Ischemia stimulates the release of atrial natriuretic peptide from rat cardiac ventricular myocardium in vitro

Uusimaa, Paavo; Peuhkurinen, Keijo; Hassinen, Ilmo E.; Vuolteenaho, Olli; Ruskoaho, Heikki

doi:10.1016/0024-3205(92)90438-u

Cited by 17 publications

(10 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…hypoxia has also proved to be a powerful stimulus for the release of natriuretic peptides from the rodent heart (Baertschi et al 1986, Lew & Baertschi 1989, Uusimaa et al 1992a,b, Chen et al 1993, Arad et al 1994, T oth et al 1994, Focaccio et al 1995, Svorak et al 1996, Zhang et al 2004) and from isolated cell lines of human cardiac origin (Ljusegren & Andersson 1994, Klinger et al 2001, Hopkins et al 2004, Casals et al 2009). Also, both the A-and B-type peptides have a hypoxia-responsive element in the promoter sequence of their respective genes (Chun et al 2003, Luo et al 2006 and hypoxia has been shown to be a direct and sufficient stimulus for the transcription of the gene encoding B-type peptide (Weidemann et al 2008).…”

mentioning

confidence: 99%

Hypoxia exposure and B‐type natriuretic peptide release from Langendorff heart of rats

et al. 2016

View full text Add to dashboard Cite

AimWe studied whether available oxygen without induced mechanical stretch regulates the release of the biologically active B‐type natriuretic peptide (BNP) from Langendorff heart.MethodsRat hearts were isolated and perfused with a physiological Krebs–Henseleit solution at a constant hydrostatic pressure in Langendorff set‐up. The basal O2 level of perfusate (24.4 ± 0.04 mg L−1) was gradually lowered to 3.0 ± 0.01 mg L−1 over 20 min using N2 gas (n = 7). BNP and O2 level were measured from coronary flow. During control perfusions (n = 5), the O2 concentration was kept at 26.6 ± 0.3 mg L−1.ResultsA low oxygen concentration in the perfusate was associated with a significant increase in BNP release (F = 40.4, P < 0.001). Heart rate decreased when the oxygen concentration in the perfusate reached 9.1 ± 0.02 mg L−1 and continued to fall in lower oxygen concentrations (F = 14.8, P < 0.001). There was also a significant but inverse correlation between BNP and oxygen in the coronary flow (R 2 = 0.27, P < 0.001).ConclusionIn the spontaneously beating Langendorff rat heart, a decreasing concentration of oxygen in the ingoing perfusion increased the secretion of BNP. The effect of oxygen was independent of mechanical stretch of the heart as it occurred even when the heart rate decreased but the pressure conditions remained constant. The difference in the oxygen capacitance of blood and Krebs–Henseleit solution appears to be a major factor affecting secretion of BNP, which is correlated with the oxygen tension of myocardial cells and affected both by the oxygen concentration and capacitance of solution perfusing the heart and by the coronary flow.

show abstract

mentioning

confidence: 99%

Hypoxia exposure and B‐type natriuretic peptide release from Langendorff heart of rats

et al. 2016

View full text Add to dashboard Cite

show abstract

“…One plausible mechanism is that the elevated left atrial pressure caused by myocardial ischemia stimulates secretion of ANP. On the contrary, Uusimaa et al (33) have reported that myocardial ischemia directly stimulates secretion of ANP from the ventricle via energy metabolic mechanism. The secretion of ANP in HCM was closely correlated with tau, and the increase in ANP secretion was not significantly correlated with the increase in LVEDP but with the lactate production during rapid pacing.…”

Section: Discussionmentioning

confidence: 96%

“…Tachycardia is also a stimulation to induce myocardial ischemia. It has been reported that myocardial ischemia per se enhances secretion of ANP in clinical as well as experimental studies (11,13,20,33). Myocardial ischemia has been repeatedly related to a pathophysiological background of HCM (3,6,27,30,34).…”

Section: Discussionmentioning

confidence: 99%

Tachycardia-induced myocardial ischemia and diastolic dysfunction potentiate secretion of ANP, not BNP, in hypertrophic cardiomyopathy

Kido

Hasebe

Ishii

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Kido, Shinsuke, Naoyuki Hasebe, Yoshinao Ishii, and Kenjiro Kikuchi. Tachycardia-induced myocardial ischemia and diastolic dysfunction potentiate secretion of ANP, not BNP, in hypertrophic cardiomyopathy. Am J Physiol Heart Circ Physiol 290: H1064 -H1070, 2006. First published September 19, 2005 doi:10.1152/ajpheart.00110.2005.-The aim of this study was to investigate what factor determines tachycardia-induced secretion of atrial and brain natriuretic peptides (ANP and BNP, respectively) in patients with hypertrophic cardiomyopathy (HCM). HCM patients with normal left ventricular (LV) systolic function and intact coronary artery (n ϭ 22) underwent rapid atrial pacing test. The cardiac secretion of ANP and BNP and the lactate extraction ratio (LER) were evaluated by using blood samples from the coronary sinus and aorta. LV end-diastolic pressure (LVEDP) and the time constant of LV relaxation of tau were measured by a catheter-tip transducer. These parameters were compared with normal controls (n ϭ 8). HCM patients were divided into obstructive (HOCM) and nonobstructive (HNCM) groups. The cardiac secretion of ANP was significantly increased by rapid pacing in HOCM from 384 Ϯ 101 to 1,268 Ϯ 334 pg/ml (P Ͻ 0.05); however, it was not significant in control and HNCM groups. In contrast, the cardiac secretion of BNP was fairly constant and rather significantly decreased in HCM (P Ͻ 0.01). The cardiac ANP secretion was significantly correlated with changes in LER (r ϭ Ϫ0.57, P Ͻ 0.01) and tau (r ϭ 0.73, P Ͻ 0.001) in HCM patients. Tachycardia potentiates the cardiac secretion of ANP, not BNP, in patients with HCM, particularly when it induces myocardial ischemia and LV diastolic dysfunction. left ventricular outflow tract obstruction; lactate extraction ratio; left ventricular diastolic function; cardiac event; atrial and brain natriuretic peptides THE CLINICAL SIGNIFICANCE of natriuretic peptides has been widely accepted in the management of heart failure. The plasma levels of brain natriuretic peptide (BNP) correlate well with the clinical severity of heart failure and hypertrophy (2,8,14). BNP is secreted mainly from the ventricle, whereas atrial natriuretic peptide (ANP) is produced and secreted not only from the atrium but from the ventricle in the hypertrophied heart (4, 23, 32). ANP synthesis is also enhanced in patients with heart failure (21, 36); however, the plasma ANP levels fluctuate more easily compared with BNP levels.The plasma levels of natriuretic peptides have been reported to be increased despite the intact contractile function of the left ventricle (LV) in patients with hypertrophic cardiomyopathy (HCM). The hypertrophied heart is prone to complicate with diastolic dysfunction (35). Tachycardia induces heart failure in patients with hypertrophied LV because diastolic dysfunction can be aggravated by shortening of diastolic phase (1,12,31). Tachycardia is also prone to induce myocardial ischemia even in HCM with angiographically normal coronary arteries. Although rapid pacing linearly increases coro...

show abstract

“…Es wurden auch erhöhte ANP-Konzentrationen durch kurze Ischämien im Bereich des linken Ventrikels bei der percutanen, transluminalen Coronarangioplastie (PTCA) beobachtet (17). Verschiedenste Untersuchungen zeigten ebenfalls, dass links-und rechtsventrikuläre Infarzierungen ein potenter Stimulus für erhöhte ANP-Ausschüt-tungen sind (5,18,22,26,29). Die erhöhten ANP-Konzentrationen bei Ischämie scheinen mit der ventrikulären Dysfunktion sowie mit dem atrialen Druck und der atrialen Dehnung als stärkstem Reiz für die ANP-Ausschüttung positiv korreliert zu sein (10,14,22).…”

Section: Atrial Natriuretic Peptide (Anp)-levels Reveal Mild Postoperunclassified

Das atriale natriuretische Peptid als Indikator einer milden postoperativen kardialen Dysfunktion nach unkomplizierter Bypasschirurgie

Langenbach¹,

Korbmacher

Schulte

et al. 2000

Z Kardiol

View full text Add to dashboard Cite

Plasma levels of ANP (pg/ml; radioimmunoassay) as a parameter for postischemic dysfunction and levels of Troponin T (TnT) (ng/ml; ELISA test) as a parameter for postischemic cellular damage were determined in 15 patients with coronary artery disease (CAD) (mean age: 58 +/- 6.1 years; 13 m, 2 w; with no history of myocardial infarction and no signs for congestive heart failure) prior to, during and after extracorporal circulation (ECC). Under standardized conditions during the ECC basic parameters concerning the cardial hemodynamic (heart rate (HR); systolic (RRsys, mmHg), diastolic pressure (RR dia, mmHg) central venous pressure (CVP, mmHg); left atrial pressure (LAP, mmHg); left ventricular enddiastolic pressure (LVEDP, mmHg)) and ECG monitoring blood samples were performed: 1) prior to operation (op); 2) prior to CPB; 3) 1 h CPB; 4) 5 min after CPB; 5) 1 h after CPB; 6) 6 h postoperative (postop); 7) 24 h postop; 8) 48 h postop; 9) 10 days postop. Also the left atrial diameter (LAD, mm) and the left ventricular enddiastolic diameter at Q (LVEDD, mm) pre- and postop were documented with m-mode echocardiography (Echo) and ejection fraction (EF, %) was calculated. The bypass operations were performed with intermittent aortic cross-clamping with open venae cavae (CVP: 0-5 mmHg) and moderate hypothermia. For the determination of ANP levels and TnT levels in arterial and venous blood, a double-antibody (AB) radioimmunoassay and an ELISA test were used. Concerning the patients with CAD there was a maximal increase of ANP from preoperative 90 +/- 10 (M +/- SEM) pg/ml (p < 0.05) up to intraoperative 380 +/- 38 pg/ml. Ten days postop, the ANP level was with 262 +/- 33 pg/ml still increased threefold in comparison to the preoperative level. TnT showed an increase from preoperative 0.02 +/- 0.01 ng/ml up to intraoperative 3.44 +/- 0.47 ng/ml. Ten days postop the TnT concentration was at the preoperative level with 0.13 +/- 0.11 ng/ml. Five minutes after bypass up to 48 h postop, ANP and TnT levels were correlated (p < 0.05, r = 3.4). There was an increase of the LAD from preoperative 42.2 +/- 1.1 mm up to 46.8 +/- 1.2 mm (p < 0.05) 10 days postop as determined by m-mode echo. LVEDD and EF changed from preoperative 51.1 +/- 0.9 mm and 73 +/- 2% to 54.5 +/- 1.2 mm and 65 +/- 4% 10 days postop. The significant increase of TnT (172-fold) indicates the cellular, myocardial injury, caused by the operation without signs in ECG recordings and no signs of congestive heart failure. The significantly increased ANP level up to the 10th day postop indicate sa very sensitive prolonged, postischemic dysfunction, which is not compensated 10 days postop.

show abstract

Ischemia stimulates the release of atrial natriuretic peptide from rat cardiac ventricular myocardium in vitro

Cited by 17 publications

References 35 publications

Hypoxia exposure and B‐type natriuretic peptide release from Langendorff heart of rats

Hypoxia exposure and B‐type natriuretic peptide release from Langendorff heart of rats

Tachycardia-induced myocardial ischemia and diastolic dysfunction potentiate secretion of ANP, not BNP, in hypertrophic cardiomyopathy

Das atriale natriuretische Peptid als Indikator einer milden postoperativen kardialen Dysfunktion nach unkomplizierter Bypasschirurgie

Contact Info

Product

Resources

About