Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “atrial function”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 829 records · Page 46Linked to original sources
PubMed1985

Release of atrial natriuretic peptide by atrial distension.

A heterologous radioimmunoassay was used to measure the concentration of immunoreactive atrial natriuretic peptide (iANP) in plasma from the femoral artery of eight chloralose anaesthetized dogs. Mitral obstruction which increased left atrial pressure by 11 cmH2O increased plasma iANP from 97 +/- 10.3 (mean +/- SE) to 135 +/- 14.3 pg/mL. Pulmonary vein distension increased heart rate but did not increase plasma iANP. Bilateral cervical vagotomy and administration of atenolol (2 mg/kg) did not prevent the increase in iANP with mitral obstruction. Samples of blood from the coronary sinus had plasma iANP significantly higher than simultaneous samples from the femoral artery confirming the cardiac origin of the iANP. Release of iANP depends on direct stretch of the atrium rather than on a reflex involving left atrial receptors.

Animals↗
PubMed1987

Mechanisms for the release of atrial natriuretic peptide.

In assessing the role that atrial natriuretic peptide (ANP) might have in the homeostasis of fluid volume and blood pressure, it is important to define the physiological and pathophysiological conditions that determine its release into the circulation. There is substantial evidence that ANP is released through atrial distension under a variety of conditions. There are also some indications that ANP may be released through humoral factors, although it is not clear whether this is a result of direct action on the myocytes or simply a result of ensuing haemodynamic changes. There is no evidence to suggest that ANP can be released through stimulation of efferent fibres innervating the atria, but it may be released as a result of changes in myocardial work and oxygen consumption. Plasma levels of ANP are elevated in several disease states and that release appears to be a result of the haemodynamic disturbances in those conditions.

Atrial Function↗
PubMed1991

The effect of isoproterenol on right and left atrial dynamics and plasma atrial natriuretic factor in anesthetized rabbits.

The effect of isoproterenol on mean right and left atrial pressures (RAP, LAP) and dimensions (RAD, LAD), and plasma immunoreactive atrial natriuretic factor (IR-ANF) was investigated in anesthetized rabbits. Infusion of isoproterenol (10 micrograms.kg-1.min-1 for 10 min) significantly increased plasma IR-ANF and heart rate. There were no significant changes in mean RAP or LAP following isoproterenol. Neither mean RAD, systolic RAD and diastolic RAD nor mean LAD, systolic LAD or diastolic LAD changed significantly. Systolic right and left atrial wall stress and diastolic right and left atrial wall stress did not change significantly during the infusion of isoproterenol. Since atrial dimensions did not increase, it is unlikely that the release of IR-ANF in response to isoproterenol is mediated by atrial stretch. These results suggest that the release of IR-ANF in response to this dose of isoproterenol is mediated by factors other than stretch or changes in atrial dynamics.

Animals↗
PubMed1992

Plasma atrial natriuretic factor and atrial wall stress in hypertensive and normotensive rabbits after pacing and volume expansion.

Atrial natriuretic factor (ANF) is present in high concentration in atria but in very low concentration in the ventricles. Under conditions of haemodynamic overload ventricular gene expression may become activated, but it is not clear if ventricular ANF can be released through a regulated or constitutive pathway. The purpose of this study was to determine whether basal and stimulated release of ANF are increased in perinephritic rabbits with mild hypertension. Six rabbits were rendered hypertensive by wrapping both kidneys in cellophane, and six sham-operated rabbits were used as controls. Eight weeks after renal wrapping, mean arterial pressure was approximately 20 mmHg higher in the experimental group. After anaesthesia, the renal-wrapped group had a higher vascular resistance. Right and left atrial wall stress was measured using sonomicrometry. Volume expansion by 30% of blood volume, using donor blood, caused a small increase in right and left atrial diastolic and systolic wall stress but did not significantly increase plasma ANF. Pacing the heart at 6 Hz caused increases in systolic but not diastolic wall stress and caused a significant increase in plasma ANF; the increase was larger after volume expansion. There were no significant differences between the responses of the experimental and control groups. It is concluded that mild hypertension, in the rabbit, does not lead to changes in atrial wall stress or either basal or stimulated release of ANF.

Anesthesia↗
PubMed1989

Determinants of atrial natriuretic peptide secretion in cultured atrial myocytes.

Atrial natriuretic peptide (ANP) secretion by atrial myocytes in 7- to 8-day primary cultures from adult rats was measured by radioimmunoassay under conditions designed to separate primary effects on secretion from effects caused by contractions. Abolishing contraction with 10 microM tetrodotoxin significantly reduced ANP accumulated in 2 h. Raising external Ca2+ concentration from 0.2 to 1.2 mM in the presence of tetrodotoxin did not increase ANP secretion. Substantial ANP secretion persisted in a nominally Ca2+-free medium containing 10 mM ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) and was not diminished by 100 microM ryanodine. In the presence of EGTA, 100 nM 12-O-tetradecanoylphorbol 13-acetate (TPA) significantly increased ANP secretion; this increment was unaffected by 100 microM ryanodine. These experiments suggest 1) that in absence of contractions, ANP secretion requires neither transplasmalemmal Ca2+ influx nor ryanodine-inhibitable Ca2+ release by sarcoplasmic reticulum (SR) and 2) that TPA stimulates ANP secretion without requiring Ca influx or ryanodine-inhibitable SR Ca release.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1990

Basal and stretch-augmented natriuretic peptide secretion by quiescent rat atria.

Absolute rates of immunoreactive atrial natriuretic peptide (ANP) secretion were measured in vitro at 37 degrees C in noncontracting preparations of combined right and left rat atria at constant distending pressures of 0 or 5.1 mmHg in presence of 0.2 mM extracellular Ca2+ concentration [( Ca2+]o), 10 microM ryanodine, and either 1 microM saxitoxin or 10 microM tetrodotoxin. By systematic deletion of external Na+, K+, Mg2+, Cl-, or HCO3-, and reduction of [Ca2+]o, and by selective ion transport inhibitors, neither net transplasmalemmal fluxes of Na+, Cl-, HCO3-, and Mg2+ nor ryanodine-sensitive Ca2+ release from sarcoplasmic reticulum (SR) was found necessary for stretch augmentation of secretory rate (Ra). Ra 1) was near zero within 20 min when extracellular Na+ concentration = 0 and [Ca2+]o = 20 microM and within 5 min or less after preincubation with caffeine, 8-chlorophenylthioadenosine 3',5'-cyclic monophosphate, or at 18 degrees C; 2) was significantly decreased by Cd2+, Ni2+, the isoquinoline H-7, and trifluoperazine but not 100 microM ryanodine; 3) was increased by neomycin; and 4) had an apparent activation energy of 18.5 +/- 4.1 x 10(3) cal/mol between 23 and 42 degrees C. These experiments strongly implicated transplasmalemmal Ca2+ influx and cAMP but not SR Ca2+ release in control of Ra under the experimental conditions studied.

Amiloride↗
PubMed1988

Effect of alpha- and beta-adrenergic stimulation on atrial natriuretic peptide release in vitro.

The role of intracellular signals in the regulation of atrial natriuretic peptide (ANP) release was studied using the isolated left and right atria from a rat. The atria were perfused with Tyrode's solution, equilibrated with 95% O2-5% CO2 at 37 degrees C with a constant flow of 0.5 ml/min. Addition of epinephrine (10(-6) M), an alpha- and beta-agonist, to the perfusate induced the biphasic release of ANP from the right atrium without effect on the left. The initial peak (19.2 +/- 2.6 pg.min-1.ml-1) occurs 2-4 min after the administration of epinephrine, which lasted 4-6 min and returned to base line (10.4 +/- 1.1 pg.min-1.mg-1). The second peak (16.5 +/- 2.0 pg.min-1.ml-1) appeared 30-35 min after epinephrine administration and was sustained for 100 min, at which time the experiment was terminated. The first peak was stimulated by isoproterenol (10(-6) M), a beta-agonist, and blunted by propranolol (10(-6) M), a beta-antagonist. The second peak appeared following methoxamine (10(-6) M), an alpha-agonist, and could be suppressed by phentolamine (10(-6) M), an alpha-antagonist. These studies indirectly suggest that the adenosine 3',5'-cyclic monophosphate system and the inositol triphosphate system are involved in ANP secretion, with the former responsible for the initial rapid release and the latter maintaining the secretion.

Animals↗
PubMed2004

Augmentation of moxonidine-induced increase in ANP release by atrial hypertrophy.

Imidazoline receptors are divided into I(1) and I(2) subtypes. I(1)-imidazoline receptors are distributed in the heart and are upregulated during hypertension or heart failure. The aim of this study was to define the possible role of I(1)-imidazoline receptors in the regulation of atrial natriuretic peptide (ANP) release in hypertrophied atria. Experiments were performed on isolated, perfused, hypertrophied atria from remnant-kidney hypertensive rats. The relatively selective I(1)-imidazoline receptor agonist moxonidine caused a decrease in pulse pressure. Moxonidine (3, 10, and 30 micromol/l) also caused dose-dependent increases in ANP secretion, but clonidine (an alpha(2)-adrenoceptor agonist) did not. Pretreatment with efaroxan (a selective I(1)-imidazoline receptor antagonist) or rauwolscine (a selective alpha(2)-adrenoceptor antagonist) inhibited the moxonidine-induced increases in ANP secretion and interstitial ANP concentration and decrease in pulse pressure. However, the antagonistic effect of efaroxan on moxonidine-induced ANP secretion was greater than that of rauwolscine. Neither efaroxan nor rauwolscine alone has any significant effects on ANP secretion and pulse pressure. In hypertrophied atria, the moxonidine-induced increase in ANP secretion and decrease in pulse pressure were markedly augmented compared with nonhypertrophied atria, and the relative change in ANP secretion by moxonidine was positively correlated to atrial hypertrophy. The accentuation by moxonidine of ANP secretion was attenuated by efaroxan but not by rauwolscine. These results show that moxonidine increases ANP release through (preferentially) the activation of atrial I(1)-imidazoline receptors and also via different mechanisms from clonidine, and this effect is augmented in hypertrophied atria. Therefore, we suggest that cardiac I(1)-imidazoline receptors play an important role in the regulation of blood pressure.

Adrenergic alpha-Agonists↗
PubMed1988

Mechanism of inhibition by methacholine of norepinephrine-stimulated ANP secretion.

We have previously reported that methacholine inhibits norepinephrine-stimulated immunoreactive atrial natriuretic peptide (ANP-IR) secretion by 65% in vitro. In the present study, we examined the mechanism by which methacholine inhibits norepinephrine-stimulated secretion using isolated, paced rat left atria superfused in vitro. Norepinephrine has beta- and alpha-adrenergic properties, both of which stimulate ANP secretion. Thus we separately examined the effect of 10 microM methacholine on ANP-IR secretion stimulated by the beta-adrenergic agonist isoproterenol (0.1 microM) and by the alpha-adrenergic agonist phenylephrine (10 microM). Methacholine lowered isoproterenol-stimulated ANP-IR secretion to base line but did not inhibit phenylephrine-stimulated ANP-IR secretion. Atria were superfused with 0.5 mM dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP) to determine whether inhibition of isoproterenol-stimulated secretion by methacholine occurred by a reduction in adenylate cyclase activity or at a point distal to cAMP. Methacholine inhibited dibutyryl cAMP-stimulated ANP-IR secretion by 50%. This inhibition could not be reversed by 20 microM isobutylmethylxanthine. We conclude that 1) methacholine completely blocks isoproterenol-stimulated ANP-IR secretion; 2) inhibition appears to be primarily due to a decrease in adenylate cyclase activity; however, inhibition occurs at a point(s) distal to cAMP production; 3) methacholine does not inhibit phenylephrine-stimulated ANP-IR secretion; and 4) inhibition by methacholine of norepinephrine-stimulated ANP-IR secretion reflects a block in beta-adrenergic activity.

Animals↗
PubMed1989

Effect of manipulations of Ca2+ environment on atrial natriuretic factor release.

The effects of Ca2+ on the kinetics of atrial natriuretic factor (ANF) release [measured as immunoreactive cardionatrin (IRC)] were studied on an in vitro, spontaneously beating rat atrial preparation. It was found that ethylene glycolbis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) and Ca2+-free media induced a significant increase in the rate of basal IRC release. Reintroduction of Ca2+ reversed the augmented basal IRC release induced by EGTA and restored mechanical activity. It was also found that the stretch-induced IRC release was independent of extracellular Ca2+ and took place even in the presence of EGTA. The presence of absence of Ca2+ had no apparent effect on ANF processing. In all instances, cardionatrin I (ANF 99-126) was found to be the most abundant peptide released. Morphologically, no obvious differences were observed during either basal or stretch-induced IRC release. These results suggest that, unlike most other endocrine secretory systems, a reduction of cytosolic Ca2+ stimulates basal IRC release. These findings suggest an adaptation of atrial cardiocytes to accomplish their dual role as secretory and contractile cells.

Animals↗
PubMed1991

Release of ANF, proANF 1-98, and proANF 31-67 from isolated rat atria by atrial distension.

The purpose of the present study was to determine if ANF and the NH2-terminus of the ANF prohormone are secreted simultaneously in response to atrial distension in isolated perfused rat atria. The experiments were conducted in paced left atria perfused with a modified Krebs buffer. Atrial pressure was increased from a baseline level of 2 mmHg to 8-9 mmHg for 60 minutes (distension) and then returned to 2 mmHg for 60 minutes in one group (n = 9) of isolated atria. In a second group of atria (n = 6), atrial pressure was maintained at approximately 2 mmHg throughout the experimental period. ANF secretion averaged 100 pg/min during the three 10-minute periods immediately preceding the increased atrial pressure and increased to 600-800 pg/min (P less than 0.001) when atrial pressure was raised. Secretion of the proANF 31-67 peptide increased from a value of approximately 100 pg/min immediately prior to distension to a peak of over 200 pg/min during distension (P less than 0.01). Secretion of proANF 1-98 increased from an average of 1.25 ng/min during the three periods immediately prior to distension to a peak of 2.5 ng/min during distension (P less than 0.01). These data indicate that ANF and the NH2-terminus of the ANF prohormone appear to be simultaneously secreted by isolated paced atria.

Animals↗
PubMed1991

Rate-induced increase in plasma atrial natriuretic factor can occur independently of changes in atrial wall stretch.

Tachycardia is known to increase the plasma level of atrial natriuretic factor (ANF). The aim of the study was to determine whether such release of ANF can occur independently of increased atrial wall stretch. Seven anesthetized dogs were instrumented with pressure catheters and sonomicrometer crystals to measure left and right auricular and atrial free wall dimensions. During atrial pacing, the measured atrial dimensions were kept constant by adjusting vascular constrictors placed around the great vessel trunks. When atrial rate was increased progressively by pacing at 150, 200, and 250 min-1, plasma ANF increased from 40.8 +/- 5.4 to 43.0 +/- 6.0 (P = NS) and 103.1 +/- 17.6 (SE) pmol/l (P less than 0.05), respectively. Repeating the pacing sequence at two different levels of elevated left atrial pressure caused at each level a similar increase in plasma ANF at 250 min-1. The relationship between plasma ANF and atrial dimensions was shifted upward by pacing, such that ANF was higher for any given atrial dimension. In conclusion, pacing tachycardia elevates plasma ANF in the presence of constant atrial dimensions. These results support the hypothesis that chronotropic stimulation can cause release of ANF by a mechanism that is independent of atrial stretch.

Animals↗
PubMed1991

Regional blood flow effects of ANP in conscious dogs: preferential gastrointestinal vasoconstriction.

We studied total and regional blood flow responses to human atrial natriuretic peptide (alpha-hANP) using radioactive microspheres in six conscious dogs. Hemodynamic responses to infusions of alpha-hANP at 75 ng.kg-1.min-1 were determined in each dog in the presence and absence of autonomic reflexes using the ganglion blocking agent pentolinium. When autonomic reflexes were blocked, alpha-hANP caused a substantial reduction in gastrointestinal (GI) vascular conductance (35%) but had no significant effects in brain, kidneys, liver, skeletal muscle, or skin. This alpha-hANP-induced fall in GI conductance contributed more than 40% to the fall in total peripheral conductance (TPC) of 24% occurring after autonomic blockade. A fall in myocardial vascular conductance, most prominent in the left ventricle, contributed a further 40% to the fall in TPC. When autonomic reflexes were intact, alpha-hANP caused vasoconstriction in the GI region (29% fall in vascular conductance), had no significant effects on myocardial vascular conductance but significantly increased splenic vascular conductance. In addition to these systemic responses, alpha-hANP infusion also significantly reduced pulmonary vascular conductance, independent of autonomic reflex activity or changes in pulmonary artery pressure. Thus our results in conscious dogs demonstrate that alpha-hANP causes a systemic vasoconstriction, most pronounced in the GI region.

Animals↗
PubMed1993

Role of tachycardia and V wave wall stress in the release of ANF during volume loading.

Heart rate is believed to be a primary determinant of atrial natriuretic factor (ANF) release; however, we postulated that V wave wall stress is the main signal for ANF release during volume loading. Conscious dogs were volume loaded with 1,000 ml of saline while the heart rate was allowed to vary and on another day while the heart was paced at 240 beats/min. During volume loading, plasma ANF increased from 58 +/- 10 to 221 +/- 31 pg/ml (P < 0.05), and heart rate increased from 97 +/- 3 to 182 +/- 9 beats/min. During pacing, plasma ANF increased from 42 +/- 8 to 85 +/- 10 pg/ml. A wave atrial pressures were increased during pacing and were fixed due to contraction against a closed atrioventricular valve. Volume loading increased plasma ANF to 180 +/- 25 pg/ml. V wave atrial pressure increased markedly, and V wave atrial wall stress increased from 25 +/- 10 to 131 +/- 44 and from 7 +/- 4 to 116 +/- 25 g/cm2, respectively. A wave pressure and wall stress were not increased by volume loading. V wave wall stress and ANF were significantly correlated. V wave atrial wall stress accounts for the majority of change in plasma ANF (60%), while tachycardia and A wave wall stress account for a smaller fraction (40%) of change.

Animals↗
PubMed1996

Neural influences on renal responses to acute volume expansion in rats with heart failure.

Experiments were performed to test the postulate that neural influences underlie the suppressed excretory response to acute volume expansion (VE) typically observed 3-4 wk after myocardial infarction to induce chronic heart failure (CHF). Responses to VE were assessed in innervated (intact) and denervated (DNX) kidneys of anesthetized CHF rats and sham-operated controls. CHF rats exhibited blunted natriuretic responses to VE in both intact kidneys (35% of sham response) and DNX kidneys (55% of sham DNX response). CHF rats also displayed suppressed excretory responses to atrial natriuretic factor (0.25 microgram.kg-1.min-1 iv) in both intact kidneys (74% of sham response) and DNX kidneys (63% of sham DNX response). Additional experiments confirmed that the compliance of the venoatrial junction did not differ between sham rats (52 +/- 2 mmHg/microliter) and CHF rats (54-2 mmHg/microliter). The observations support the contention that both tonic renal sympathetic renal nerve activity and suppressed renal atrial natriuretic factor responsiveness likely contribute to the blunted excretory response to VE during CHF.

Animals↗
PubMed1997

Atrial systolic pressure, as well as stretch, is a principal stimulus for release of ANF.

The mechanism for increased secretion of atrial natriuretic factor (ANF) during tachycardia and atrial fibrillation has remained unsettled. In seven open-chest pigs, the plasma concentration of ANF increased from 49.8 +/- 12.4 to 131.8 +/- 15.7 pg/ml when heart rate was increased from 133 +/- 13 to 212 +/- 4 beats/min by atrial pacing. Right atrial maximal diameter, recorded by ultrasonic technique at the maximal atrial filling, did not increase. During pacing tachycardia, the atrial contraction (a wave) occurs during atrial filling, and the a wave becomes superimposed on the v wave. In the present study the systolic atrial pressure (a wave) increased from 5.8 +/- 0.8 to 9.6 +/- 0.5 mmHg. The significance of this pressure rise was subsequently examined. After complete atrioventricular (AV) block, the AV delay was progressively increased, without altering heart rate, until the a wave was similar to the the a wave during the preceding tachycardia. Plasma ANF increased to 113.8 +/- 14.7 pg/ml, which showed that the increase in atrial pressure during atrial systole is a stimulus for ANF release. In the second part of the study, atrial fibrillation was induced in six open-chest pigs by rapid atrial pacing after complete AV block. Plasma ANF increased from 83.5 +/- 7.2 to 269.0 +/- 45.4 pg/ml during atrial fibrillation. No increase in atrial dimensions occurred during atrial fibrillation, but atrial pressure was substantially elevated. Thus, although passive atrial stretch stimulates ANF release during blood volume expansion, the present study shows that the increase in atrial pressure during atrial contraction is a stimulus for release of ANF during tachycardia and atrial fibrillation.

Animals↗
PubMed2000

C-type natriuretic peptide inhibits ANP secretion and atrial dynamics in perfused atria: NPR-B-cGMP signaling.

The purpose of the present experiments was to define the role of C-type natriuretic peptide (CNP) in the regulation of atrial secretion of atrial natriuretic peptide (ANP) and atrial stroke volume. Experiments were performed in perfused beating and nonbeating quiescent atria, single atrial myocytes, and atrial membranes. CNP suppressed in a dose-related fashion the increase in atrial stroke volume and ANP secretion induced by atrial pacing. CNP caused a right shift in the positive relationships between changes in the secretion of ANP and atrial stroke volume or translocation of the extracellular fluid (ECF), which indicates the suppression of atrial myocytic release of ANP into the paracellular space. The effects of CNP on the secretion and contraction were mimicked by 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP). CNP increased cGMP production in the perfused atria, and the effects of CNP on the secretion of ANP and atrial dynamics were accentuated by pretreatment with an inhibitor of cGMP phosphodiesterase, zaprinast. An inhibitor of the biological natriuretic peptide receptor (NPR), HS-142-1, attenuated the effects of CNP. The suppression of ANP secretion by CNP and 8-BrcGMP was abolished by a depletion of extracellular Ca(2+) in nonbeating atria. Natriuretic peptides increased cGMP production in atrial membranes with a rank order of potency of CNP > BNP > ANP, and the effect was inhibited by HS-142-1. CNP and 8-BrcGMP increased intracellular Ca(2+) concentration transients in single atrial myocytes, and mRNAs for CNP and NPR-B were expressed in the rabbit atrium. From these results we conclude that atrial ANP release and stroke volume are controlled by CNP via NPR-B-cGMP mediated signaling, which may in turn act via regulation of intracellular Ca(2+).

Animals↗
PubMed1986

Effect of atrial natriuretic factor in rat pregnancy.

Protocols were designed to 1) identify atrial natriuretic factor (ANF) bioactivity in pregnant rats, 2) compare ANF activity in atria from gravid and virgin Sprague-Dawley animals, and 3) assess renal and vascular responsiveness to ANF during gestation. Similar quantities of ANF were extracted from atria of term gravid and age-matched controls (assayed as the natriuretic response in awake virgins). We then purified by high-performance liquid chromatography a peptide identical to the synthetic 23 amino acid atriopeptin II (AP II). With equimolar injections of ANF, gravid rats had a blunted natriuretic response (P less than 0.05). However, when dose was based on estimated extracellular volume, awake virgin and pregnant animals displayed similar highly significant dose-response curves to infused AP II (R's 0.8). When hydropenic rats were assayed, both gravid and virgins required 10 times more ANF to initiate a diuresis; dose-response curves again being similar and highly significant. Decrements in blood pressure were also similar in pregnant and nongravid animals. Thus, despite an increased intravascular volume of 70% during gestation, cardiac content of ANF and the renal and vascular responsiveness to this peptide are similar to those in virgin rats, suggesting resetting of ANF-volume relationships during pregnancy.

Animals↗