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At least 739 records · Page 41Linked to original sources
PubMed1990

Delayed decline in plasma atrial natriuretic peptide levels after an abrupt reduction in atrial pressures: observation in patients with dual-chamber pacing.

The effect of an abrupt reduction in atrial pressures on atrial natriuretic peptide (ANP) secretion was studied in four patients with complete atrioventricular block with a dual-chamber pacemaker when the pacing mode was changed from the VVI to the DVI mode at an equal rate of 70/min. Simultaneous continuous hemodynamic monitoring was performed using a balloon-tipped thermodilution catheter. With DVI pacing, there was an immediate decrease of right atrial pressure from 4.5 +/- 0.9 to 1.8 +/- 1.1 mm Hg, and a reduction of pulmonary arterial wedge pressure from 7 +/- 0.8 to 4.5 +/- 0.9 mm Hg, together with a rise in cardiac output from 3.1 +/- 0.2 to 3.7 +/- 0.2 L/min. However, despite a constant hemodynamic status after dual-chamber pacing, the arterial ANP level steadily decreased from 151 +/- 26 pg/ml to a steady low level of 78 +/- 15 pg/ml after 20 minutes of dual-chamber pacing (percentage reduction- 48 +/- 8%, p less than 0.05). This persisted until the end of the study at 60 minutes. The time-dependent decay in ANP secretion after an abrupt and constant change in hemodynamic status should be considered when interpreting ANP levels.

Aged↗
PubMed1991

Influence of dilated cardiomyopathy, myocarditis and cardiac transplantation on the relation between plasma atrial natriuretic factor and atrial pressures.

To determine whether dilated cardiomyopathy, myocarditis or cardiac transplantation affect the relation between plasma immunoreactive atrial natriuretic factor (ANF) and cardiac filling pressures, right atrial plasma ANF concentration, pulmonary arterial wedge pressure and right atrial pressure were measured in patients with dilated cardiomyopathy (n = 48), dilated cardiomyopathy secondary to myocarditis (n = 20) and prior cardiac transplantation (n = 34). ANF level significantly correlated with both pulmonary arterial wedge and right atrial pressures in patients with dilated cardiomyopathy; however, the presence or absence of myocarditis did not significantly alter these relations (p = 0.88 and p = 0.33 for interaction terms, respectively). For the combined group the ANF-pulmonary arterial wedge pressure relation had a slope of 8.1 pg/ml/mm Hg (95% confidence interval (CI), 5.4 to 10.8; p = 0.0001) and the ANF-right atrial pressure relation a slope of 13.6 pg/ml/mm Hg (CI, 8.5 to 18.7; p = 0.0001). Receiver operator curve analysis identified an optimal dividing point of ANF 150 pg/ml with 100% (CI, 72 to 100%) of patients with right atrial pressure greater than or equal to 8 mm Hg having ANF greater than or equal to 150 pg/ml, but only 56% (CI, 42 to 69%) with pressure less than 8 mm Hg having ANF less than 150 pg/ml. Unlike the patients with cardiomyopathy (with or without myocarditis), cardiac transplant recipients displayed no correlation between ANF level and either pulmonary arterial wedge pressure (p = 0.50) or right atrial pressure (p = 0.29) despite similarly elevated ANF concentrations (mean +/- standard deviation 168 (83) pg/ml in transplant patients versus 185 (114) pg/ml in cardiomyopathy patients). It is concluded that left and right intracardiac pressures are important determinants of circulating ANF level unaffected by inflammation in patients with cardiomyopathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Impaired response of atrial natriuretic factor to blood volume expansion in acute right ventricular infarction.

To assess the role of atrial natriuretic factor (ANF) in right ventricular (RV) infarction, 30 patients with inferior wall acute myocardial infarction (15 with RV involvement) and normal left heart filling pressures were studied 39 +/- 12 hours after the onset of symptoms. Serial measurements of cardiac output, right atrial, pulmonary artery and pulmonary wedge pressures, as well as plasma ANF, plasma renin activity, plasma aldosterone and vasopressin were obtained before and 30 minutes after acute volume expansion to raise wedge pressure greater than or equal to 20 mm Hg. Baseline mean right atrial pressure and plasma ANF levels were greater in patients with than without RV infarction (8 +/- 3 vs 5 +/- 2 mm Hg; p less than 0.0001, and 4.6 +/- 2.9 vs 2.7 +/- 1.5 fmol/ml; p less than 0.05, respectively). There were no differences in other baseline hemodynamic or humoral parameters between both groups. After volume expansion, pulmonary wedge pressure was similar in both groups, but right atrial pressure increased to higher levels in patients with RV infarction (19 +/- 2 vs 14 +/- 2 mm Hg; p less than 0.0001). Despite this greater stimulus for ANF secretion, the increase in plasma ANF was less pronounced in patients with RV infarction (63 +/- 81 vs 455 +/- 417%; p less than 0.002), especially among those with paroxysmal supraventricular tachyarrhythmias. Thus, despite higher baseline plasma levels of ANF, response to volume loading is markedly attenuated in patients with RV infarction complicating an inferior wall acute myocardial infarction.

Adult↗
PubMed1995

Hemodynamic and hormonal responses to atrial distension in the ovine fetus.

OBJECTIVE: Our purpose was to evaluate the hemodynamic and endocrine responses to elevations of atrial pressure in fetal sheep. STUDY DESIGN: By use of a randomized block design, 10 ovine fetuses underwent pulmonary artery constriction proximal to the ductus arteriosus with and without propranolol pretreatment. RESULTS: Atrial pressure doubled (p < 0.05), whereas mean arterial pressure remained unchanged (p > 0.05), in response to pulmonary artery constriction in both groups. Atrial natriuretic peptide tripled (p < 0.01), arginine vasopressin tripled (p < 0.05), and plasma renin activity doubled (p < 0.05) in both the constriction and constriction plus propranolol groups. No changes in fetal hematocrit values were demonstrated in any group. CONCLUSIONS: The fetal sheep responds to increased atrial pressure with not only increased levels of atrial natriuretic peptide but also with arginine vasopressin and plasma renin activity over time. These changes occur in spite of increases in both atrial pressure and atrial natriuretic peptide. We speculate that the fetal heart may participate in redistribution of cardiac output by releasing atrial natriuretic peptide and augmenting secretion of arginine vasopressin and plasma renin activity.

Animals↗
PubMed1984

Purification and complete amino acid sequence of beta-rat atrial natriuretic polypeptide (beta-rANP) of 5,000 daltons.

A survey for natriuretic factors in rat atrial extract was performed by the aid of a simple assay for the relaxant effect on the contractility of chick rectum, in a manner similar to our previous purification of alpha-human atrial natriuretic polypeptide (alpha-hANP). Three distinct components (alpha, beta and gamma) of a potent relaxant activity with varying molecular weights, were found in the chromatographic regions of a crude extract. From the beta-component of rectum activity corresponding to about 5,000 daltons, a 48-amino acid peptide has been purified to homogeneity and found to elicit a potent natriuretic activity, when injected into the assay rats. Accordingly, the peptide was designated as "beta-rat atrial natriuretic polypeptide (beta-rANP)". The complete amino acid sequence of the peptide has been determined by microsequencing the S-carboxymethylated beta-rANP and its tryptic peptides.

Amino Acid Sequence↗
PubMed1985

Release of atriopeptin in the rat by vasoconstrictors or water immersion correlates with changes in right atrial pressure.

Vasopressin, its 1-deamino analog (dAVP), angiotensin II, and phenylephrine, administered intravenously, increased plasma atriopeptin immunoreactivity in chloral hydrate-anesthetized rats. A continuous one hour infusion of either dAVP or phenylephrine caused a sustained elevation in: a) systemic blood pressure; b) right atrial pressure; c) left ventricular end diastolic pressure; and d) plasma atriopeptin immunoreactivity. While continuous infusion of angiotensin II also produced a sustained elevation in left ventricular end diastolic pressure, the changes in right atrial pressure and plasma atriopeptin were only transient. These data suggest that plasma atriopeptin most closely correlates with right atrial pressure. Consistent with this hypothesis, we found that the release of atriopeptin directly correlated with changes in right atrial pressure in anesthetized, water-immersed rats.

Angiotensin II↗
PubMed1985

ANF (Arg 101--Tyr 126) is the peptide secreted by rat atrial cardiocytes in culture.

The atrial natriuretic factor (ANF) secreted from rat cardiocytes in culture was purified and characterized. The purification procedure involves extraction of ANF by activated Vycor glass, followed by HPLC on C18 mu Bondapak and Vydac columns. The detection of ANF in column eluates was performed by a simple and sensitive radioimmunoassay. The amino acid composition and N-terminal amino acid sequencing appeared to be identical to the Arg 101 - Tyr 126 peptide. The isolated ANF showed biological activity, inhibiting basal and ACTH-stimulating aldosterone secretion from rat zona glomerulosa cells with the same potency as the synthetic peptide.

Adrenal Glands↗
PubMed1990

Effects of temperature and osmolality on the release of atrial natriuretic peptide.

In isolated rat atria a 10 degrees C increase in temperature approximately doubled the output of atrial natriuretic peptide during relaxation and stretch. The effect was not due to the increased rate of contraction. Increasing the osmolality of the superfusate within the physiological range (290 to 320 m osmols) with sodium, potassium or glucose had no appreciable effect on the release of atrial natriuretic peptide.

Animals↗
PubMed1990

Sequential mechanism of atrial natriuretic peptide secretion in isolated perfused rabbit atria.

It is well known that the secretion of atrial natriuretic peptide (ANP) is dependent on the atrial stretch. It has been claimed in this laboratory that the secretion of ANP occurs with a reduction in atrial distension. It was shown in the present experiment that the secretion of immunoreactive (ir) ANP occurs coincidently with a translocation of extracellular space marker (3-H)-inulin in the isolated perfused rabbit atria. Translocation of extracellular space fluid was observed with a reduction in atrial distension. The secretion of irANP into the atrial lumen occurs less than 15 sec of the reduction in atrial distension. It is therefore suggested that the incremental response of irANP secretion to the reduction in atrial distension is a sequential mechanism of ANP secretion, in which first is the release of ANP from the atrial myocytes into the extracellular space and then second is the translocation of ANP with extracellular space fluid into the atrial lumen with a reduction in atrial distension.

Animals↗
PubMed1988

Right atrial dilatation increases inositol-(1,4,5)trisphosphate accumulation. Implications for the control of atrial natriuretic peptide release.

Stretching the right atrium of isolated perfused [3H]inositol-labelled rat hearts was shown to stimulate the phosphatidyl-inositol turnover pathway as demonstrated by the accumulation of [3H]inositol-(1,4,5)trisphosphate and its degradation products. Stimulation was detectable after 1 min with larger increases observed after 10 or 20 min. These findings demonstrate that the myocardium can respond to dilatation by an activation of the phosphatidylinositol turnover pathway. Such a mechanism has implications for the release of atrial natriuretic peptide following right atrial distention.

Animals↗
PubMed1989

Stretch-induced centrifugal movement of atrial specific granules--a preparatory step in atrial natriuretic peptide secretion.

Atrial natriuretic peptide (ANP) is a circulating hormone produced by atrial muscle cells which acts upon renal vascular smooth muscle to raise glomerular filtration pressure, thereby increasing salt and water excretion and reducing blood pressure [2, 5, 8]. As in other peptide hormone-secreting cells, ANP is packaged and stored in dense Golgi-derived secretory granules [4-6]. These atrial specific granules [6] occur predominantly in large clusters deep in the myocyte's interior, associated with Golgi cisternae in myofibril-free cytoplasm at the nuclear poles [5, 6]. Smaller clusters and individual granules are distributed beneath the sarcolemma and between myofibrils [6, 10]. Expansion of the blood volume raises the level of circulating ANP [7], a response mediated by mechanical stretch of the atrial wall [1, 3, 9]. The mechanism by which cell stretch induces release of ANP from atrial myocytes is, however, unknown. We show here that one component of this unusual secretory mechanism involves a sudden centrifugal movement of atrial specific granules toward the cell surface.

Animals↗
PubMed1990

Arrested exocytosis of atrial secretory granules.

Release of atrial natriuretic peptide (ANP) from atrial muscle cells is thought to occur by exocytosis of secretory granules, as in other secretory systems. However, in the atrial myocyte, exocytosis has previously proved difficult to detect ultrastructurally. In order to study the mechanism of ANP release and related events, we have applied two separate techniques--tannic acid perfusion and ultrarapid freezing--specifically designed to arrest exocytosis. An increased number of fusion sites was found after ultrathin sectioning and freeze-fracture of tannic acid-treated atria enabling a hypothetical release sequence to be constructed. Detail of granule substructure was also obtained, suggesting the presence of a coat to the secretory granule core. Ultrarapid freezing, followed by freeze-fracture and freeze substitution, has confirmed aspects of the proposed exocytotic sequence, suggesting that this release is not due to the application of tannic acid, and these techniques also produced further evidence for the existence of the granule-core coat. Coated pits and vesicles were also found in large numbers in tannic acid-treated atria and interactions between coated vesicles and secretory granules were visualized. The possible role of coated vesicles in an exocytotic/endocytotic membrane retrieval pathway is discussed.

Animals↗
PubMed1987

Release of atrial natriuretic polypeptide by graded right atrial distension in anesthetized dogs.

In order to verify the contribution of right atrial pressure to atrial natriuretic polypeptides (ANP) release, we measured plasma levels of immunoreactive (ir)-ANP when graded rise of right atrial pressure was executed in anesthetized dogs. Increasing right atrial pressure (RAP) from 2.7 +/- 0.6 to 9.0 +/- 0.7 mmHg, plasma levels of ir-ANP in aorta tended to increase by 33% but not significantly (p greater than 0.05). However, when RAP was increased from 9.0 +/- 0.7 to 17.0 +/- 1.1 mmHg, ir-ANP levels in aorta were significantly (p less than 0.05) increased by 132% of control within 5 min from the start of RAP elevation. The RAP elevation produced a sustained increase in plasma levels of ir-ANP. There was a positive correlation between right atrial pressure and plasma levels of ir-ANP. The plasma levels of ir-ANP were similar between aorta and pulmonary artery. These results demonstrate that increasing atrial pressure is closely correlated with ANP release and ANP is not greatly metabolized by pulmonary circulation.

Animals↗
PubMed1988

The concentration of atrial natriuretic peptide (ANP) is decreased in plasma but not in atria in hypophysectomised rats.

To study the role of the pituitary gland in the release of Atrial Natriuretic Peptide (ANP) plasma and atrial concentrations were measured both in intact and in hypophysectomized rats. The plasma concentration of ANP (pg/ml) was significantly (p less than 0.01) decreased from 143 +/- 35 to 82 +/- 29 (mean +/- SD, n) while the tissue concentration (ng/wet tissue mg) remained unchanged, 192 +/- 46 and 194 +/- 39, respectively. The total atrial amount of ANP (ug) was, however, significantly (p less than 0.01) decreased from 29.7 +/- 7.8 to 17.0 +/- 3.3 after hypophysectomy. In intact animals, a volume load (1.1ml/100 body weight g 0.9% NaCl) resulted in 2-fold (p less than 0.001) increase in the plasma ANP levels whereas similar load had no effects on plasma ANP levels in hypophysectomized animals. In both groups, the right atrial pressure was increased from about 2 to about 6 mmHg. We conclude that in the absence of pituitary gland the right atrial pressure and the atrial ANP concentration do not change but plasma ANP levels and the response to volume stimulus are attenuated.

Animals↗
PubMed1988

A calmodulin antagonist (W-7) and a protein kinase C inhibitor (H-7) have no effect on atrial natriuretic peptide release induced by atrial stretch.

The role of intracellular signals in the regulation of atrial natriuretic peptide (ANP) release was investigated using isolated rat left atria. Dibutyryl cyclic AMP and dibutyryl cyclic GMP had no effect on ANP release. Arginine vasopressin and phenylephrine, both of which activate the polyphosphoinositide system and consequently both the diacylglycerol-protein kinase C system and the Ca2+-Ca2+ receptor system, stimulated ANP release dose-dependently. The ANP release stimulated by phenylephrine was inhibited by N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7), a calmodulin antagonist, and 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7), a protein kinase C inhibitor. Atrial stretch stimulated ANP release, but the release was not inhibited by W-7 or H-7. These results suggest that the mechanism responsible for phenylephrine-induced ANP release differs from that for stretch-induced ANP release.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗