonidine on humoral factors in patients with arterial hypertension]. 214 Feb 96

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