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

Forty-one patients with essential hypertension were classified as salt-sensitive (SS) or non-salt-sensitive (NSS) from the changes in mean blood pressure (MBP) with alterations in sodium intake from 35 mmol (low-sodium) to 250 mmol/day (high-sodium). Whereas there was no difference in plasma levels of atrial natriuretic factor (ANF) on a normal-sodium diet (120 mmol) between the 2 groups, the degree of increase in the plasma ANF level between the low- and high-sodium intake was significantly greater in NSS than in SS (p less than 0.001). In addition, the urinary sodium excretion on a high-sodium diet was smaller in SS than in NSS. There was a significant positive correlation between the plasma ANF and MBP after the high-sodium intake in both SS (r = 0.67, p less than 0.01) and NSS (r = 0.60, p less than 0.01); however, the relation of plasma ANF to MBP shifted apparently to a lower level in SS compared with NSS. These findings not only indicate that there exists a hyporesponsiveness of ANF release by the heart of SS patients in response to high-sodium loading, but also imply that such a response contributes to blood pressure-elevating mechanisms due to sodium loading in this type of human hypertension.
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PMID:Attenuated release of atrial natriuretic factor due to sodium loading in salt-sensitive essential hypertension. 182 68

Atrial natriuretic peptide has been considered to be a major regulator in the body's water and salt homeostasis. Antagonizing those mechanisms leading to volume retention and overload (renin, angiotensin, aldosterone), ANP has been suggested to play a critical role in the pathology of certain diseases like renal failure, congestive heart failure or hypertension. In this regard, we measured ANP plasma concentration in normal healthy dogs and dogs with renal failure, congestive heart failure and Cushing syndrome. ANP levels were slightly decreased in dogs with Cushing disease (n = 9; 5.5 +/- 2 fmol/ml), increased in renal failure (n = 7; 16.2 +/- 5.8 fmol/ml, p less than 0.05) and markedly augmented in dogs with congestive heart failure (n = 14; 52.9 +/- 29.75 fmol/ml, p less than 0.01) as compared to healthy dogs (n = 6; 8.3 +/- 3.5 fmol/ml). Furthermore, characterization of the measured immunoreactivity (IR-ANP) revealed, that up to 50% of the IR-ANP in dogs with congestive heart failure corresponds to the ANP precursor molecule, not found in healthy subjects. This fact might present one possible explanation for the attenuated response to ANP in congestive heart failure. In addition, this finding may also serve a diagnostical purpose.
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PMID:[Diagnostic possibilities of ANP blood measurements in dogs]. 182 66

Atrial natriuretic factor (ANF) is a peptide secreted by auricular cardiac cells and acts on the brain; it is a diuretic, a natriuretic and a vasodilator and inhibits the renin angiotensin aldosterone system at several levels. The lungs are rich in specific ANF receptors present both at a vascular cellular level and in the mesothelial cells. These receptors participate in the extraction of ANF during its pulmonary intravascular transit and also in its enzymatic degradation. Endogenous ANF (and exogenous) is a vasodilator of the pulmonary arterial bed, representing a regulatory system for right ventricular afterload and probably modifying pulmonary capillary permeability. Hypoxia and hypercapnia contribute by direct and indirect mechanisms to the stimulation of ANF secretion explaining their elevated levels in pulmonary arterial hypertension and chronic respiratory insufficiency. The lung can under certain conditions synthesise ANF itself as can neuro-endocrine bronchial tumours. ANF may be involved in the understanding of sodium retention during ventilation with PEEP and in the paraneoplastic hyponatraemia of certain bronchial tumours. Finally acute bronchial obstruction leads to hypersecretion of ANF which has some bronchodilator properties.
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PMID:[Atrial natriuretic factor and the lung]. 183 Mar 97

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

Atrial natriuretic factor (ANP) is present in neuronal cells of the locus coeruleus and its vicinity in the pontine tegmentum and moderate amount of ANP is detectable in this area by radioimmunoassay. The ANP (both peripheral and brain-born) is known as a neuropeptide which may influence the body salt and water homeostasis and blood pressure by targeting both central and peripheral regulatory mechanisms. Whether this pontine ANP cell group is involved in any of these regulatory mechanisms, the effect of various types of hypertension and experimental alterations in the salt and water balance on ANP levels was measured by radioimmunoassay in the locus coeruleus of rats. Adrenalectomy, as well as aldosterone and dexamethasone treatments failed to alter ANP levels in the locus coeruleus. Reduced ANP levels were measured in spontaneously hypertensive (both young and adult) rats, and in diabetes insipidus (Brattleboro) rats with vasopressin replacement. In contrast to these situations, elevated ANP levels were found in rats with DOCA-salt or 1-kidney-1-clip hypertension. These data suggest a link between ANP levels in the locus coeruleus and fluid volume homeostasis. Whether this link is causal and connected with the major activity of locus coeruleus neurons (noradrenergic influence on brain regulatory activities) needs further informations.
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PMID:Atrial natriuretic peptide in the locus coeruleus and its possible role in the regulation of arterial blood pressure, fluid and electrolyte homeostasis. 183 23

The present study was designed first to investigate the pulmonary hypertensive effects of chronic hypoxia in spontaneously hypertensive rats and second to compare the cardiovascular effects of atrial natriuretic factor on rats exposed to hypoxia and on control rats kept at sea level. Catheters were placed in the femoral and pulmonary arteries for measurement of mean systemic arterial pressure and mean pulmonary arterial pressure. The cardiac output was measured by thermodilution method. It was found that 4 weeks of simulated 18,000-foot hypoxia led to polycythemia, right ventricular hypertrophy, and pulmonary hypertension, which resulted from an increased pulmonary vascular resistance. However, systemic arterial pressure was not significantly different between the two groups of rats. Atrial natriuretic factor administration decreased systemic arterial pressure and pulmonary arterial pressure to a lesser extent in the hypoxic group compared with the sea level control group. It is concluded that these animals showed an impaired response to atrial natriuretic factor after long-term exposure to hypoxia.
Hypertension 1991 Sep
PMID:Effects of atrial natriuretic factor in chronic hypoxic spontaneously hypertensive rats. 183 12

To investigate the effects of salt loading on cardiopulmonary and arterial baroreceptor reflexes, 34 hypertensive patients underwent two 4-day periods with different dietary sodium intakes (70 and 370 meq/day). The patients were classified as salt-sensitive or salt-resistant depending on whether the mean arterial pressure value obtained on day 4 of high salt intake did or did not increase by 8% or more. In 22 patients cardiopulmonary and carotid baroreceptor reflexes were assessed during each dietary period by measuring the reflex responses to the application of -10 mm Hg lower body negative pressure and of +60 mm Hg increase in neck tissue pressure. Salt-resistant patients (n = 16) retained less sodium than salt-sensitive patients (n = 6) and showed a reduction in plasma norepinephrine and forearm vascular resistance during high sodium intake, whereas the salt-sensitive patients did not. During low sodium diet, no significant differences could be detected in the reflex responses to cardiopulmonary and carotid baroreceptor unloading between the two groups. High salt diet, however, potentiated the gain of cardiopulmonary baroreceptor reflex, which was expressed as the increase in plasma norepinephrine or forearm vascular resistance per millimeter of mercury decrease in pulmonary capillary wedge pressure, only in the salt-resistant hypertensive patients. In addition, the atrial natriuretic factor response to changes in pulmonary capillary wedge pressure was significantly enhanced by high salt intake only in the salt-resistant hypertensive patients. The reflex responses to carotid baroreceptor unloading were unaffected by salt loading in either group. In the remaining 12 patients, the hemodynamic effects of graded lower body negative pressure (-5, -10, -15 mm Hg) and neck tissue positive pressure (+30, +45, +60 mm Hg) were tested for both diets. Again, high salt intake significantly potentiated the cardiopulmonary baroreceptor reflex gain, expressed as the slope of the linear correlation between the changes in forearm vascular resistance (mm Hg/ml/min/100 g) and pulmonary capillary wedge pressure (mm Hg), in salt-resistant (from 3.8 +/- 0.9 to 7.2 +/- 1.0, p less than 0.05) but not in salt-sensitive patients (from 4.2 +/- 0.9 to 3.2 +/- 0.6, NS). In conclusion, the present study demonstrates that high salt diet potentiates cardiopulmonary baroreceptor reflexes and enhances atrial natriuretic factor response in salt-resistant but not in salt-sensitive hypertensive patients. The salt-induced plasticity of cardiopulmonary baroreceptor reflexes may exert a protective effect against the development of salt-induced hypertension by augmenting the reflex vasodilatory response to volume expansion.(ABSTRACT TRUNCATED AT 400 WORDS)
Hypertension 1991 Oct
PMID:Salt-induced plasticity in cardiopulmonary baroreceptor reflexes in salt-resistant hypertensive patients. 183 20

Atrial natriuretic peptide is stored by atrial myocytes in secretory granules, known as atrial specific granules, and is released from these granules by exocytosis. We have isolated a group of atrial proteins by affinity chromatography that bind to atrial specific granules in a calcium-dependent manner. The two major proteins isolated (32.5 kd and 67 kd) are calcium-binding proteins and have been identified as annexins V and VI by immunoblotting with specific antisera. The calcium dependence of their binding to atrial specific granules has been characterized in vitro and indicates that this interaction takes place at micromolar levels of calcium. In addition, the group of proteins isolated includes another calcium-binding protein of 20 kd, as well as GTP-binding proteins of 22 to 26 kd. Membrane interactions during exocytosis are presumably mediated by the interaction of specific proteins with the granule membrane. The properties of the proteins described here, and their ability to bind to atrial specific granules in a calcium-dependent manner, make them likely candidates in the search for regulatory proteins mediating atrial natriuretic peptide secretion.
Hypertension 1991 Nov
PMID:Annexins V and VI: major calcium-dependent atrial secretory granule-binding proteins. 183 52

We investigated possible relations between excitation-contraction coupling and atrial natriuretic factor (ANF) release in rat atrial muscle using the isolated perifused atria preparation. To this purpose, the extracellular ionic environment was manipulated by replacement of Ca2+ with the polyvalent cations Ba2+, Sr2+, and La3+. Intracellular Ca2+ was altered by treatment with caffeine and ryanodine and by chemical (49 mM K+) depolarization. Replacement of Ca2+ with Ba2+ or Sr2+ abolished atrial spontaneous mechanical activity but did not prevent ANF release. Chemical depolarization also abolished spontaneous mechanical activity and significantly reduced ANF release in Ca(2+)-free media and in 0.625 mM extracellular Ca2+ but had no effect in the presence of 1.25 or 2.5 mM Ca2+, suggesting that changes in cytosolic Ca2+ levels do not affect ANF release in media containing Ca2+ in the physiological concentration range. The kinetics of ANF release observed during caffeine (10(-6) to 10(-2) M) treatment was similar to that seen in atrial preparations without treatment. At 10(-2) M, caffeine induced an increase in atrial beating rate and resting tension. Ryanodine (10(-4) M) pretreatment reduced stretch-induced ANF release by an average 34%, in addition to inhibiting tension development and beating. These findings clearly show marked differences between atrial cardiocytes and most other endocrine cells in terms of the effect of specific changes in the ionic environment on the secretory response; they also support the view that basal ANF release from atrial cardiocytes is not dependent on contractile atrial activity or Ca2+. In fact, Ca2+ appears to tonically inhibit the rate of basal ANF release. We conclude that, although indispensable for excitation-contraction coupling, intracellular Ca2+ transients by influx or from intracellular stores are not essential for basal ANF release. However, a ryanodine-sensitive compartment appears to be partly responsible for the increased ANF output after muscle stretch.
Hypertension 1991 Nov
PMID:Stretch-secretion coupling in atrial cardiocytes. Dissociation between atrial natriuretic factor release and mechanical activity. 183 55

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


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