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At least 19 recordsLinked to original sources
PubMed1986

Inhibition of vasopressin action by atrial natriuretic factor.

Atrial natriuretic factor results in diuresis in animals and humans, perhaps because atrial natriuretic factor increases renal blood flow. The possibility that this diuresis is due to direct inhibition of renal tubular epithelial water transport was examined in rabbit collecting tubules perfused in vitro. Atriopeptin III inhibition of the hydraulic conductivity response to the hormone arginine vasopressin but not to either 3'5'-cyclic adenosine monophosphate or forskolin was found. These results suggest that atriopeptin III acts proximal to cyclic adenosine monophosphate formation to directly affect vasopressin-stimulated water transport in the mammalian nephron. They also suggest a potential role for inhibition by atrial natriuretic factor of the renal response to arginine vasopressin as a contributor to a diuretic state.

Animals↗
PubMed1988

Contribution of blood and systemic circulation to the processing of pro-(atrial natriuretic factor).

Atrial natriuretic factor-(Asn1-Tyr126)-peptide, the 13.6 kDa propeptide of atrial natriuretic factor (ANF), is stored in the secretory granules of atrial cardiocytes. ANF-(Ser99-Tyr126)-peptide, the 28-amino-acid species, is the circulating form of this hormone in the rat. As the site of maturation of the prohormone is still unknown, the present study was undertaken to understand the contribution of the circulation to the maturation process of pro-ANF. 125I-ANF-(Asn1-Tyr126)-peptide was incubated with whole rat blood, plasma or serum for different time intervals, and the products were analysed. There was minimal activation of the propeptide in either whole blood or plasma. Incubation with serum, however, resulted in the formation of an 11 kDa and a 3 kDa peptide which corresponded respectively to the N-terminal and C-terminal parts of the propeptide. These results suggest that hydrolysis of the propeptide in serum is brought about by enzymes that may be stimulated during coagulation but which may not play a major role in the activation of pro-ANF in the circulation. Plasma analysis at different time intervals after prohormone injection indicated a non-specific hydrolysis of the pro-ANF molecule. The disappearance rate curves, obtained with radiolabelled pro-ANF, suggested the presence of two components with half-lives of 2.1 +/- 0.4 min and 52.5 +/- 8.4 min respectively. A metabolic clearance rate of 1.49 +/- 0.22 ml/min and an initial distribution volume of 47.4 +/- 8 ml were calculated. These results indicate that the maturation of pro-ANF to its active circulating form takes place before it is released into the circulation.

Animals↗
PubMedDate not supplied

Is there a pericardial restriction to the cardiac secretion of atrial natriuretic factor?

Atrial natriuretic factor (ANF) is secreted from atrial myocytes in response to increased atrial wall stress caused by increased transmural pressure. This study investigates whether the presence of an intact pericardium restricts the ANF secretory response to an increment in left atrial pressure caused by acute aortic constriction in anaesthetized open-chest pigs. The rise in ANF plasma concentration secondary to constriction was higher when the pericardium had been surgically opened than when it was left intact. Furthermore, an opened pericardium led to a larger increase during constriction in left atrial diameter as measured by sonomicrometry. The results suggest that the intact pericardium restricts the cardiac release of ANF secondary to aortic constriction, probably by restricting left atrial dilatation.

Animals↗
PubMed1987

On the physiological role of atrial natriuretic factor.

Atrial natriuretic factor, a family of peptides present in saline extract of cardiac atria, was discovered by deBold and colleagues in 1981. It was shown subsequently that ANF is synthesized in, and secreted from, myocytes in cardiac atria, that it circulates in the bloodstream, and that it acts on receptor sites in kidney and blood vessels. It is appropriate, therefore, to consider ANF as a new endocrine system which may be important in body fluid volume and blood pressure regulation. However, despite extensive investigation in many laboratories the regulatory roles of this hormone remain largely speculative. Although a causative contribution of endogenous ANF in the natriuretic response to acute hypervolemia is well established, its participation in the maintenance of salt balance during large variations in dietary Na intake is less certain. Depending on species studied (and laboratory) a range of more than 30-fold may or may not alter plasma levels of ANF, which, in any case, remain lower than those resulting in acute natriuresis. In addition to increased sodium excretion, atrial factor also inhibits aldosterone and renin release, both in vitro and in vivo. The in vitro effects occur at concentrations which are 10- to 100-fold higher than circulating plasma ANF levels. In addition, atrial factor reduces blood pressure when injected in the whole animal, and causes relaxation of precontracted smooth muscle in vitro. The vasorelaxant effect is detectable at concentrations which fall in the range of normal endogenous levels of the hormone. Although hypotension in vivo generally requires natriuretic doses of ANF, this may be due to compensatory reflexes in the intact animal.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1986

Inhibition of aldosterone synthesis by atrial natriuretic factor.

Atrial natriuretic factor (ANF) inhibits basal and stimulated aldosterone synthesis in adrenal glomerulosa cells. ANF probably acts through specific membrane receptors. Alterations in cyclic GMP and cyclic AMP levels do not account for ANF's inhibitory effect. ANF does not block angiotensin II (AngII) receptors nor does it interfere with phosphoinositide metabolism or calcium movements stimulated by adrenal agonists. ANF does not inhibit protein synthesis nor does it work by inhibiting NA+,K+-ATPase or depleting cell potassium. ANF decreases conversion of endogenous cholesterol to pregnenolone, the step stimulated by adrenocorticotropin and AngII. ANF does not affect the conversion of 20-alpha-hydroxycholesterol, which easily penetrates mitochondrial membranes to the site of the cholesterol side-chain cleavage enzyme. These results suggest that ANF inhibits the ability of endogenous cholesterol to reach or interact with the side-chain cleavage enzyme. ANF does not act like a calcium channel-blocking agent. However, ANF is less effective at high-calcium concentrations, which suggests that it may inhibit a step that calcium stimulates. Understanding ANF action will probably require identification of the specific biochemical changes (mediators) that it induces. Parallel efforts to understand how other agents stimulate steroidogenesis (particularly in the areas of protein synthesis, protein phosphorylation, and cholesterol movements) will further this understanding.

Aldosterone↗
PubMed1994

[Current knowledge on the atrial natriuretic factor].

Atrial natriuretic factor (ANF) is a polypeptidic hormone released by the atria in response to an increase in atrial stretch. Kidneys, vessels and adrenal are the major ANF target tissues. ANF inhibitory effect on renin-angiotensin-aldosterone system potentiates its natriuretic and vasodilatory actions. By decreasing the venous return to the heart, ANF exerts an indirect negative feedback on its own synthesis. Since ANF discovery by De Bold in 1981, progress have been accomplished including the description of a family of natriuretic peptides derived from ANF and therapeutic trials of neutral endopeptidase inhibitors, a new pharmacologic class of diuretics.

Animals↗
PubMed1993

Cardiovascular and renal effects of atrial natriuretic factor.

Atrial natriuretic factor (ANF) reduces cardiac output and systemic arterial blood pressure. The reduction in systemic arterial blood pressure is not caused by dilation of arterial resistance vessels, since total peripheral vascular resistance often increases during infusion of ANF. The reduction in cardiac output with subsequent hypotension can be explained by a decrease in venous return. The decrease in venous return is not due to pooling of blood in the capacitance vessels, since ANF reduces venous compliance. Reduced venous return during infusion of ANF can be explained by a reduction in circulating blood volume and an increase in resistance to venous return. The reduction in circulating blood volume is due to increased urine output and to a shift of circulating fluid into the interstitial space. The increase in renal sodium and water excretion is mediated by an increase in glomerular filtration rate and reduced sodium and chloride reabsorption in the collecting ducts. ANF also inhibits the renin-angiotensin-aldosterone system. The plasma level of ANF may be a parameter for the severity of heart diseases with increased preload. In congestive heart failure and supraventricular tachycardia, the increase in plasma ANF concentration may augment sodium excretion, but anti-natriuretic factors, such as reduction in renal perfusion pressure, may override the natriuretic effect of ANF. Reduced sodium excretion during mechanical ventilation with positive end-expiratory pressure (PEEP) is partly due to a decrease in ANF secretion.

Animals↗
PubMed1986

Extra-atrial expression of the gene for atrial natriuretic factor.

Atrial natriuretic factor (ANF) is a group of peptides, originally isolated from the cardiac atria, that have a number of important effects on blood pressure, renal function, and salt balance. In the current study, expression of the ANF gene in certain extra-atrial tissues of the rat has been examined by radioimmunoassay of extracted ANF protein and by blot-hybridization, nuclease S1 analysis, and primer-extension analysis of the ANF mRNA. ANF peptides and mRNA were detected in cardiac ventricles, lung, and pituitary gland at levels generally less than or equal to 1% those of cardiac atria. The ANF transcripts in extra-atrial tissue appear to be very similar to those synthesized in the atria. They are polyadenylylated, are equivalent in overall length (950-1050 nucleotides), and have identical 5' termini. A secondary transcription start site mapping approximately 80 base pairs upstream from the primary start site is employed in atria and to a lesser extent in other tissues. The ANF transcript is present throughout the cardiac ventricles from apex to base and in the septum as well as the ventricular free walls. The transcript is more prevalent in the left ventricle and interventricular septum than in the right ventricle. Immunocytochemistry using various anti-rat ANF antibodies localized ANF immunoreactivity to the atrial myocytes; the ventricular myocytes, particularly along the endothelial surface of the ventricular chamber; perialveolar cells in the lung; and the gonadotropin-producing cells of the pituitary. The data indicate that the capacity for ANF gene expression extends beyond atrial tissue, albeit at much reduced levels, and may suggest alternative, perhaps paraendocrine, functions for the peptide in these tissues.

Animals↗
PubMed1990

Neutral endopeptidase inhibition potentiates the renal actions of atrial natriuretic factor.

Atrial natriuretic factor (ANF) is degraded by neutral endopeptidase. We hypothesized that neutral endopeptidase inhibition (NEP-I) increases sodium excretion and that this effect would be potentiated in the presence of an isolated increase in intrarenal ANF. In seven anesthetized dogs, ANF was infused into one renal artery to produce pathophysiologic concentrations in the supplemented kidney while the control kidney received physiologic circulating concentrations of ANF. In the control kidney, NEP-I (SQ 28,603) produced significant increases in urine flow, absolute sodium excretion and fractional sodium excretion while glomerular filtration rate (GFR) remained constant. These renal actions of NEP-I were associated with marked increases in urinary excretion of ANF and cyclic GMP consistent with decreased renal degradation and increased biologic activity of ANF. All of these effects were significantly greater in the supplemented kidney. The present study suggests that NEP-I produces natriuresis which appears to be independent of changes in GFR. In addition, while NEP-I mimics the renal action of pathophysiologic levels of ANF, NEP-I also potentiates the natriuretic effects of pathophysiologic concentrations of ANF as observed in congestive heart failure or hypertension.

Alanine↗
PubMed1987

Angiotensin decreases cyclic GMP accumulation produced by atrial natriuretic factor.

Atrial natriuretic factor (ANF) produced rapid increases in cyclic GMP (cGMP) in cultured aortic smooth muscle cells. Angiotensin II (ANG II) markedly decreased the accumulation of cGMP that was evoked by ANF. Arginine vasopressin and ATP, which evoke transient increases in free Ca2+ similarly to ANG II, also inhibited cGMP accumulation. The effect of the calcium mobilizing neurohormones was mimicked by the divalent cation ionophore, A23187. The cyclic nucleotide phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine, prevented ANG II from inhibiting ANF-evoked cGMP accumulation. ANG II also inhibited cGMP accumulation induced by nitroprusside, a compound that activates cytosolic guanylate cyclase. These findings support the hypothesis that ANG II decreases cGMP accumulation by stimulating cGMP hydrolysis, apparently via a Ca2+-activated cGMP phosphodiesterase.

1-Methyl-3-isobutylxanthine↗
PubMed1989

The effect of subarachnoid hemorrhage on blood and CSF atrial natriuretic factor.

Atrial natriuretic factor (ANF) is a diuretic natriuretic peptide hormone produced by both the heart and brain which has been postulated to play a role in the hemodynamic and sodium instability that frequently follows subarachnoid hemorrhage (SAH). Levels of ANF were measured in 12 patients with nontraumatic SAH and nine control patients with unruptured cerebral aneurysms. At surgery, the mean plasma ANF level (+/- standard deviation) of the SAH group was significantly higher than that of the control group (158.1 +/- 83.8 vs. 57.8 +/- 45.3 pg/ml, respectively; p = 0.01). There was no significant difference in serum sodium concentration, blood pressure, or central venous pressure between these groups. Nine patients with SAH due to aneurysm rupture had plasma ANF levels similar to those in three patients with SAH due to other causes. Four patients with moderate to severe SAH had significantly higher mean cerebrospinal fluid (CSF) ANF values (17.7 +/- 12.8 pg/ml) than five patients with minimal SAH (0.6 +/- 0.9 pg/ml) or the control group of nine patients (3.7 +/- 1.3 pg/ml) (p less than 0.05). Five patients with moderate to severe SAH had significantly higher plasma ANF values (202.6 +/- 72.2 pg/ml) than five with minimal SAH (86.8 +/- 29.2 pg/ml) or the control group (57.8 +/- 45.3 pg/ml) (p less than 0.05). Plasma ANF values were substantially higher than CSF ANF content in the SAH group (p less than 0.01) and in the control group (p = 0.05). From these data it is concluded that: 1) plasma ANF is elevated significantly after SAH; 2) this rise appears unrelated to the cause of hemorrhage, serum sodium concentration, blood pressure, or central venous pressure, but is related to the extent of the hemorrhage; 3) ANF concentrations in the CSF are significantly lower than in plasma, and are elevated after moderate to severe SAH; and 4) the source of CSF ANF is probably the plasma, and the source of plasma ANF is likely the heart.

Adult↗
PubMed1987

Cellular mechanisms of action of atrial natriuretic factor.

Atrial natriuretic factor (ANF) interacts with its target cells through specific receptors. This interaction induces, in most cell types, the activation of particulate guanylate cyclase and decreased Calcium mobilisation. In addition, ANF also decreases adenylate cyclase activity in some tissues. Activation of particulate guanylate cyclase, and additionally inhibition of adenylate cyclase, appear to initiate the cellular responses to circulating ANF. The activation of particulate guanylate cyclase is tissue-specific, immediate and can be demonstrated also on the solubilized enzyme. The ANF receptor appears to be tightly coupled to particulate guanylate cyclase. The increased formation of cyclic GMP induces cGMP-dependent protein phosphorylation in target cells. In addition, cyclic GMP inhibits Calcium mobilisation in several tissues. This may explain observations of inhibition of Calcium mobilisation after ANF. Cyclic GMP is not only degraded by phosphodiesterase, but is also extruded from target cells. As a consequence of cGMP extrusion, ANF increases the levels of cyclic GMP in plasma and urine in animals and man. Cyclic GMP is also increased in various disease states, in which ANF is increased. In contrast, cyclic AMP plasma levels are unaltered after ANF elevations. At present, the exact mechanisms, by which cellular functions are altered by ANF are still incompletely understood. It is anticipated, that the close correlation between the cyclic GMP system and effects of ANF in various target tissues is a key finding that will help elucidate the exact mechanisms of ANF action.

Adenylyl Cyclase Inhibitors↗
PubMed1985

The gene for rat atrial natriuretic factor.

Atrial natriuretic factor (ANF), a peptide hormone recently isolated from heart atria, appears to play an important role in the regulation of extracellular fluid volume and blood pressure. Indeed, natural and synthetic ANF rapidly and markedly stimulate natriuresis and diuresis and produce smooth muscle relaxation. Consistent with the hypothesis that ANF is a novel hormone, it was recently shown that ANF is present in circulation, and high affinity membrane receptors specific for ANF have been described in renal, vascular, and adrenal tissues. These important biological activities suggest that conditions like hypertension could be associated with defective ANF gene expression. We and others have shown by cDNA cloning that ANF is part of a larger precursor, pro-natriodilatin (PND). We now describe the isolation and structural analysis of the rat PND gene. Southern blot analysis of rat genomic DNA suggests the presence of a single PND gene per haploid genome. The PND coding sequences are interrupted by two short introns. A long alternating purine-pyrimidine tract (GT)9GATG(GT)27 is found 111 base pairs downstream of the polyadenylation site; such sequences could adopt Z-DNA configuration and they have been associated with sequences that appear very active in intergenic recombination. Comparison of the rat and human PND genomic sequences shows highest homology in 5'-flanking as well as in coding sequences. The rat PND gene will be a useful model to study the physiology and pathology of this important regulator of the cardiovascular system.

Animals↗
PubMed1989

Effect of posture on the plasma levels of atrial natriuretic factor.

Atrial natriuretic factor (ANF) is a peptide with potent natriuretic, diuretic and vasorelaxant activities. Stretching of the right atria causes release of ANF into the circulation. Therefore, changes in central blood volume or acute volume expansion are likely to change the plasma levels of ANF. In this study we investigated the effects of changes in posture on the plasma levels of ANF, plasma renin activity (PRA) and plasma aldosterone (aldo). Eight male and five female volunteers ranging in age from 23 to 26 years were placed on a normal sodium intake and on the experimental day blood was obtained for ANF, PRA, and aldo after 30 minutes of lying supine, 30 minutes of 10 or 20 degrees head-down tilt, and 30 minutes of standing. Plasma ANF increased significantly after 30 minutes of head-down tilt from the supine value of 33.7 +/- 5.2 pg/ml to 47.7 +/- 7.7 pg/ml (p less than 0.02) and suppressed to 14.1 +/- 0.02) after 30 minutes of standing. PRA did not change significantly with head-down tilt, (supine 1.64 +/- 0.44 ngAI/ml/h vs. 30 minutes tilt 1.28 +/- 0.32 ngAI/ml/h (p = NS). Plasma aldosterone decreased by head-down tilt from 11.2 +/- 1.2 ng/ml to 8.4 +/- 0.8 ng/dl (p less than 0.02) and returned to the supine level after standing. In conclusion ANF levels change significantly with posture. Increase in central blood volume by head-down tilt increases ANF levels and suppresses plasma aldosterone with no effect on PRA. Standing decreases ANF significantly. These results suggest that for proper interpretation of plasma levels of ANF, posture at the time of sampling has to be standardized.

Adult↗
PubMed1991

Endogenous natriuretic factors: atrial natriuretic hormone and digitalis-like substance in Cushing's syndrome.

In order to investigate the effect of chronic hypercortisolaemia on endogenous natriuretic factors (atrial natriuretic hormone (ANH) and the Na+/K+ pump inhibitor) digitalis-like substance (DLS), and their relation to hypertension, 28 patients with pituitary- or adrenal-dependent Cushing's syndrome and six patients on high-dose prednisone treatment were studied. Plasma ANH levels were increased in patients with Cushing's syndrome (36.0 +/- 1.4 (S.E.M.) ng/l) compared with those in healthy controls (28.6 +/- 1.3 ng/l, P less than 0.01). In prednisone-treated patients, ANH levels (43.8 +/- 4.5 ng/l) were higher than those in patients with Cushing's syndrome and in controls (P less than 0.05 and P less than 0.01 respectively). DLS measured by radioimmunoassay and binding of [3H]ouabain to erythrocytes was not altered in patients with hypercortisolaemia. Slightly decreased DLS activity in the erythrocyte 86Rb uptake inhibition assay was found in patients with Cushing's syndrome (52.9 +/- 2.7%) compared with that in controls (60.9 +/- 1.8%, P less than 0.02). With the exception of cortisol (r = 0.52, P less than 0.01), none of the other factors determined correlated with the mean arterial pressure in patients with Cushing's syndrome. Thus, a chronic excess of endogenous and exogenous glucocorticoids increases plasma levels of ANH, but does not substantially influence DLS activity or plasma levels. Neither natriuretic factor is directly related to hypertension in Cushing's syndrome.

Adult↗
PubMed1984

Atrial natriuretic factor: atrial conversion of high to low molecular weight forms.

The atrial natriuretic factor elutes by gel filtration in high and low molecular weight fractions. Extraction and elution of rat atria in 1.0 M acetic acid yielded a predominance of the high molecular weight form(s); whereas when these procedures were carried out in 0.1 M acetic acid, there was a predominance of the low molecular weight forms. When partially purified high molecular weight natriuretic activity was eluted in 0.1 M acetic acid, the high molecular weight form(s) remained intact. When partially purified high molecular weight natriuretic activity was mixed with crude atrial extract in 0.1 M acetic acid, there was an apparent conversion to the low molecular weight forms. Extraction of rat atria in boiling 0.1 M acetic acid blocked this conversion. It is concluded that rat atria contain a heat labile factor that converts high molecular weight natriuretic activity to the low molecular weight forms.

Acetates↗
PubMed1987

Atrial natriuretic factor during atrial fibrillation and supraventricular tachycardia.

Plasma immunoreactive atrial natriuretic factor was measured in 10 patients with chronic atrial fibrillation before and after cardioversion to sinus rhythm, and in 14 patients during electrophysiologic evaluation of paroxysmal supraventricular tachycardia. The mean plasma concentration of atrial natriuretic factor in atrial fibrillation was 138 +/- 48 pg/ml and decreased to 116 +/- 45 pg/ml 1 hour after cardioversion to sinus rhythm (p less than 0.005). The mean plasma concentration of atrial natriuretic factor increased from 117 +/- 53 pg/ml in sinus rhythm to 251 +/- 137 pg/ml during laboratory-induced supraventricular tachycardia (p less than 0.005). Right atrial pressures were recorded in 12 patients; the baseline atrial pressure was 4.3 +/- 1.9 mm Hg and increased to 7.4 +/- 3.6 mm Hg during supraventricular tachycardia (p less than 0.005). A modest but significant linear relation was noted between the changes in plasma atrial natriuretic factor and right atrial pressure measurements during induced supraventricular tachycardia (r = 0.60, p less than 0.05). In conclusion, changes in atrial rhythm and pressure may be an important factor modulating the release of atrial natriuretic factor in the circulation and raised levels of this hormone may be a contributing factor for the polyuria and the hypotension associated with paroxysmal supraventricular tachyarrhythmias.

Aged↗