(Circulation. 1995;92:1558-1564.)
© 1995 American Heart Association, Inc.
Articles |
Rapid Ventricular Induction of Brain Natriuretic Peptide Gene Expression in Experimental Acute Myocardial Infarction
From the Second Division, Department of Medicine (N.H., H.I., O.N., S.S., Y.O., I.M., T.Y., K. Nakao) and Department of Anesthesia (G.S.), Kyoto University School of Medicine; the Department of Pharmacy (Y.H., M.Y., R.H.), Kyoto University Hospital; the Department of Pathology (K. Nakanishi), National Defense Medical College; and the Division of Cardiology (H.Y.), Kumamoto University School of Medicine, Japan.
Correspondence to Kazuwa Nakao, MD, PhD, Second Division, Department of Medicine, Kyoto University School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606, Japan.
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Abstract |
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Background We have demonstrated that brain natriuretic peptide (BNP) is a cardiac hormone predominantly synthesized in and secreted from the ventricle. We have also reported that, compared with atrial natriuretic peptide (ANP), the plasma concentration of BNP is increased to a greater degree in patients with congestive heart failure and more rapidly in patients with acute myocardial infarction (AMI).
Methods and Results To investigate ventricular gene expression of BNP in AMI, we analyzed plasma and ventricular BNP concentrations along with ventricular BNP mRNA in rats with AMI produced by coronary artery ligation. The BNP concentration in the left ventricle increased about 2-fold as early as 12 hours postinfarction and 5-fold 1 day postinfarction compared with sham-operated rats, whereas left ventricular ANP concentration remained unchanged within 1 day. The tissue concentration of BNP increased in the noninfarcted region as well as in the infarcted region. The surviving myocytes in and around the necrotic tissues in the infarcted region were intensely stained with the anti-BNP antiserum, indicating augmented production in the remaining myocytes in the infarcts. The BNP concentration in the right ventricle also increased about 10-fold 12 hours postinfarction, whereas the ANP concentration remained unchanged within 12 hours. Northern blot analysis revealed that BNP mRNA expression was augmented 3-fold in the left ventricle as early as 4 hours postinfarction. In contrast, ANP mRNA expression was unchanged. Reflecting the rapid induction of ventricular BNP production, the plasma BNP concentration rose to about 100 pg/mL 12 hours postinfarction (sham-operated rats, <70 pg/mL).
Conclusions These results demonstrate the rapid induction of ventricular BNP gene expression in rats with AMI compared with ANP and suggest that BNP gene expression in the ventricle is regulated distinctively from ANP gene expression against acute ventricular overload. They also suggest that the BNP gene can be one of the acutely responsive cardiac genes for the ventricular overload and suggest a possible pathophysiological role of BNP distinct from ANP in AMI.
Key Words: natriuretic peptides • myocardial infarction
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Introduction |
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Atrial natriuretic peptide (ANP) is a cardiac hormone with potent diuretic, natriuretic, and vasodilatory activities and plays an important role in body-fluid and cardiovascular homeostasis.1 2 3 A second natriuretic peptide, brain natriuretic peptide (BNP), first isolated from the porcine brain,4 has a remarkable sequence homology to ANP and exhibits peripheral and central actions similar to those of ANP.5 6 We first reported that BNP is synthesized in and secreted from the porcine heart7 to demonstrate that BNP is a cardiac hormone. Later, we and others isolated and sequenced rat BNP with 45 amino acids8 9 10 and human BNP with 32 amino acids from the heart.11 Recently, using the specific radioimmunoassay (RIA) for BNP, we made the crucial observation that BNP is predominantly synthesized in and secreted from the ventricle, in contrast to ANP, the major producer of which is the atrium.12 13 14 15 We also demonstrated that in patients with chronic congestive heart failure, the plasma level of BNP increases, in proportion to the severity of the disease, more markedly than that of ANP and surpasses the level of ANP in severe cases.13 16 This observation suggested that BNP is a cardiac hormone that reflects ventricular function. More recently, we have observed that in patients with acute myocardial infarction (AMI), the plasma level of BNP increases acutely and much more prominently than that of ANP in the early phase of the disease.17 18 This observation suggested the possibility that BNP is synthesized rapidly in the infarcted ventricle. However, there were no reports concerning BNP synthesis in the ventricle after AMI. In this context, in the present study, we attempted to determine the temporal profile of ventricular BNP production evaluated both at BNP peptide and mRNA levels, using the experimental rat model of AMI.
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Methods |
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Animals With Myocardial Infarction
Male Wistar rats weighing 250 to 300 g (Shimizu Experimental Supplies) were used for the present study. Myocardial infarction was produced by a method previously described.19 In brief, rats were anesthetized with intraperitoneal injection of pentobarbital. Under mechanical ventilation, a left thoracotomy was performed, and the heart was rapidly exteriorized. The left coronary artery was ligated between the pulmonary artery outflow tract and left atrium with 6-0 silk suture. The heart was returned to its normal position, and the incision was closed. Sham-operated rats were prepared with the coronary artery loosely ligated. Rats were allowed free access to standard rat chow, and water was provided ad libitum. The mortality rate was 50% within 12 hours after the operation.
Rats were killed at three time points: 12 hours, 1 day, and 3 days after the operation. First, to assess ventricular function in rats with AMI, hemodynamic measurement was performed with 6 rats with AMI and 6 sham-operated rats 1 day after the operation. Second, myocardial infarct size and plasma concentrations of BNP and ANP were evaluated in 21 rats with AMI (MI group) and 18 sham-operated rats (Sham group): 12 hours (MI, n=5; Sham, n=3), 1 day (MI, n=10; Sham, n=9), and 3 days (MI, n=6; Sham, n=6) after the operation. Then, tissue concentrations of BNP and ANP were evaluated in another 21 rats with AMI and 15 sham-operated rats: 12 hours (MI, n=7; Sham, n=5), 1 day (MI, n=7; Sham, n=5), and 3 days (MI, n=7; Sham, n=5) after the operation. Tissue levels of mRNA of ANP and BNP were evaluated in rats with AMI and sham-operated rats 4 hours, 12 hours, and 3 days (n=3 each) after the operation.
Hemodynamic Measurements
Rats were anesthetized with 2%
halothane
anesthesia. The internal carotid artery was exposed and
cannulated with a fluid-filled PE-50 tube connected to a Gould
Statham P23ID pressure transducer and San-Ei Biophysiograph 180 system
(NEC San-Ei). Systemic arterial pressure was monitored and
recorded. Then the catheter was advanced into the left ventricle,
and left ventricular pressure was measured.
Plasma Sampling
Under halothane anesthesia, the abdomen was
opened.
Blood (4 mL) was rapidly obtained by puncture of the abdominal aorta.
Blood was transferred to chilled tubes containing aprotinin (1000
KIU/mL) and Na2EDTA (1 mg/mL) and immediately
centrifuged at 4°C. Plasma samples were stored at -20°C
until assay. Then a thoracotomy was performed, and the heart was
obtained for the measurement of infarct size.
Infarct Size Measurement
The atria and the right ventricle
were excised. The left
ventricle was weighed and cut into four slices perpendicular to the
apex-base axis. These slices were placed in 1%
triphenyltetrazolium chloride solution for
10 minutes at 37°C to dye the normal region as previously
described.20 The undyed region was cut out and weighed.
The myocardial infarct size was expressed as a percentage of the weight
of the left ventricle.
Tissue Preparation for Analysis of BNP and ANP
Concentrations and mRNAs
Thoracotomy was performed under halothane
anesthesia, and the heart was removed immediately. The
heart was cut transversely 3 mm beneath the
atrioventricular groove to avoid contamination of
atrial tissues. Then the right ventricle was excised from the remaining
heart. The left ventricle was further divided into four equal regions
by two planes parallel to the apex-base axis and containing the
center of the left ventricular cavity as illustrated in Fig 1
:
anterior wall, lateral wall, posterior wall, and
septum. Since we confirmed that the infarcted area covered most of the
anterior and lateral walls (>80%) and did not extend to the posterior
wall or septum, we defined the anterior and lateral walls as the
infarcted portion of the left ventricle and the posterior wall and
septum as the noninfarcted portion of the left ventricle. These five
pieces of cardiac tissues were frozen in liquid nitrogen and stored at
-70°C until use. The cardiac tissues obtained were subjected to RNA
or peptide extractions.
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Tissue Extraction and Determination of Tissue Levels of BNP
and ANP
Cardiac tissues (the right ventricle and four pieces of the
left
ventricle) were boiled for 10 minutes in 10 vol% 0.1 mol/L acetic acid
containing 0.1% Triton X-100 to avoid intrinsic proteolysis,
homogenized with a polytron homogenizer
(Kinematica GmbH Kriens), and extracted as previously
reported.21 BNP and ANP concentrations were measured by
their respective RIAs as previously reported.12 21
Cross-reactivity with 
–rat ANP in the RIA for rat BNP was
<0.01 mol%, as was the cross-reactivity with rat BNP in the RIA
for –rat ANP.
The peptide concentration of the infarcted left ventricle was thus calculated by averaging the peptide concentration of anterior and lateral walls, taking tissue weight into account. The peptide concentration of the noninfarcted left ventricle was calculated by averaging the peptide concentration of posterior wall and septum. Further, the peptide concentration of the whole left ventricle was calculated by averaging the peptide concentrations of the infarcted and noninfarcted regions.
Total RNA Extraction and Northern Blot
Analysis
Total RNA was extracted from cardiac tissues in 4 mol/L
guanidinium thiocyanate buffer, and tissue concentrations of BNP mRNA
and ANP mRNA were measured by Northern blot analysis as
previously reported.15 22 A 468-bp fragment of rat
BNP
cDNA was prepared by polymerase chain reaction and used to detect rat
BNP mRNA.15 A 368-bp restriction fragment of rat ANP cDNA
was used to detect rat ANP mRNA.22 These fragments were
labeled with [-32P]dCTP (3000 Ci/mmol, Amersham
International) to a specific activity of 1x109 cpm/µg by
the random priming method. Autoradiographs were quantified by
densitometric scanning.
Measurement of the Plasma Levels of BNP and ANP
The plasma
concentration of BNP was measured with 50 µL rat
plasma without extraction by the RIA described above. The minimum
detection limit of the plasma BNP concentration was 70 pg/mL. The
plasma concentration of ANP was measured with 25 µL rat plasma by the
RIA described above.23
Immunohistochemistry
A cross section of the left ventricles
of sham-operated rats
and MI rats 3 days postinfarction was made perpendicular to the long
axis of the heart at the middle of the base and apex. These tissues
were embedded in OCT compound (Tissue Tek, Miles Inc), quickly frozen
in dry ice/acetone, and stored at -80°C until use. The indirect
immunoperoxidase method was applied to the frozen
section.24 The frozen sections, 4 µm thick, were
prepared on a 3-aminopropyltrimethoxy silane–coated glass slide
and then postfixed in acetone at room temperature for 10 minutes. The
primary rabbit antisera against -rat ANP and rat BNP diluted at
1:200 were reacted at room temperature for 1 hour, followed by a
10-minute rinse in 0.01 mol/L PBS, pH 7.2. Horseradish
peroxidase–labeled secondary antibody to rabbit immunoglobulins
(Chemicon International Inc) diluted at 1:250 was then incubated at
room temperature for 30 minutes. Immunoperoxidase staining was absent
from samples incubated with both antisera preabsorbed with –rat
ANP and rat BNP, respectively.
Statistical Analysis
All data are presented as
mean±SEM. In the
hemodynamic study, comparisons were done with
Student's t test. In the tissue concentrations of ANP and
BNP, comparisons were done with two-way ANOVA for group (Sham
versus MI, infarcted region versus noninfarcted region) and time. When
appropriate, comparisons to determine the significance of changes
within the same group over time and between groups at each time
interval were performed with Scheffé's test for multiple
comparisons. Statistical significance was accepted at the 95%
confidence limit (P<.05).
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Results |
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Myocardial Infarct Size
The infarct sizes as measured by a percentage weight of the left ventricle were 49±1.5% (n=5) 12 hours postinfarction, 53±2.3% (n=10) 1 day postinfarction, and 37±1.7% (n=6) 3 days postinfarction.
Progressive thinning of the infarcted wall with reduction in the volume of the infarcted myocardium occurs25 ; thus, myocardial infarct size as measured by weight was smaller 3 days postinfarction than 12 hours or 1 day postinfarction.
Hemodynamic Measurement
The Table shows
hemodynamic
parameters in rats with AMI and sham-operated rats 1
day after the operation. Measurement of systemic arterial
pressure indicated that a fall in systolic, diastolic, and
mean pressures developed. In contrast, heart rate was unchanged. Left
ventricular end-diastolic pressure
increased 1.8-fold, and left ventricular systolic pressure
decreased by 14%. These results indicate depressed left
ventricular performance in rats with AMI in this
study. After hemodynamic measurement, hearts were
removed, and we confirmed that infarct size was almost half of the left
ventricle.
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BNP and ANP Concentrations in the Ventricles of Rats With
AMI
Fig 2A depicts BNP concentration in the left
ventricle in rats with AMI and sham-operated rats. According to
two-way ANOVA, there was a significant difference between rats with
AMI and sham-operated rats. Twelve hours postinfarction, the BNP
concentration in the whole left ventricle of MI rats was already
elevated compared with Sham rats (2-fold). The BNP concentration showed
further increase 1 day (5-fold) and 3 days (7-fold) postinfarction. Fig
2B depicts BNP concentration in the right ventricle in rats
with AMI
and sham-operated rats. There was also a significant difference
between rats with AMI and sham-operated rats. The BNP concentration
of the right ventricle also increased about 10-fold 12 hours
postinfarction and remained elevated until 3 days postinfarction. In
contrast to the rapid increase of the BNP concentrations, the ANP
concentrations of the left and right ventricles were unchanged until 1
day (Fig 2C and 2D).The significant elevation of
ANP concentrations was
first observed only 3 days postinfarction. Fig 3A
depicts the comparison of the BNP concentration change in the infarcted
area and the noninfarcted area of the left ventricle after AMI. In
sham-operated rats, the average of the BNP concentration of
anterior and lateral walls was not different from that of posterior
wall and septum. There was no significant difference between the two
regions. In rats with AMI, the BNP concentration of the noninfarcted
region showed almost the same magnitude of increase as the infarcted
region. Similar results were also obtained in the ANP concentration
(Fig 2B).
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BNP and ANP mRNA Expression in the Ventricles of Rats With
AMI
As shown in Fig 4, BNP mRNA expression was
augmented in the left and right ventricles as early as 4 hours
postinfarction. In contrast, ANP mRNA expression was unchanged 4 hours
postinfarction. In the left ventricle, BNP mRNA expression was
augmented in the noninfarcted region as well as in the infarcted
region. In sham-operated rats, BNP mRNA and ANP mRNA were unchanged
throughout 3 days postoperation compared with normal rats.
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The levels of BNP mRNA and ANP mRNA of the noninfarcted region of the left ventricle in rats with AMI were quantified by densitometric scanning, and mRNA levels were expressed by folds of increase from those of normal rats. The levels of BNP mRNA were 3.3±0.4 4 hours postinfarction, 4.7±0.3 12 hours postinfarction, and 3.5±0.7 3 days postinfarction. The levels of ANP mRNA were not increased 4 hours postinfarction (1.1±0.6), modestly increased 12 hours postinfarction (2.6±0.4), and further increased 3 days postinfarction (5.5±0.9).
Plasma Level of BNP and ANP in Rats With AMI
Fig
5 shows the change of the plasma BNP
concentration in rats with AMI. The plasma BNP concentration of Sham
rats was always below the detection limit (<70 pg/mL). In rats with
AMI, the plasma BNP concentration increased to about 100 pg/mL 12 hours
postinfarction and persisted until 3 days postinfarction. The plasma
ANP concentration of MI rats was also significantly higher than that of
Sham rats: 1570±130 versus 180±45 pg/mL (P<.001) 12
hours
postinfarction, 1260±180 versus 310±50 pg/mL
(P<.001) 1
day postinfarction, and 1900±150 versus 210±40 pg/mL
(P<.001) 3 days postinfarction.
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Immunohistochemical Staining for BNP and ANP in the Ventricles of
Rats With AMI
The left ventricular myocytes in the control heart
were weakly immunostained for BNP (Fig 6A).
In contrast, intense immunostaining for BNP was
observed in the myocytes surrounding the infarcts (Fig 6B) and
in the
surviving myocytes in the infarcts (Fig 6C). No
immunostaining was observed in the necrotic myocytes,
infiltrating cells, or fibrous tissue in the infarcts. Strongly
immunostained myocytes for ANP were localized as for BNP
(data not shown).
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Discussion |
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The present study demonstrates that both ventricular BNP concentration and BNP mRNA level increase as early as 12 hours postinfarction and that these increases are much earlier than those of ANP in the ventricles of rats with AMI. BNP concentration and BNP mRNA showed parallel increases during the early phase of AMI in this study. As reported,15 26 27 ventricular ANP and BNP are secreted immediately after synthesis from ventricular cardiocytes with a small storage capacity. Thus, the increase of peptide content of the ventricular cardiocyte together with the increase of mRNA level reflects augmented biosynthesis of the peptides. The present study, therefore, is the first demonstration of the rapid induction of BNP gene expression, in comparison to ANP, in AMI in vivo using an experimental animal model.
Rats with MI involving >30% of the left ventricle are reported to
have overt congestive heart failure, with elevated left
ventricular end-diastolic pressure and
reduced cardiac output.19 28 The rats with AMI in the
present study had myocardial infarction involving 
50% of the
left ventricle, and hemodynamic measurement showed
depressed left ventricular performance. Thus, the
experimental MI rats used in the present study are an appropriate
model of acute heart failure. The present study, therefore,
indicates markedly rapid induction of ventricular BNP gene
expression in response to acute ventricular overload. A
previous study revealed that BNP mRNA and ANP mRNA expressions are
regulated in a concordant manner in the ventricles in end-stage
heart failure.29 In contrast, the present study raises
the possibility that BNP and ANP gene expressions are regulated
differently in the ventricle in the acute phase of myocardial
infarction or acute heart failure.
Clinically, the plasma level of BNP increases in the acute phase of AMI,17 18 but the mechanism of release of BNP from the heart into the circulation is not clear. Is BNP released from the irreversibly injured or necrotic myocardial cells like creatine phosphokinase, glutamic-oxaloacetic transaminase, or lactate dehydrogenase? In this study, we show for the first time that elevated plasma BNP in AMI is not due to a leakage of BNP from the necrotic tissue but rather is attributable to its augmented synthesis in the ventricle in AMI.
There are several reports as to tissue weight change after infarction in rats. Fishbein et al25 reported that tissue edema in infarcts is at a peak 24 to 48 hours postinfarction and that edema decreases by 3 days. Further, Mannisi et al30 reported that water content of the infarcted region was increased no more than 5% of total weight compared with the noninfarcted region 24 hours postinfarction. Thus, although peptide concentration in the infarcted region may be underestimated within 1 day postinfarction, there is little effect of water content on peptide concentration, which shows a dramatic increase. Ventricular dilatation after infarction has been documented as architectural rearrangements of myocytes, which leads to thinning of the ventricular wall and increased mural stress.31 32 33 Previous reports demonstrated that ANP concentration or ANP mRNA expression increases in the noninfarcted region as well as the infarcted region in patients with old myocardial infarction,27 34 35 and they suggested that regional mechanical stress as well as hemodynamic overload may be closely associated with ventricular ANP expression. Similarly, in the present study, the BNP concentration and BNP mRNA were also increased in the noninfarcted region as well as the infarcted region of the left ventricle. The BNP concentration and BNP mRNA in the right ventricle, which receives pressure overload, were also increased. These findings suggest that the stimulus for BNP biosynthesis is the ventricular overload.
To clarify which cell types of the infarcted region contribute to the increased production of BNP or ANP, we next performed immunohistochemical study using our anti-BNP and anti-ANP antisera. The immunohistochemical study indicates that the surviving myocytes in and around the necrotic tissues synthesize more BNP. Similar results were also obtained by immunostaining with anti-ANP antiserum. Recent reports demonstrated that the productions of several growth factors, such as transforming growth factor-ß and basic fibroblast growth factor, are augmented in the surviving myocyte in the surroundings of the infarcted region.36 37 Moreover, Parker et al38 reported that these growth factors stimulated ANP gene expression in cultured rat neonatal cardiocytes. We also reported that transforming growth factor-ß potently stimulated the secretion of C-type natriuretic peptide from the cultured endothelial cells.39 These growth factors or other substances produced at the augmented level may be responsible for ANP or BNP synthesis in the infarcted region. In addition, the infarcted region is thinner than the noninfarcted region,31 and surviving myocytes in the infarcts are considered to suffer from more regional wall stress according to Laplace's law. The increased regional wall stress may also be related to augmented ANP or BNP synthesis in the surviving myocytes in the infarcted region. Further study is necessary on the mechanisms of BNP production in the infarcts. In the present study, the plasma BNP concentration increased as early as 12 hours postinfarction. We have demonstrated that BNP is mainly synthesized in and secreted from the ventricle in humans and rats.12 13 14 15 BNP biosynthesis is increased in the ventricle of rats with AMI in this study. Therefore, the considerable amount of the increase of the plasma BNP concentration was thought to be of ventricular origin. On the other hand, the increase of plasma ANP concentration is attributed to augmented atrial secretion, because ANP biosynthesis is not increased in the ventricles in the early phase of MI in the present study. This finding is in contrast to the state of chronic heart failure. We and others have demonstrated that ANP and BNP biosynthesis is augmented in the ventricle in chronic heart failure13 15 27 40 41 and that the ventricle is a substantial source of both circulating ANP and BNP in chronic heart failure.13 27 41 The present study, therefore, demonstrates that in acute heart failure, BNP is secreted rapidly from the ventricle via de novo synthesis against ventricular overload, whereas ANP is secreted from the storage in the atrium. Thus, BNP can be a more sensitive marker of ventricular function than ANP.
Previously, we reported that infusion of BNP in patients with congestive heart failure showed beneficial hemodynamic effects.42 Recently, we demonstrated the chronic action of BNP in blood pressure regulation, using a BNP gene–overexpressing transgenic mouse.43 Thus, augmented synthesis of BNP in rats with AMI may have some roles in acute heart failure.
In summary, this study demonstrates that BNP biosynthesis is more rapid than ANP biosynthesis in the ventricle of rats with AMI. The present results also indicate that expression of the BNP gene in the ventricle is regulated distinctively from that of ANP. The elucidation of the molecular mechanism of the rapid gene expression of ventricular BNP is now ongoing in our laboratory.
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Acknowledgments |
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This work was supported in part by research grants from the Japanese Ministry of Education, Science, and Culture; the Japanese Ministry of Health and Welfare Disorders of Adrenal Hormone Research Committee and Molecular Approach for the Pathogenesis of Immunological Disorder Research Committee; the Smoking Research Foundation; the Yamanouchi Foundation for Research on Metabolic Disorders; the Salt Science Research Foundation; the Uehara Memorial Foundation; and the Japanese Society for Cardiovascular Disease. We gratefully thank S. Mori for her technical assistance. We also thank C. Yamamoto, K. Kito, A. Takakoshi, and M. Shida for their secretarial assistance.
Received July 25, 1994; revision received March 3, 1995; accepted March 10, 1995.
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T. Langenickel, I. Pagel, K. Hohnel, R. Dietz, and R. Willenbrock Differential regulation of cardiac ANP and BNP mRNA in different stages of experimental heart failure Am J Physiol Heart Circ Physiol, May 1, 2000; 278(5): H1500 - H1506. [Abstract] [Full Text] [PDF]
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M. Ueno, T. Miyauchi, S. Sakai, T. Kobayashi, K. Goto, and I. Yamaguchi Effects of physiological or pathological pressure load in vivo on myocardial expression of ET-1 and receptors Am J Physiol Regulatory Integrative Comp Physiol, November 1, 1999; 277(5): R1321 - R1330. [Abstract] [Full Text] [PDF]
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M. Harada, H. Itoh, O. Nakagawa, Y. Ogawa, Y. Miyamoto, K. Kuwahara, E. Ogawa, T. Igaki, J. Yamashita, I. Masuda, et al. Significance of Ventricular Myocytes and Nonmyocytes Interaction During Cardiocyte Hypertrophy : Evidence for Endothelin-1 as a Paracrine Hypertrophic Factor From Cardiac Nonmyocytes Circulation, November 18, 1997; 96(10): 3737 - 3744. [Abstract] [Full Text]
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N. Tamura, Y. Ogawa, H. Chusho, K. Nakamura, K. Nakao, M. Suda, M. Kasahara, R. Hashimoto, G. Katsuura, M. Mukoyama, et al. Cardiac fibrosis in mice lacking brain natriuretic peptide PNAS, April 11, 2000; 97(8): 4239 - 4244. [Abstract] [Full Text] [PDF]
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