Diagnóstico radiográfico de la discordancia aurículo ventricular / Radiographic diagnosis of atrioventricular discordance

En un período de 10 años se diagnosticaron por angiocardiografía 21 pacientes con discordancia auriculoventricular. Veinte presentaron conexión ventriculoarterial discordante (transposición corregida de grandes vasos) y sólo uno tenía una doble salida del ventrículo anatómicamente derecho. Tres de los pacientes con transposición corregida de grandes vasos tenían dextrocardia y 17 levocardia con situs solitus, de los cuales 16 presentaron el aspecto típico descritos en la mayoría de estos casos, tanto en el telecardiograma como en el estudio contrastado. Otro paciente presentaba el tabique interventricular dispuesto horizontalmente. La anomalía asociada más frecuente fue la comunicación interventricular. Dos pacientes no presentaron anomalías asociadas y en uno de ellos el diagnóstico se hizo a los 47 años, al realizarse una coronariografía por sospecha de aterosclerosis coronaria. Teniendo en cuenta la posición del tabique interventricular y las anomalías asociadas más frecuentes en la discordancias auriculoventricular, se recomienda cuando se sospecha esta entidad comenzar el estudio contrastado con ventriculografía selectiva bilateral en las proyecciones frontal y lateral y recurrir después, si fuera necesario, a las vistas axiales e inyecciones en las aurículas, aorta y pulmonar

Chicken hypotensive peptide: purification and characterization.

We have purified and isolated a novel, hypotensive peptide from avian ventricular tissue. Ventricular homogenates have been shown to exhibit potent hypotensive activity in the avian and mammalian species, with little natriuresis or diuresis. Using avian mean arterial pressure (MAP) as a bioassay, we were able to purify a peptide which decreased MAP 30% in adult, female chickens. Amino acid analysis indicated that it contained 20 amino acids (including two cysteine residues), and was not similar to the amino acid composition of mammalian atrial natriuretic factors, or other known hypotensive peptides.

Synthesis and secretion of atrial natriuretic factor during chronic hypoxia: a study in the conscious instrumented rat.

1. To investigate the mechanisms leading to enhanced synthesis and release of atrial natriuretic factor during chronic hypoxia, we measured immunoreactive plasma atrial natriuretic factor, blood gases, packed cell volume, pulmonary artery pressure and systemic artery pressure in male Sprague-Dawley rats exposed to 1, 2 or 3 weeks of normobaric hypoxia. Rats were implanted with pulmonary and carotid artery catheters and studied conscious, 23 h after return to hypoxia. 2. The concentration of atrial natriuretic factor messenger RNA was measured in the right and left ventricular free walls of rats exposed to 3 weeks of hypoxia and in normoxic control rats. 3. There was a trend for plasma atrial natriuretic factor to increase with the duration of exposure to hypoxia but only the 3-week hypoxic rats had a significantly higher level (1080 +/- 193 pg/ml) than the normoxic control rats (318 +/- 46 pg/ml, P less than 0.05, mean +/- SEM). When all the data from normoxic and hypoxic rats were considered together, plasma atrial natriuretic factor was positively correlated with packed cell volume (r = 0.66, P less than 0.001), pulmonary artery pressure (r = 0.68, P less than 0.002), and the index of right ventricular hypertrophy (r = 0.54, P less than 0.01), but after analysis of partial correlation, packed cell volume was the only independent contributing factor to the variance in the level of plasma atrial natriuretic factor (r2 = 0.24).(ABSTRACT TRUNCATED AT 250 WORDS)

[The topographic characteristics and changes in the ontogeny of light-chain myosin in the human myocardium]. / Izuchenie topograficheskikh osobennostei i izmenenii v ontogeneze legkikh tsepei miozina v miokarde cheloveka.

Pattern of myosin light chain in human atrium and ventricles was studied using two-dimensional electrophoresis. Minor fraction was found in ventricles and atria of adult man that coincided in molecular weight, isoelectric point and staining specificity with fetal myosin light chain. The 23 kDa and 24 kDa fractions of auricles were not detected in ventricles.

[A two-dimensional map of proteins from left ventricle of the human heart]. / Dvumernaia karta belkov levogo zheludochka serdtsa cheloveka.

A two-dimensional map of human heart left ventricular proteins for 213 polypeptide fractions has been constructed. A quantitative analysis of variability of the fraction position at 60 selected spots with the use of a CVIT computer system revealed a high reproducibility of the material distribution on electrophoregrams. Differences were found in the protein composition of eight heart muscle atrial and ventricular polypeptide fractions. Left ventricular proteins were shown to be represented by six electrophoretical variants. The methodological peculiarities of construction at the two-dimensional map of heart muscle proteins are discussed.

Effects of potassium or potassium/magnesium supplementation on potassium content of body tissues and fluids in furosemide-treated rats on magnesium-deficient or magnesium-sufficient diet.

Persistent Mg2+ deficiency may interfere with restoration of normal tissue K+ levels. This study examined: a) the effects of chronic furosemide treatment on K+ of sartorius, aorta and ventricle of rats fed Mg2(+)-deficient (100 ppm) or Mg2(+)-sufficient (400 ppm) diet and deionized water; b) whether normal tissue K+ is restored by oral K+ or K+/Mg2+ supplementation with continued furosemide therapy. Levels of Mg2+ were also measured. Furosemide (20 mg/kg i.p.) decreased K+ in sartorius, aorta and ventricle by 5.5, 4.3 and 19.9 microEq/gm (p less than .05), respectively, in rats fed 100 ppm Mg2+ diet. Furosemide did not alter K+ levels in rats fed 400 ppm Mg2+ diet. K+ supplementation (1 mEq/kg for 7 days) restored K+ to normal in sartorius but the addition of Mg2+ supplementation was necessary to restore K+ levels to normal in ventricle and aorta. These data indicate that furosemide can decrease tissue K+ in rats on a Mg2(+)-deficient diet. This decrease can be reversed during diuretic administration by K+ supplementation in sartorius, or K+ plus Mg2+ supplementation in ventricle and aorta.

Changes of atrial natriuretic peptide and its messenger RNA with development and regression of cardiac hypertrophy in renovascular hypertensive rats.

We assessed the changes in atrial natriuretic peptide (ANP) and its messenger RNA (mRNA) levels in atria and ventricles in relation to hemodynamic factors during antihypertensive treatments in two-kidney, one-clip renovascular hypertensive rats (RHRs). Hypertension of 10-week duration caused a twofold increase in the left ventricular weight/body weight ratio, a significant increase in left ventricular end-diastolic pressure, and an eightfold increase in left ventricular ANP mRNA levels in RHRs, as compared with the levels in control rats. Uninephrectomy or 4 weeks of treatment with the converting enzyme inhibitor enalapril reduced the blood pressure to the control level, with the complete reversal of left ventricular hypertrophy, left ventricular end-diastolic pressure, and ANP mRNA levels. Four weeks of treatment with the arterial vasodilator hydralazine significantly, but not completely, reduced the high blood pressure, but it did not influence left ventricular hypertrophy, end-diastolic pressure, and ANP mRNA levels. The increased ANP synthesis observed in the right ventricles of RHRs also reverted to the control level by uninephrectomy or enalapril treatment, but not by hydralazine, with a time course similar to that of left ventricular ANP. In addition, uninephrectomy caused the left and right ventricular ANP and ANP mRNA levels of RHRs to fall to the levels of control rats as early as 1 week, despite persistent left ventricular hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)

Relationship between alterations in atrial and ventricular histamine content and cardiac function during cardiac anaphylaxis of isolated guinea pig hearts.

Antigen-induced histamine release from sensitized cardiac tissue has been shown to contribute significantly to the increases in atrial rate, atrioventricular nodal conduction, and ventricular contractile force that occur during cardiac anaphylaxis. These findings suggest that there might be a strong negative correlation between changes in these variables and the residual histamine content in the tissue after the anaphylactic reaction. In the present study using isolated hearts of passively sensitized guinea pigs, antigen challenge evoked transient increases in atrial automaticity, P-R intervals, vascular resistance, and left ventricular pressure. The histamine content of atrial and ventricular tissue from antigen-challenge hearts (1,475 +/- 296 and 4,543 +/- 360 ng/g, respectively) was significantly less than that of nonchallenged hearts (2,652 +/- 335 and 6,298 +/- 251 ng/g, respectively). Significant correlations found were between the residual histamine content of the ventricular tissue or the total histamine released and the magnitude of the antigen-induced increase in left ventricular systolic pressure. These findings suggest that antigen-induced increases in left ventricular systolic pressure can be used as an index of the local ventricular histamine release. The lack of significant correlations between local residual histamine levels and changes in atrial rate, P-R intervals, or coronary vascular resistance suggests that complicated interactions between histamine and other mediators or factors may be involved in the antigen-induced chronotropic, dromotropic, and vasoconstrictive alterations in these preparations.

Alterations in the regional beta adrenergic system in experimental left ventricular hypertrophy.

STUDY OBJECTIVE - The aim of the study was to determine the changes in the beta adrenergic system induced by cardiac hypertrophy due to valvular aortic stenosis. DESIGN - Density of beta adrenoceptors, cardiac tissue noradrenalime concentrations, coronary blood flow (using radioactive microspheres), and haemodynamic variables were compared in a model of experimental aortic valve stenosis of 6 month's duration and in sham operated controls. SUBJECTS - 14 mongrel dogs with aortic stenosis and eight sham operated litter mates were used in the studies. MEASUREMENTS and RESULTS - Heart weight to body weight ratio was 33% greater in dogs with aortic valve stenosis than in controls. There were no haemodynamic differences except for a left ventricular to aortic systolic pressure gradient of 38 (SD 22) mm Hg in the aortic stenosis group. Response of left ventricular dP/dtmax to dopamine was similar in the two groups, as was coronary flow. Density of beta adrenoceptors (Bmax) as measured by (125I)-iodopindolol binding was reduced in ventricles from the aortic stenosis group compared to control: 41.2(13.3) v 59.1(8.1) fmol.mg-1 protein, p less than 0.005. Affinity of receptor for ligand (Kd) was not affected by cardiac hypertrophy. Tissue noradrenaline concentration was reduced in the hypertrophy group: 1108(402) (control) v 438(13) ng.g-1 initial wet weight (aortic stenosis), p less than 0.05. There were no significant subepicardial v subendocardial differences in any variable. CONCLUSIONS - Cardiac hypertrophy induced by aortic valve stenosis over a 6 month period is accompanied by a decrease in the density of ventricular beta adrenoceptors per gram and a decrease in ventricular noradrenaline concentration, though responsiveness of the whole heart is maintained.

Distribution and molecular forms of brain natriuretic peptide in porcine heart and blood.

Although brain natriuretic peptide (BNP) is a novel natriuretic peptide originally identified in porcine brain, recent investigation has verified the presence of BNP in porcine heart. In order to identify BNP as a circulating hormone, we analyzed the regional distribution and molecular form of immunoreactive (ir-) BNP in heart and blood. Tissue concentration of ir-BNP was high in atrium, but low in ventricle, in a manner similar to that of atrial natriuretic peptide (ANP). However, the concentration of ir-BNP in atrium was only about 1/50 that of ir-ANP. In plasma, ir-BNP was found at a concentration of 1-3 fmol/ml, which was about 1/20 that of ir-ANP. Both ir-BNP and ir-ANP were present as low molecular weight forms. Three forms of ir-BNP of about 3K daltons, including BNP-26, BNP-29 and BNP-32, are thought to circulate in blood.

Distribution and molecular forms of brain natriuretic peptide in the central nervous system, heart and peripheral tissue of rat.

The amino acid sequence of rat brain natriuretic peptide (rBNP) precursor has recently been deduced by the cDNA cloning method (1). In the present study, a radioimmunoassay (RIA) system for rBNP was newly established, and regional distribution of rBNP in the central nervous system, heart and other peripheral tissue of rat was investigated. In heart, especially in cardiac atrium, a high concentration of immunoreactive (ir-) rBNP was detected and identified as rBNP-45 and gamma-rBNP. No significant amount of ir-rBNP was found in other tissues examined including the central nervous system. Especially in brain, no ir-rBNP was detected, while ir-rat atrial natriuretic peptide (rANP) was observed at a relatively high concentration. These results demonstrate a sharp contrast between rat and porcine brains in ir-BNP distribution.

Dissociation between reperfusion induced arrhythmias and increases in ventricular alpha 1 receptor density in the anaesthetised rat.

Using anaesthetised rats we have assessed (1) whether the density of alpha 1 adrenergic receptors increases during coronary artery occlusion, (2) whether any change in density can be associated with the onset of reperfusion induced ventricular fibrillation, and (3) whether alpha 1 blockade with prazosin modifies the incidence of reperfusion induced ventricular fibrillation. The incidence of fibrillation upon reperfusion after 3, 5, 10, 20 and 30 min occlusion was 20, 75, 50, 16 and 10% (n = 10-12 in each group) respectively. alpha 1 Receptor density was measured using [3H]-prazosin in non-ischaemic and ischaemic tissue obtained after 0, 5 and 30 min ischaemia. Receptor density was not significantly altered at the time of maximum incidence of reperfusion induced ventricular fibrillation (5 min occlusion) but did significantly increase in both non-ischaemic and ischaemic tissue after 30 min occlusion, when the incidence of fibrillation upon reperfusion was very low (8%). At this time the values were 17.0(SEM 2.3) and 18.4(0.6)fmol.mg-1 protein in non-ischaemic and ischaemic zones as compared to 10.7(0.6) and 12.8(1.0)fmol.mg-1 protein in sham operated control animals (p less than 0.05 in both cases). Prazosin (0.1 or 1.0 mg.kg-1 body wt intravenously, 5 min prior to coronary occlusion) did not alter the incidence of ventricular fibrillation, ventricular tachycardia or total number of premature ventricular complexes upon reperfusion. We conclude that ischaemia induced changes in alpha 1 receptor density do not parallel changes in vulnerability to reperfusion induced arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)

Density of beta adrenoceptors in rat heart and lymphocytes 48 hours and 7 days after acute myocardial infarction.

Down regulation of the beta adrenoceptor is thought to play an important role in the diminished response to catecholamines in heart failure. beta Adrenoceptor densities were measured on membrane homogenates of rat right ventricle and lymphocytes 48 h or 7 d after experimental myocardial infarction, and in rats exposed to a continuous infusion of isoprenaline (400 micrograms.kg-1.h1). The performance of the rat hearts was also evaluated 48 h post infarction in an isolated retrograde perfused heart preparation. In contrast to a 60% down regulation in right ventricle and a 20% down regulation in lymphocyte membranes after isoprenaline infusion, there was no change in right ventricle and lymphocyte beta adrenoceptor densities after myocardial infarction. Left ventricular contractile performance was significantly depressed 48 h after myocardial infarction. Mean basal left ventricular pressure decreased from 108(SEM 3) to 63(4) mm Hg while the maximal response to dobutamine was decreased from 204(4) to 105(12) mm Hg (n = 8). No correlation was found between the receptor densities of right ventricular and lymphocyte membranes. We conclude that diminished response to beta sympathomimetics after myocardial infarction cannot be attributed to a loss of surface beta adrenoceptors, and that the lymphocyte beta adrenoceptor does not provide an adequate system to monitor small receptor changes on the myocardium.

Basic fibroblast growth factor in atria and ventricles of the vertebrate heart.

Extracts from atrial and ventricular heart tissue of several species (chicken, rat, sheep, and cow) are strongly mitogenic for chicken skeletal myoblasts, with the highest apparent concentration of biological activity in the atrial extracts. Using several approaches (biological activity assay and biochemical and immunological analyses), we have established that (a) all cardiac extracts contain an 18,000-D peptide which is identified as basic fibroblast growth factor (bFGF) since it elutes from heparin-Sepharose columns at salt concentrations greater than 1.4 M and is recognized by bFGF-specific affinity-purified antibodies; (b) bFGF is more abundant in the atrial extracts in all species so examined; (c) avian cardiac tissue extracts contain the highest concentration of immunoreactive bFGF; and (d) avian ventricles contain a higher relative molecular mass (23,000-D) bFGF-like peptide which is absent from atrial extracts. Examination of frozen bovine cardiac tissue sections by indirect immunofluorescence using anti-bFGF antibodies shows bFGF-like reactivity associated with nuclei and intercalated discs of muscle fibers. There is substantial accumulation of bFGF around atrial but not ventricular myofibers, resulting most likely from more extensive endomysium in the atria. Blood vessels and single, nonmuscle, connective tissue cells react strongly with the anti-bFGF antibodies. Higher bFGF content and pericellular distribution in atrial muscles suggest a correlation with increased regenerative potential in this tissue. Distribution within the myofibers is intriguing, raising the possibility for an intimate and continuous involvement of bFGF-like components with normal myocardial function.

Noradrenaline, atrial natriuretic peptide, bombesin and neurotensin in myocardium and blood of rats in congestive cardiac failure.

Rats given monocrotaline develop severe right ventricular hypertrophy often accompanied by ascites and pleural effusions. In rats with right ventricular hypertrophy and no serous effusions ("hypertrophy" group), ventricular concentrations of noradrenaline were reduced but ventricular contents were unchanged. Atrial concentrations of noradrenaline were unaffected. Those with more severe right ventricular hypertrophy and serous effusions ("failure" group) had greatly reduced concentrations of noradrenaline in all four chambers, particularly on the right side; the right and left ventricular contents of noradrenaline were also diminished. The distributions of ir-ANP, ir-bombesin and ir-neurotensin in the normal rat heart are presented. ANP concentration fell to 33% in the right atrium and 46% in the left atrium of "failure" animals and to 57% in the right atrium of "hypertrophy" animals. Right ventricular content of ANP, normally low, increased more than two-fold in both groups, the concentration remaining unchanged. Left ventricular content of ANP decreased in the "failure" group. Concentrations of bombesin and neurotensin fell in both ventricles of both groups. Ventricular contents of bombesin did not change, but ventricular contents of neurotensin decreased, especially on the right side. Plasma ANP rose nearly six-fold while plasma bombesin and neurotensin fell in the "failure" group. Plasma peptide concentrations were unchanged in the "hypertrophy" group. The studies show the utility of the monocrotaline model in distinguishing between the effects of hypertrophy and those associated specifically with the syndrome of congestive cardiac failure.

Evidence for expression of a common myosin heavy chain phenotype in future fast and slow skeletal muscle during initial stages of avian embryogenesis.

We have utilized a key biochemical determinant of muscle fiber type, myosin isoform expression, to investigate the initial developmental program of future fast and slow skeletal muscle fibers. We examined myosin heavy chain (HC) phenotype from the onset of myogenesis in the limb bud muscle masses of the chick embryo through the differentiation of individual fast and slow muscle masses, as well as in newly formed myotubes generated in adult muscle by weight overload. Myosin HC isoform expression was analyzed by immunofluorescence localization with a battery of anti-myosin antibodies and by electrophoretic separation with SDS-PAGE. Results showed that the initial myosin phenotype in all skeletal muscle cells formed during the embryonic period (until at least 8 days in ovo) consisted of expression of a myosin HC which shares antigenic and electrophoretic migratory properties with ventricular myosin and a distinct myosin HC which shares antigenic and electrophoretic migratory properties with fast skeletal isomyosin. Similar results were observed in newly formed myotubes in adult muscle. Future fast and slow muscle fibers could only be discriminated from each other in developing limb bud muscles by the onset of expression of slow skeletal myosin HC at 6 days in ovo. Slow skeletal myosin HC was expressed only in myotubes which became slow fibers. These findings suggest that the initial commitment of skeletal muscle progenitor cells is to a common skeletal muscle lineage and that commitment to a fiber-specific lineage may not occur until after localization of myogenic cells in appropriate premuscle masses. Thus, the process of localization, or events which occur soon thereafter, may be involved in determining fiber type.

Intracellular distribution of adrenoceptors in the failing human myocardium.

Although it is increasingly recognized that the density of cardiac membrane-bound beta adrenoceptors declines in heart failure, the mechanisms involved are unclear. Furthermore, it is not known whether cardiac alpha-1 adrenoceptors are similarly affected. Inasmuch as agonist-induced desensitization results in translocation of adrenoceptors from the plasma membrane to an intracellular vesicular fraction, we determined the intracellular distribution of cardiac adrenoceptors in two groups: group 1 (n = 9) consisted of papillary muscles from patients with mild-to-moderate heart failure undergoing valve replacement, and group 2 (n = 8) consisted of severely failing hearts removed during orthotopic cardiac transplantation. The density of cardiac beta adrenoceptors was lower in membranes from group 2 (17.8 +/- 3.3 fmol/mg protein vs 27.8 +/- 3.7 fmol/mg in group 1; (p less than 0.01), and the percentage of beta receptors recovered in the vesicular fraction was higher in group 2 (47.1 +/- 3.3% vs 36.8 +/- 5.0% in group 1; p less than 0.01). In group 1 but not group 2 there was a significant inverse correlation (r = -0.87; p less than 0.001) between the density of membrane-bound beta receptors and the percentage of beta receptors recovered in the vesicular fraction. Alpha-1 adrenoceptors were lower in both membrane and vesicular fraction of group 2 compared to group 1; in group 2 but not group 1 there was a significant negative correlation between the density of membrane-bound alpha-1 adrenoceptors and the percentage of alpha-1 receptors in the vesicular fraction (r = -0.8; p less than 0.01). These results suggest that the regulation of alpha-1 and beta adrenoceptors differs in the failing myocardium. Furthermore, agonist-induced desensitization may play a predominant role only in mild-to-moderate heart failure.

Improved gas chromatography with electron-capture detection using a reaction pre-column for the determination of blood cyanide: a higher content in the left ventricle of fire victims.

We developed a head-space method for the determination of blood cyanide by gas chromatography with electron-capture detection. In this technique, a reaction pre-column, packed with chloramine-T, was used for the conversion of hydrogen cyanide into cyanogen chloride. Since the reaction pre-column eliminated the necessity for trapping hydrogen cyanide from the biological samples, blood cyanide was quickly analysed by acidification only. The reaction pre-column was durable for at least several months. The calibration curve gave good linearity when dichloromethane was used as the internal standard, and the lower detection limit taken from this plot was ca. 0.05 micrograms/ml. The relative standard deviation of spiked blood samples was in the range 0.6-3.9%. We determined blood cyanide levels at autopsy in victims who had died from fire using this method. A significantly higher cyanide content was detected in the left ventricular blood than in the right. There was a positive correlation between blood cyanide and carboxylhaemoglobin contents. This simple and sensitive technique could be very useful for the determination of cyanide in various samples.

Role of alpha 1-adrenoceptor activity in progression of cardiac hypertrophy in guinea pig hearts with pressure overload.

To elucidate the role of alpha 1- and beta-adrenergic activities in pressure overload hypertrophy, changes of alpha 1- and beta-adrenoceptors were measured by radioligand binding assay, and the preventive effects of alpha 1- and beta-adrenoceptor blockade on cardiac hypertrophy were assessed in guinea pigs after aortic banding. Five days after banding, dry weight of left ventricle had not increased, though wet weight increased due to marked intercellular oedema. In this period, the maximum binding capacity of [3H] prazosin increased to 31.1 (SEM 2.2) fmol.mg-1 from (sham operation) 17.0(2.1) fmol.mg protein-1, p less than 0.01, whereas the maximum binding capacity of [3H]dihydroalprenolol did not increase: 143(16) fmol.mg-1 (banded) v 153(13) fmol.mg-1 (sham). Three weeks after aortic banding, the maximum binding capacity of both ligands increased to 45.6(5.5) fmol.mg-1 and 232(21) fmol.mg-1, respectively, accompanied by a significant increase in left ventricular dry weight, from 0.46(0.02) mg.g-1 (sham) to 0.62(0.08) mg.g-1 (banded), p less than 0.01. Continuous subcutaneous administration of the alpha 1-blocker bunazosin (0.1 mg.kg-1.d-1) significantly attenuated the increase in left ventricular dry weight whereas the beta-blocker propranolol (5 mg.kg-1.d-1) did not: 0.55(0.03) v 0.66(0.04) mg.g-1 respectively, after 3 weeks. These results show that pressure overload elicited an increase in myocardial alpha 1-adrenoceptors before the onset of cardiac hypertrophy, and that an alpha 1-blocker could prevent the development of hypertrophy in the pressure overloaded heart.

An immunocytochemical study on co-localization of cathepsin B and atrial natriuretic peptides in secretory granules of atrial myoendocrine cells of rat heart.

To examine localization of cathepsin B, a representative lysosomal cysteine protease, in atrial myoendocrine cells of the rat heart, immunohistochemistry at the light and electron microscopic level was applied to the atrial tissue, using a monospecific antibody for rat liver cathepsin B. In serial semi-thin sections, immunoreactivity for cathepsin B and atrial natriuretic peptides (ANP) was detected in the para-nuclear region of atrial myoendocrine cells. Several large granules and many fine granules in the region of the cells were positively stained by the cathepsin B antibody. Gold particles indicating cathepsin B antigenicity labeled secretory granules in the cells, which were also labeled by those indicating ANP, using thin sections of the Lowicryl K4M-embedded material. Moreover, some granules labeled densely by immunogold particles for cathepsin B seemed to be lysosomes. By double immunostaining using thin sections of the Epon-embedded material, gold particles indicating cathepsin B and ANP antigenicities were co-localized in secretory granules of the cells. By enzyme assay, activity of cathepsin B was three times higher in atrial tissue than ventricular tissue. The results suggest that co-localization of cathepsin B and ANP in secretory granules is compatible with the possibility that cathepsin B participates in the maturation process of ANP.