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PubMed1990

Norepinephrine-induced atriopeptin release in conscious dogs is mediated by alterations in atrial pressure.

This study was designed to determine whether the increase in atriopeptin secretion induced by an intravenous infusion of norepinephrine is mediated directly by adrenergic receptor stimulation or indirectly by the associated increase in atrial pressure. Norepinephrine was infused at 0.5 microgram.kg-1.min-1 for 30 min into both sham-operated (intact) and cardiac-denervated conscious dogs. The infusion increased mean arterial pressure in all dogs. On the other hand, left atrial pressure increased from 5.0 +/- 0.7 to 9.6 +/- 1.6 mmHg (p less than 0.01) in intact dogs, but decreased from 5.5 +/- 1.0 to 2.0 +/- 0.7 (p less than 0.01) in cardiac-denervated dogs. Right atrial pressure changes followed similar trends, but were not significant in the intact group. Plasma atriopeptin increased from 73 +/- 12 to 110 +/- 18 pg/ml (p less than 0.01) as left atrial pressure increased in intact dogs and decreased from 79 +/- 15 to 54 +/- 10 pg/ml (p less than 0.01) as left atrial pressure decreased in cardiac-denervated dogs. The changes in plasma atriopeptin correlated closely with the changes in left atrial pressure (r = 0.941, p less than 0.001) and to a lesser extent with the changes in right atrial pressure (r = 0.413, p less than 0.05). These results suggest that the change in plasma atriopeptin induced by infusion of norepinephrine into conscious dogs is mediated by the concomitant change in atrial pressures.

Animals↗
PubMed1991

Cardiac electrophysiologic effects of adaprolol maleate, a new beta-blocker, in closed chest dogs.

Adaprolol maleate (adaprolol) is a new beta-adrenergic receptor blocker. The cardiac electrophysiologic characteristics and the duration of action of adaprolol were studied in intact anesthetized dogs. The electrophysiologic parameters were evaluated before drug administration and 10 min after the administration of maintenance infusion of adaprolol (N = 5). The duration of action was measured during constant infusion of isoproterenol, giving the adaprolol as a single i.v. bolus in different concentrations (N = 5). Results of this study showed that adaprolol has marked electrophysiologic effects. Its major action was on sinus node; it prolonged the basic sinus cycle length and had significant effect on intrinsic automaticity as reflected by the prolonged corrected sinus node recovery time and sinuatrial conduction time. There was, also, direct effect on atrial function and AV nodal function. Adaprolol prolonged the effective refractory period of the His-Purkinje system and the ventricle. The onset of action was very rapid (within seconds) and the duration of action was relatively prolonged (3 hrs). The potency of adaprolol's electrophysiologic effects are higher compared to other widely used beta-blockers. Adaprolol appears to be a potent beta-blocker with particularly strong antiarrhythmic effect and it would be very useful in the treatment of both supraventricular and ventricular tachyarrhythmias and ectopic beats.

Adamantane↗
PubMed1987

Beta-adrenergic control of atrial natriuretic factor secretion from dispersed rat atrial myocytes.

Adrenergic control of atrial natriuretic factor (ANF) secretion was studied using perifused, dispersed atrial myocytes. ANF secretion was stimulated by as little as 1 nM epinephrine (EPI) or the beta-adrenergic agonist isoproterenol (ISO). The response to EPI was completely blocked by equimolar propranolol but not by phenoxybenzamine suggesting that, at least in this system, the adrenergic control of ANF secretion is mediated by beta-adrenergic receptors.

Animals↗
PubMed1988

Characteristics of distension-induced release of immunoreactive atrial natriuretic peptide in isolated perfused rabbit atria.

Atrial pressure- or distension-induced release of atrial natriuretic peptide (ANP) has been considered as an important regulatory mechanism of ANP release in cardiac atria. A new technique to permit graded continuous atrial distension has been developed in an isolated perfused single rabbit atrium. Graded atrial distension was induced by changing the elevation of the outflow catheter tip. Intra-atrial volume expansion resulted in an increase in immunoreactive ANP release. The graded increase in atrial distension from 43.9 +/- 10.2 to 207.7 +/- 29.1 microliter resulted in 6.2-27.1-fold increases in volume-dependent immunoreactive ANP release. A rise in immunoreactive ANP release induced by increasing atrial distension did not occur in the state of atrial distension but occurred only after return to the reduced distension. However, in the case of atrial distension with pacing, an increase in immunoreactive ANP release was observed during atrial distension with pacing and after return to the basal level. The present study shows that the new technique is applicable to the study of the 'stretch-secretion coupling' mechanism of ANP release in vitro, and that the more important factor involved in the release of immunoreactive ANP induced by atrial distension may be the atrial reduction to basal level after distension rather than the stretch itself.

Animals↗
PubMed1990

Capsaicin-sensitive nerves influence the release of atrial natriuretic factor by atrial stretch in the rat.

Although many factors may modulate the release of atrial natriuretic factor (ANF), the primary mechanism has been demonstrated to be atrial stretch. Recent studies have led to the suggestion that the peptidergic innervation of the heart, through the release of peptides, may be involved in the control of ANF secretion. We have examined the influence of chronic capsaicin treatment on three models of atrial stretch that release ANF. This treatment inhibited ANF released through in vivo blood volume expansion and through balloon inflation in the right atrium of in vitro isolated perfused hearts. Immunohistochemical and electron microscopical analysis confirmed the absence of innervation of the heart by calcitonin gene related peptide and substance P immunoreactive nerve fibres and apparent lack of effect on atrial granules in capsaicin treated rats. We conclude that capsaicin-sensitive cardiac innervation is a component modulating the release of ANF, stimulated by atrial stretch in the rat.

Animals↗
PubMed1991

Synergism of atrial pressure and adrenergic stimulation for ANF release in the rat.

The effect of adrenergic stimulation on atrial natriuretic factor (ANF) release was studied in conscious rats. 60 min i.v. infusion of 15 micrograms/kg/min phenylephrine produced an elevation in mean arterial pressure of about 50 mmHg that was associated with an immediate, transitory increase in both central venous (CVP) and left ventricular end-diastolic (LVEDP) pressures. Heart rate was not changed. The elevation in CVP, but not LVEDP, persisted until 5 min, together with a 50-fold increase in plasma C-terminal ANF concentrations (from 19 +/- 5 to 1010 +/- 339 fmol/ml); at 30 min, in the absence of any increases in CVP or LVEDP, plasma ANF was still elevated by 5-fold (114 +/- 35 fmol/ml). It is suggested that adrenergic stimulation 'per se' can induce ANF release, independently of atrial pressure. Furthermore, combined adrenergic stimulation and increased atrial wall tension could result in a potentiation of the ANF secretory response 'in vivo', in the case where both stimuli are present concomitantly.

Animals↗
PubMed1990

Atrial strain is the main determinant of release of atrial natriuretic peptide.

We studied the response of atrial natriuretic peptide to the hemodynamic and renin-aldosterone variations occurring in four patients who developed cardiac tamponade, either occurring in idiopathic fashion in one or secondary to metastatic involvement of the pericardium in three. Right atrial pressure, heart rate and arterial blood pressure were monitored and serial blood samples were taken before and over three hours after pericardiocentesis. During cardiac tamponade, normal levels of atrial natriuretic peptide (mean +/- SEM: 54 +/- 7.4 pg/ml) were observed in the plasma despite increased right atrial pressure (23 +/- 3.8 cm H2O) and heart rates (98 +/- 4.4). Removal of pericardial fluid (540 to 1160 ml) was associated at first with a 200% increase in plasma concentrations of atrial natriuretic peptide (108 +/- 8.8 pg/ml; P less than 0.001), then with a gradual decline toward normal levels, simultaneous with the normalization of right atrial pressure and heart rate. Activity of renin and concentrations of aldosterone in the plasma were increased during tamponade and returned gradually to normal after pericardiocentesis (3.8 +/- 0.9 to 1.2 +/- 0.3 ng/ml/h and 20 +/- 4.2 to 9 +/- 3.2 ng/dl, respectively; P less than 0.01). These data confirm that atrial strain, not intracavitary pressure in itself nor heart rate, is the main determinant of the acute release of atrial natriuretic peptide, which is associated with a suppressing effect on the renin-aldosterone system. In addition, our data indicate that secretion of atrial natriuretic peptide during cardiac tamponade is not stimulated by secondary hyperaldosteronism.

Adult↗
PubMed1994

The pericardium acts as a restricting factor on the release of ANF (1-98) and ANF (99-126) after volume loading in pigs.

The stimulus for secretion of the atrial peptides from the heart is a mechanical distension of the atria. We studied the changes in plasma levels of immunoreactive ANF (1-98) and ANF (99-126) after volume loading (NaCl 0.9%, 50 ml/kg in 10 min) in pigs that had their pericardium opened (peric-, n = 8) and compared these changes to those of pigs subjected to sham operation (peric+, n = 8). For irANF (99-126), the maximum increase was achieved 10 min after the start of loading: 18.6 +/- 5.5 pmol/l to 31.4 +/- 15.6 pmol/l. (P < 0.05) in peric+ and 23.9 +/- 6.5 pmol/l to 110.2 +/- 46.2 pmol/l (P < 0.05) in peric-. The maximum increase in irANF (1-98) took place after 15 min: 658.8 +/- 223.9 pmol/l to 791.0 +/- 229.4 pmol/l (P < 0.05) in peric+ and 769.9 +/- 228.5 pmol/l to 1136.7 +/- 348.6 pmol/l (P < 0.05) in peric-. For both peptides the maximal increase after loading was significantly greater when the pericardium had been removed. The results demonstrate that the intact pericardium restricts peptide release secondary to volume infusion in closed-chest pigs.

Animals↗
PubMed1992

Effect of methyl methacrylate on isolated atria and interaction with isoproterenol, atropine and calcium chloride.

1. Spontaneous rate and contractile force of isolated rat and rabbit atria suspended in a tissue bath were recorded before and after drugs. Methyl methacrylate monomer (MMA) alone both decreased force and increased rate dose-dependently. 2. Concentrations of calcium chloride or isoproterenol that alone increased both rate and force of rat atrial contraction were fully and only partially able, respectively, to restore force to normal after MMA. 3. Atropine prevented changes in rat atrial function from low-effective doses of MMA, but not higher ones; it also failed to prevent the reduction of contractile force by a calcium channel blocker, verapamil. 4. There are similarities but also differences between actions of MMA and verapamil on rat atria.

Animals↗
PubMed1993

The effects of glyburide and insulin on the cardiac performance in rats with non-insulin-dependent diabetes mellitus.

1. The effects of glyburide were studied on the myocardial contractile force and heart rate in the atria isolated from non-diabetic and non-insulin-dependent diabetic rats (diabetic). 2. In order to examine the myocardial changes in the alloxan model of non-insulin-dependent diabetes, atrial functions of 11-week old diabetic rats were evaluated by comparing with the atria from their age-matched controls. 3. Diabetic atria were found to possess an increased contractile force and reduced inotropic responses to isoprenaline as a consequence of non-insulin-dependent diabetes induced by neonatal alloxan injection. 4. However, no significant change was observed in the heart rate of diabetic atria in response to isoprenaline when compared with controls. 5. Since apparent affinity constant (pD2 value) calculated for the inotropic response of diabetic atria to isoprenaline was also reduced, it might be suggested that non-insulin-dependent-diabetes causes a decrease in the beta-adrenoceptor affinity of the rat atria. 6. Glyburide treatment (5 mg/kg/day per os) for 3 weeks was able to improve the reduced responsiveness of rat atria due to non-insulin-dependent diabetes as well. The results obtained in this study indicated that glyburide possesses an improving effect on the decreased beta-adrenergic responses of rat atria with non-insulin-dependent diabetes mellitus.

Animals↗
PubMed1989

Atrial natriuretic peptide levels during and after acute cardiac tamponade in dogs.

The ability of the atrial wall to secrete atrial natriuretic peptide was studied in eight dogs during 2 h of cardiac tamponade and for 2 h after decompression of the pericardium. Cardiac tamponade was induced by instillation of 5% dextrose in water into the pericardial cavity until aortic systolic pressure was reduced by 30% to 35%. Heart rate, cardiac output and atrial, pericardial and aortic pressures were measured at 60 and 120 min of tamponade and at 5, 30, 60, 90 and 120 min after decompression. Blood samples were withdrawn at the same time for the determination of atrial natriuretic peptide and aldosterone levels. Aortic pressure decreased significantly during tamponade and increased after decompression to near control levels. Right and left atrial pressures as well as intrapericardial pressure increased significantly during tamponade and returned to control levels after decompression. The effective transmural pressure, which was reduced during tamponade, was increased significantly at 5 min after decompression. Cardiac output was significantly reduced during tamponade and returned to pretamponade levels after decompression. Over the total experimental period, no significant changes in the levels of atrial natriuretic peptide were observed, whereas aldosterone increased significantly. It is concluded that the increased atrial pressure observed during cardiac tamponade did not stimulate the secretion of atrial natriuretic peptide. Furthermore, atrial distension observed immediately after decompression was not sufficient or of long enough duration to induce measurable increases in atrial natriuretic peptide levels. Finally, the secondary hyperaldosteronism did not activate atrial natriuretic peptide secretion either during cardiac tamponade or after decompression.

Aldosterone↗
PubMed1990

Response of atrial natriuretic factor to postural change in patients with heart failure versus subjects with normal hemodynamics.

The response of atrial natriuretic factor to an acute increase in atrial pressures produced by changing from a 45 degrees upright to a -15 degrees Trendelenburg tilt was examined in 21 patients with heart failure and 8 control subjects with normal hemodynamics. In the control subjects, baseline (45 degrees upright tilt) pulmonary capillary wedge and right atrial pressures increased from 3.1 +/- 0.9 (mean +/- SEM) and 4.4 +/- 0.3 mm Hg to 6.9 +/- 1.9 and 8.5 +/- 0.4 mm Hg, respectively (p less than 0.05 for both), 30 min after the -15 degrees tilt. Baseline arterial plasma atrial natriuretic factor concentration increased from 34 +/- 4 to 44 +/- 1 pg/ml (p less than 0.05) 30 min after the tilt, with an increase observed in every patient. In the group with heart failure, baseline pulmonary capillary wedge and right atrial pressures increased from 17.5 +/- 2.0 and 5.3 +/- 1.2 mm Hg to 24.6 +/- 1.8 and 9.7 +/- 1.3 mm Hg, respectively (p less than 0.01 for both), 30 min after the tilt. Plasma atrial natriuretic factor concentration was 326 +/- 38 pg/ml at baseline and 347 +/- 34 pg/ml (p = NS) 30 min after tilt. Compared with the 7 patients with heart failure who had increased atrial natriuretic factor concentrations after the tilt (responders), the 14 patients with unchanged or decreased atrial natriuretic factor concentrations after the tilt (nonresponders) had a higher baseline right atrial pressure and atrial natriuretic factor concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Function↗
PubMed1991

Disturbed secretion of atrial natriuretic peptide in patients with persistent atrial standstill: endocrinologic silence.

Persistent atrial standstill is a very rare pathophysiologic condition whose diagnosis is established when both electrical and mechanical silence of the atria are confirmed. To test the hypothesis that secretion of atrial natriuretic peptide is disturbed in patients with persistent atrial standstill, the response of atrial natriuretic peptide secretion and other neurohormonal factors during exercise was investigated in three patients with a rate-responsive ventricular demand (VVI) pacemaker implanted for confirmed persistent atrial standstill. The results were compared with those observed in eight normal subjects and patients with a rate-responsive VVI (Group A) or atrial demand (AAI) (Group B) pacemaker implanted for confirmed sick sinus syndrome. Patients in Group A displayed significant elevation of alpha-human atrial natriuretic peptide secretion both before and during exercise (122.5 +/- 14.8 and 207.5 +/- 8.3 pg/ml, respectively) compared with those in Group B (55 +/- 14.1 and 116.4 +/- 51.5 pg/ml, respectively) and the normal subjects (18.9 +/- 9.8 and 30.8 +/- 19.2 pg/ml, respectively). This indicated development of a nonphysiologic increase in atrial volume or pressure overload, or both, in rate-responsive VVI pacing because of lack of atrioventricular synchrony. However, patients with persistent atrial standstill had undetectable (less than 10 pg/ml) or almost undetectable secretion of atrial natriuretic peptide as well as lower levels of cyclic guanosine monophosphate in the circulation both before and during exercise. Changes in plasma catecholamines during exercise were similar in patients with persistent atrial standstill compared with the other groups. This study indicates that "endocrinologic silence" accompanies electrical and mechanical silence of the atria, which may constitute a third diagnostic clue to persistent atrial standstill.

Adult↗
PubMed1992

Cardiac activity of some peptide hormones in the frog, Rana tigrina.

1. The cardiac responses of isolated frog (Rana tigrina) atria to peptide hormones were studied. 2. Calcitonin gene-related peptide (CGRP), arginine vasotocin (AVT), bovine parathyroid hormone fragment (bPTH-(1-34)) and oxytocin (OXY) produced dose-related positive chronotropic and inotropic responses; atrial natriuretic peptide (ANP) was negative chronotropic and inotropic; cholecystokinin (CCK), vasoactive intestinal peptide (VIP) were without effects. 3. The dose-related responses under bPTH-(1-34) stimulation but not CGRP or AVT were attenuated in the presence of ANP (300 ng/ml, approximately 0.98 x 10(-7) M). As expected ANP decreased the basal AR and AT responses of the isolated atria and the inhibitory effects were dose-dependent. 4. As shown previously, propranolol blocked the atrial tension stimulated by bPTH (1-34) but did not alter the cardiac responses to CGRP and AVT. 5. In the presence of beta-adrenergic blocker (propranolol 10(-7) M) or ANP (10(-7) M), the AR and AT changes under ISO stimulation in the frog were also decreased. 6. These cardiac changes suggest the cardiac inhibitory effects of ANP are related to beta-adrenoceptor activity and ANP might be a beta antagonist.

Animals↗
PubMed2005

Disruption of inhibitory G-proteins mediates a reduction in atrial beta-adrenergic signaling by enhancing eNOS expression.

OBJECTIVE: Cardiac parasympathetic nerve activity is reduced in most cardiovascular disease states, and this may contribute to enhanced cardiac sympathetic responsiveness. Disruption of inhibitory G-proteins (Gi) ablates the cholinergic pathway and increases cardiac endothelial nitric oxide (NO) synthase (eNOS) expression, suggesting that NO may offset the impaired attenuation of beta-adrenergic regulation of supraventricular excitability. To test this, we investigated the role of endogenous NO production on beta-adrenergic regulation of rate (HR), contraction (CR) and calcium (Ca2+) handling in atria following blockade of Gi-coupled muscarinic receptors. METHODS: Mice were administered pertussis toxin (PTx, n=105) or saline (C, n=100) intraperitoneally. After 3 days, we measured CR, HR, and NOS protein levels in isolated atria. Intracellular calcium (Ca2+) transients and Ca2+ current density (I(Ca)) were also measured in atrial myocytes. RESULTS: PTx treatment increased atrial myocyte eNOS protein levels compared to C (P<0.05). This did not affect basal atrial function but was associated with a significant reduction in the CR and HR response to isoprenaline (ISO) compared with C. NOS inhibition normalized responses in PTx atria with respect to responses in C atria (P<0.05), which were unaffected. Furthermore, PTx did not affect ISO-stimulated HR and CR in eNOS gene knockout mice (n=40). In agreement with these findings, the ISO-mediated increase in Ca2+ transient was suppressed in PTx-treated myocytes (P<0.05), whereas I(Ca) did not differ between groups. CONCLUSION: eNOS-derived NO inhibits beta-adrenergic responses following disruption of Gi signaling. This suggests that increased eNOS expression may be a compensatory mechanism which reduces beta-adrenergic regulation of heart rate when cardiac parasympathetic control is impaired.

Adrenergic beta-Agonists↗
PubMed2004

Amylin-induced suppression of ANP secretion through receptors for CGRP1 and salmon calcitonin.

Amylin cosecretes with insulin from pancreatic beta-cells and shows high sequence homology with CGRP, adrenomedullin, and salmon calcitonin. This study aimed to investigate the effect of amylin on the atrial hemodynamics and ANP release from rat atria and to identify its receptor subtypes. Isolated perfused left atria from either control or streptozotocin-treated rats were paced at 1.3 Hz. The concentration of ANP was measured by radioimmunoassay and the translocation of ECF was measured by [3H]-inulin clearance. Rat amylin increased atrial contractility and suppressed the release of ANP. Rat CGRP showed similar effects but was approximately 300-fold more potent than amylin. Pretreatment with receptor antagonist for CGRP1 [rat alpha-CGRP (8-37)] or salmon calcitonin [acetyl-(Asn30, Tyr32)-calcitonin(8-32), (AC 187)] blocked the suppressive effect of ANP release and the positive inotropic effect by rat amylin. However, receptor antagonists for amylin [amylin (8-37), acetyl-amylin] did not block those effects. Amylin (8-37), acetyl-amylin, or rat alpha-CGRP (8-37) alone accentuated the release of ANP with no changes in atrial contractility. The effect of rat amylin and rat amylin (8-37) on the ANP release was attenuated in streptozotocin-treated rats. We suggest that amylin suppressed ANP release with increased atrial contractility through receptors for CGRP1 and salmon calcitonin and the attenuation of amylin and its antagonist on ANP release from streptozotocin-treated rat atria may be due to the downregulation of amylin receptor.

Amyloid↗
PubMed1998

N-terminal proANF in acute atrial fibrillation: a biochemical marker of atrial pressures but not a predictor for conversion to sinus rhythm. Digitalis in Acute Atrial Fibrillation (DAAF) Trial group.

BACKGROUND: Atrial filling pressures are increased in acute atrial fibrillation, which stimulates the release of atrial natriuretic factor pro-hormone, proANF. METHODS: In a randomized trial comparing digoxin with placebo in 216 patients, we investigated whether the baseline plasma level of N-terminal proANF is a predictor for conversion to sinus rhythm and the relation among N-terminal proANF, conversion to sinus rhythm, and changes in heart rate. RESULTS: N-terminal proANF was increased at baseline and decreased significantly in patients converting to sinus rhythm, whereas it was mainly unchanged in nonconverters. N-terminal proANF was not a predictor of conversion to sinus rhythm. A relation was found between relative changes in heart rate and N-terminal proANF in nonconverters. CONCLUSION: The level of N-terminal proANF does not predict conversion to sinus rhythm, which indicates that hemodynamics per se is not important. There is a correlation between relative changes in heart rate and N-terminal proANF in nonconverters.

Acute Disease↗