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At least 37 records · Page 2Linked to original sources
PubMed1989

Functional atrial natriuretic peptide receptor in human adrenal tumor.

The effects of synthetic human atrial natriuretic peptide (ANP) on the release of catecholamines, aldosterone, or cortisol were observed in human adrenal tumors obtained surgically from patients with pheochromocytoma, primary aldosteronism, or Cushing's syndrome, respectively. Each tumor tissue or adjacent normal cortical tissue was sectioned into slices, which were incubated in medium-199 in the presence or absence of adrenocorticotrophin (ACTH) and ANP. The amounts of epinephrine, norepinephrine, aldosterone, or cortisol released into the medium were measured. Existence of ANP receptors on the adrenal tissues was examined by binding assays, affinity labeling, and immunohistochemistry. Release of catecholamines from pheochromocytoma tissues was inhibited by ANP, and the presence of the ANP receptor on pheochromocytoma was further demonstrated by both binding assays and affinity labeling; Scatchard analysis revealed a single class of binding sites for ANP with a Kd of 1.0 nM and a Bmax of 0.4 pmol/mg of protein and the molecular size was estimated as 140 and a 70 kDa under nonreducing and reducing conditions, respectively. The presence of ANP receptors in pheochromocytoma was demonstrated by immunohistochemistry. ANP inhibited both basal and ACTH-stimulated aldosterone secretion in the slices of normal cortex, and localization of ANP receptors in zona glomerulosa cells was also demonstrated. However, ANP did not inhibit basal and ACTH-stimulated aldosterone and cortisol secretion in both tissue slices from aldosteronoma and Cushing's adenoma. Consistent with these observations, the absence of ANP receptors in adenoma tissues was determined by binding assays, affinity labeling, and immunohistochemistry.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex↗
PubMed1990

Comparative values of the precordial and transesophageal approaches in the echocardiographic evaluation of atrial baffle function after an atrial correction procedure.

Previous methods used to assess atrial baffle function after correction of transposition of the great arteries have included precordial echocardiography and cardiac catheterization. To evaluate whether single plane transesophageal echocardiography might provide additional information, its findings were correlated with information derived from both precordial echocardiography and cardiac catheterization in 15 patients (14 Mustard procedures, 1 Senning procedure) aged 4.2 to 33 years (mean 16.3). Precordial ultrasound with combined imaging, color flow mapping and pulsed Doppler ultrasound visualized the supramitral portion of the common systemic venous atrium in every case but could identify only superior limb obstruction in three of six patients, mid-baffle obstruction in zero of two and inferior limb obstruction in zero of two patients. Transesophageal studies with use of the same range of ultrasound methods demonstrated superior limb obstruction (severe in four, mild in two) in six of six patients, mid-baffle obstruction in two of two and inferior limb obstruction in two of two patients. The entire pulmonary venous atrium was equally well interrogated by either ultrasound approach, with both identifying three cases (two mild, one moderate) of mid-pulmonary venous atrium obstruction. However, individual pulmonary vein velocity profiles could only be recorded by transesophageal pulsed Doppler ultrasound. Precordial studies identified baffle leaks (1 large, 2 small) in only three patients, whereas transesophageal studies identified 11 such baffle leaks (1 large, 10 small), which were multiple in two patients. It is concluded that transesophageal echocardiography provides a more detailed and accurate assessment of atrial baffle morphology and function than is provided by either precordial ultrasound or cardiac catheterization.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Does atrial appendectomy aggravate secretory function of atrial natriuretic polypeptide?

The present study was designed to clarify how atrial appendectomy affects hemodynamics and secretory function of atrial natriuretic polypeptide in the failing heart. Eleven mongrel dogs were prepared for the experimental model of high-output heart failure by creation of arteriovenous fistulas between femoral arteries and veins. Two months after the first operation, effects of bilateral atrial appendectomies on basal and pacing-induced secretions of atrial natriuretic polypeptide were investigated in five dogs with simultaneous measurement of various hemodynamic indices. In the remaining six dogs, used as a control group, pacing-induced secretion of atrial natriuretic polypeptide was examined in the same way as in the appendectomy group. After excision of the atrial appendages, neither systolic blood pressure nor either atrial pressure changed, but plasma atrial natriuretic polypeptide level was decreased (292 +/- 54 to 188 +/- 47 pg/ml, p less than 0.01) and cardiac output fell (3.7 +/- 0.9 to 3.0 +/- 0.8 L/min, p less than 0.01). During pacing-induced tachycardia, the peak level of plasma atrial natriuretic polypeptide was lower in the appendectomy group than in the control groups (593 +/- 213 versus 1170 +/- 324 pg/ml, p less than 0.05), despite similar left atrial pressures in the two groups. The excised appendages contained approximately 30% of the total amount of atrial natriuretic polypeptide. These results demonstrate that atrial appendectomy decreases secretory function of atrial natriuretic polypeptide and reduces cardiac output in dogs with experimental high-output heart failure.

Animals↗
PubMed1990

Return of atrial mechanical function following electrical conversion of atrial dysrhythmias.

The return of atrial mechanical function and its relationship to embolic events following cardioversion of atrial arrhythmias is controversial. Fourteen patients with atrial arrhythmias were evaluated with pulsed Doppler echocardiography before and after direct current (DC) cardioversion. The atrial filling fraction increased significantly: 1.14 +/- 4.3% at baseline versus 14.9 +/- 13.3%, 13.4 +/- 11.4%, and 21.9 +/- 13.5% at 5 minutes, 30 minutes, and 24 hours, respectively, following cardioversion. Absent atrial mechanical activity was noted in four patients immediately after cardioversion. Mechanical activity resumed by 30 minutes in one patient and at 24 hours in two others. Those with delayed atrial function had lower stroke volumes and atrial filling fractions following cardioversion. An embolic event occurred in one patient who had immediate return of atrial mechanical activity. This patient also had the largest atrial filling fraction of any patient at 24 hours (41%). These data suggest that the degree of atrial mechanical activity following cardioversion is variable and that embolic episodes are not necessarily related to delayed return of atrial mechanical activity following cardioversion.

Adult↗
PubMed1975

Complete heart block. Studies of atrial and ventricular pacemaker site and function.

Atrial and ventricular pacemaker function was studied in 20 patients with idiopathic chronic complete heart block using the rate response to an intravenous bolus dose of isoprenaline (5 mug/70 kg bodyweight). Pacemaker responses were compared with those of 16 normal control subjects. None of the patients was having syncopal attacks at the time of admission and they were therefore selected in that none required immediate pacing. Ten of the patients had His bundle electrograms; all were shown to have a pre-His type of atrioventricular block. Two major groups emerge from the responses to isoprenaline. (a) High risk group: 11 of the 14 patients with reduced ventricular pacemaker responses had frequent syncopal attacks; 8 of the patients with Adams-Stokes syncope had a bundle-branch block pattern, while 3 had a narrow QRS. These patients require pacing. (b) Low risk group: a low risk asymptomatic group (5 patients) was identified with atrial and ventricular responses to isoprenaline within normal range. One of these patients had a bundle-branch block pattern, while 4 had a narrow QRS. These patients might be managed without pacing. The atrial response to isoprenaline was reduced in 12 of the 20 cases, 10 of whom also had reduced ventricular responses. All 9 patients with bundle-branch block had reduced ventricular responses, while 7 had reduced atrial responses. This evidence indicates that cardiac conducting tissue pathophysiology is widespread in complete heart bolck. The present work suggests that consideration of the ventricular pacemaker function is important in assessing liability to syncope in complete heart block. While patients with Adams-Stokes attacks require pacing it is suggested that all asymptomatic patients with complete heart block and those with minor symptoms are assessed using studies of both ventricular pacemaker function and site. A low risk group not requiring a pacemaker may emerge after sufficient follow-up assessment.

Adams-Stokes Syndrome↗
PubMed1989

Pulsed Doppler evaluation of atrial mechanical function after electrical cardioversion of atrial fibrillation.

Full recovery of atrial mechanical activity may not occur immediately after successful electrical cardioversion of atrial fibrillation to sinus rhythm. To examine the time course of recovery of left atrial mechanical function, serial two-dimensional, M-mode and transmitral pulsed Doppler echocardiographic studies were performed in 21 patients after elective direct current cardioversion of atrial fibrillation of 3 weeks' to 24 months' duration (mean 5 months). Over 3 months of follow-up, there were significant increases in both peak A wave velocity (p less than 0.005) and percent atrial contribution to total left ventricular filling (p less than 0.005). Compared with values in a normal control population, peak A wave velocity and percent atrial contribution to total left ventricular filling did not return to normal until 3 weeks after cardioversion in patients who remained in sinus rhythm. Left atrial dimension also decreased over the follow-up period (p less than 0.05) in patients with persistent sinus rhythm. These results may have important implications in guiding the appropriate duration of anticoagulant therapy after cardioversion, and in clinically assessing the hemodynamic benefit of restoring sinus rhythm in an individual patient.

Aged↗
PubMed1992

Effect of the pericardium on atrial systolic function.

The effect of pericardial constraint on atrial systolic function was investigated in nine acutely instrumented anesthetized dogs. Left and right atrial pressures were recorded by high-fidelity catheters; auricular diameters and free wall segment lengths were measured by sonomicrometry. Atrial function curves were constructed by relating atrial systolic dimensional shortening to atrial end-diastolic pressure during progressive volume loading. With the pericardium closed, the function curves were shifted markedly downward and rightward, such that atrial systolic shortening was reduced at any given pressure. There was a concomitant leftward and upward shift of the atrial end-diastolic pressure-dimension relationship. The relationship between atrial systolic shortening and atrial end-diastolic dimension was not shifted. These results suggest that the apparent depression of atrial systolic function with the pericardium closed is due to a restrictive effect of the pericardium on atrial filling. In conclusion, in the acutely dilated heart, the pericardium restricts atrial filling and thus causes a reduction in atrial systolic contribution to ventricular filling.

Animals↗
PubMed1991

Echo-Doppler evaluation of the effects of heart rate increments on left atrial pump function in normal human subjects.

It is commonly believed that the atrial contribution to left ventricular filling increases during heart rate increments. However, the relative contribution of the pump function (atrial systole) and of the passive role (diastasis and reservoir) of the atrium to end-diastolic left ventricular filling is not well known. In order to investigate this problem, we performed a two-dimensional echo-Doppler study during right atrial pacing. Transmitral flow velocity curves were obtained by means of pulsed Doppler. Pacing was performed (1) at the lowest heart rate at which it was possible to obtain a stable capture of the atria, (2) at the heart rate at which the early and late Doppler filling waves almost completely overlapped. In both stages pacing was interrupted for a few seconds to obtain some post-pacing beats. Doppler tracing recorded at rest, during pacing and in the immediate post-pacing beats were analysed to obtain well-known parameters of atrial contribution; atrial peak flow velocity, early to atrial peak flow velocity ratio, and time-velocity integral of the atrial wave. Furthermore, in order to distinguish end-diastolic passive flow from the active contribution of atrial systole to filling, we superimposed the envelope of the last Doppler curve obtained during atrial pacing over the envelope of the first post-pacing curve. In this way the area of the atrial wave of the paced beat was divided by the mid-diastolic part of the post-pacing one into two areas, the integrals of which correspond to the active and passive atrial contribution respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Electrocardiographic signs of atrial overload in hypertensive patients: indexes of abnormality of atrial morphology or function?

Left atrial electrocardiographic (ECG) abnormalities have been reported as common findings in hypertension; however, their relationships with atrial anatomy are still uncertain. In addition, in arterial hypertension several studies demonstrated an abnormal left ventricular filling. The aim of this study was to investigate the relationships of the ECG signs of left atrial abnormality to atrial anatomy and left ventricular filling as evaluated by pulsed-wave (PW) Doppler in a group of patients with uncomplicated essential hypertension. To this end, 53 untreated essential hypertensive patients (age 44 +/- 8 years; blood pressure 160.5 +/- 21.5/104.7 +/- 13.5 mm Hg) underwent a complete 12-lead ECG and a PW Doppler study of the transmitral flow velocities. The ECG criteria of left atrial abnormality were: P wave wider than 0.12 (or 0.10) second or higher than 0.25 mV in lead II; P wave/PR segment ratio (Macruz index) greater than 1.6 in lead II; and P wave terminal forces in lead V1 equal to or more negative than 0.04. Echocardiographic measurements were made according to American Society of Echocardiography (ASE) convention. Doppler parameters of left ventricular filling were measured as E and A peak velocity, A/E ratio, and the ratio between the velocity-time integral under the E peak and that of the whole diastolic flow, which represents the rapid filling fraction (RFF). At least one ECG sign of atrial abnormality was present in 34 patients (64%); the Macruz index gave the most common ECG index of atrial abnormality (31 patients).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Mechanism of augmented left atrial pump function in myocardial infarction and essential hypertension evaluated by left atrial pressure-dimension relation.

To analyze left atrial (LA) pump function in normal subjects, in patients with essential hypertension and in patients with a healed myocardial infarction, LA dimension (aortic-root echogram) and pressure (catheter-tip manometer) were simultaneously recorded in 25 patients (8 normal subjects, 7 with hypertension and 10 with myocardial infarction). The pressure-dimension relation of the left atrium was composed of 2 loops: the A loop (expressing the pump function of the left atrium) and the V loop. LA dimension at the beginning of active LA shortening was significantly greater in hypertensive subjects (33 +/- 3 mm) and in those with myocardial infarction (32 +/- 4 mm) than in normal subjects (28 +/- 3 mm) (p less than 0.01, p less than 0.05, respectively). The area of the A loop significantly increased in subjects with hypertension (48 +/- 3 mm Hg.mm, p less than 0.01) and in subjects with myocardial infarction (29 +/- 10 mm Hg.mm, p less than 0.05), compared with normal subjects (20 +/- 8 mm Hg.mm). The mean fractional shortening velocity of the left atrium significantly increased in subjects with hypertension, compared with normal subjects and those with myocardial infarction (p less than 0.05 for both). LA peak wall tension during the LA active contraction period significantly increased with hypertension and with myocardial infarction, compared with normal subjects (p less than 0.01, p less than 0.05, respectively). The area of the A loop was directly proportional to the LA dimension at the beginning of active LA shortening (r = 0.53), p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Endocrine function of the heart. Structure and biological properties of peptides secreted by the heart atrium].

Apart from the generally known functions, the heart has also an endocrine function. Atrial cardiocytes, being typical secretory cells, release peptide hormones into the blood stream: atrial natriuretic peptide containing 28 amino acids and cardiodilatin. The structure of atrial peptides was determined. It was shown that both peptides were derived from their common precursor, a protein containing 151 amino acids. The presence of specific receptors is demonstrated on plasmatic membranes of cells of kidney epithelium, arterial smooth muscle, arterial endothelium, kidney cortex and hypophysis. The interaction of atrial peptides with these receptors activates the guanylate cyclase system. The biological action of atrial peptides manifests itself in the quick, massive and instantaneous increase of diuresis and electrolyte excretion, elevated clearance of creatinine, decrease of kidney vascular resistance, intensification of glomerular filtration, inhibition of stimulated secretion of aldosterone, relaxation of blood vessels, elimination of arterial and intestinal spasm induced by various endogenous and exogenous vasoconstrictors and in correction of kidney hypertension. Various radioimmunoassays for the presence of atrial peptides in human plasma were developed; it was shown that in patients with congestive heart failure the content of atrial peptides is increased.

Amino Acid Sequence↗
PubMed1985

The role of the atria in fluid volume control.

Neural reflexes from the heart, in particular the atria, are well documented and are involved in sodium and water excretion. Current work also indicates that the atria have an important endocrine function. Atrial peptides, which have been recently characterized and synthesized, may play a significant role in the homeostasis of body fluids.

Animals↗
PubMed1989

Atrial wall function and plasma atriopeptin during volume expansion in conscious dogs.

Mean left atrial pressure is believed to be an accurate estimate of atrial stretch in vivo and is used to assess the stimulus for atriopeptin release in both animals and humans. However, for a number of years it has been known that atrial stretch receptor discharge occurs during specific phases of the atrial cycle and that B-receptor discharge correlates with the passive filling of the atrium, which occurs during the V wave. The purpose of this study was to develop the concept that phase-specific changes in atrial wall stress are responsible for atriopeptin secretion. In chronically instrumented conscious dogs, volume expansion (1,000 ml of saline in 5 min) increased left atrial pressure and dimensions and caused a 663 +/- 189% increase in plasma immunoreactive atriopeptin from 44 pg/ml. At this time, mean left atrial pressure increased only 202 +/- 36% (mean +/- SE), whereas A wave pressure increased 146 +/- 19% and V wave pressure increased 290 +/- 67%. A and V wave dimensions increased only a few percent. After developing atrial wall thickness constants for diastole (KCl fixation) and systole (BaCl2 fixation), calculated atrial A wave wall stress increased 163 +/- 25%, and V wave wall stress increased 346 +/- 85%. Minute wall stress (wall stress times heart rate) gave an even better correlation with changes in plasma atriopeptin. V wave minute wall stress increased 690 +/- 168%, whereas A wave wall stress increased 366 +/- 56%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Functional capacity of patients with atrial fibrillation and controlled heart rate before and after cardioversion.

OBJECTIVE: To measure exercise duration (which frequently is diminished by atrial fibrillation) and to compare the gain in exercise duration achieved by heart rate control with the gain after cardioversion. METHODS AND RESULTS: Eighteen patients (10 with structural heart condition and eight with lone atrial fibrillation) did the treadmill exercise stress test using the Bruce protocol. Resting supine heart rate was lowered below 100 beats/min by verapamil (initial exercise stress test). An exercise stress test was then repeated as often as needed to achieve 'heart rate control' (less than 130 beats/min at the end of a 3 min walk at 10 degrees elevation and 2.74 km/h speed). This heart rate control was obtained by gradual increases in verapamil dose. Subsequently, the patients were converted to normal sinus rhythm chemically (seven patients) or electrically (11 patients) and an exercise stress test was repeated. At cardioversion, patients were on antiarrhythmic therapy and verapamil was discontinued in most. All patients had left atrial size measured by echocardiogram before and after cardioversion, and all were followed for four months. Upon achieving controlled heart rate, exercise duration increased in 16 patients (average gain was 164 s). After cardioversion to normal sinus rhythm, exercise duration further increased in 13 cases with an average additional gain of 90 s. The total increase in exercise duration after cardioversion was 254 s. Post cardioversion, all patients with lone atrial fibrillation improved. A decline in exercise performance occurred in four patients with fixed cardiac output. Average gain in exercise duration was independent of drugs used. Left atrial size remained increased post cardioversion (50.4 mm before and 52 mm after). During four months of follow-up, only eight patients could continue on the same medication given for cardioversion. Three patients did not maintain normal sinus rhythm. CONCLUSIONS: Conversion to normal sinus rhythm in patients with atrial fibrillation is associated with improved exercise tolerance except in cases with fixed cardiac output. Restoration of mechanical atrial function appears to be responsible for improved exercise performance following cardioversion.

Aged↗
PubMed1991

Allosteric modulation by ATP of the bovine adrenal natriuretic factor R1 receptor functions.

Atrial natriuretic factor (ANF-R1) receptor is a 130-kDa protein that contains a cytoplasmic guanylate cyclase domain. We report that ATP interacts in an allosteric manner with the ANF-R1 receptor, resulting in reduced ANF binding and enhanced ANF-stimulated guanylate cyclase activity. The modulatory properties of various nucleotides indicate a preference for the adenine family with a rank order of potency of ATP greater than App(NH)p greater than or equal to ADP greater than or equal to AMP while cyclic and guanine nucleotides except GTP are inactive. The negative modulation by ATP of ANF binding is specific for the ANF-R1 receptor subtype since the amount of ANF bound by the guanylate cyclase uncoupled ANF-R2 subtype is increased in the presence of ATP. Furthermore, the effects of ATP on ANF-R1 receptor binding function are still observed with the affinity-purified ANF-R1 receptor, suggesting an allosteric binding site for ATP on the ANF-R1 receptor. In intact membranes, limited proteolysis of the ANF-R1 receptor with trypsin dose-dependently prevents the ATP-induced decrease in ANF binding concomitantly with the formation of a membrane-associated ANF-binding fragment of 70 kDa. These results confirm the direct modulatory role of ATP on hormone binding activity of ANF-R1 receptor and suggest that the nucleotide regulatory binding site is located in the intracellular domain vicinal to the protease-sensitive region.

Adenosine Triphosphate↗