Transient myocardial ischemia stimulates atrial natriuretic factor release

Malatino, Lorenzo; Leonardi, Carmelo; Stancanelli, Benedetta; Polizzi, Gaetano; Grassi, Rosario; Tamburino, Corrado; Tamburino, G

doi:10.1016/0002-8703(92)90508-s

Cited by 26 publications

(15 citation statements)

References 18 publications

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“…Our results support the findings of Bibbins-Domingo et al 1 ; however, we propose that N-ANP may be more useful for the discrimination of clinically significant coronary artery stenosis than BNP because of its different sites of production, mechanisms of release, and metabolic characteristics. 3 Both BNP and proBNP were markedly elevated (5-and 10-fold, respectively) in those patients as compared with individuals without coronary artery disease. Moreover, the BNP and proBNP plasma concentrations were closely associated.…”

Section: To the Editormentioning

confidence: 87%

“…Interestingly, within a group of patients undergoing coronary artery bypass surgery, the extent of elevation of both plasma BNP and proBNP concentrations in each patient was positively associated with the ventricular BNP mRNA content. 3 These data suggest that both BNP and proBNP are sensitive markers of chronic cardiac ischemia and that the elevated plasma concentrations reflect an increased BNP gene transcription. In studies of pigs, we recently found that even acute cardiac hypoxia induces BNP gene expression in the ventricular myocardium and an increase of the plasma proBNP concentration.…”

mentioning

confidence: 84%

“…[2][3][4] However, whether plasma BNP levels are increased in patients with coronary artery stenosis who have normal left ventricular function remains unknown. To examine whether coronary artery stenosis affects plasma ANP, N-ANP, and BNP levels, we recently measured these peptide levels in 104 patients with normal left ventricular systolic function who had a suspected diagnosis of angina pectoris.…”

Section: To the Editormentioning

confidence: 99%

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Letters Regarding Article by Bibbons-Domingo et al, “B-Type Natriuretic Peptide and Ischemia in Patients With Stable Coronary Disease: Data From the Heart and Soul Study”

Nishikimi

Matsuoka

2005

Circulation

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We read with great interest the recent article by BibbinsDomingo et al 1 on plasma brain natriuretic peptide (BNP) in outpatients with stable coronary disease. They concluded that elevated levels of BNP are independently associated with inducible ischemia in outpatients with stable coronary disease, particularly among those who have a history of myocardial infarction.Previous studies have demonstrated that transient myocardial ischemia stimulates the secretion of atrial natriuretic peptide (ANP) and N-terminal ProANP (N-ANP); because of its longer half-life, N-ANP may be a better marker than ANP for the detection of high-grade coronary artery stenosis. 2-4 However, whether plasma BNP levels are increased in patients with coronary artery stenosis who have normal left ventricular function remains unknown. To examine whether coronary artery stenosis affects plasma ANP, N-ANP, and BNP levels, we recently measured these peptide levels in 104 patients with normal left ventricular systolic function who had a suspected diagnosis of angina pectoris. 5 Plasma levels of all 3 of these natriuretic peptides were higher in patients with coronary artery stenosis (major coronary artery stenosis Ͼ75%) (nϭ65) than in those without stenosis (nϭ39), whereas hemodynamic variables were similar. Multiple logistic regression analysis revealed that N-ANP (per 100 fmol/mL increase; odds ratioϭ1.9 [95% CIϭ1.2 to 2.6], PϽ0.01), but not ANP (per 10 pg/mL increase; odds ratioϭ0.9 [95% CIϭ0.5 to 1.2], Pϭ0.41) or BNP (per 10 pg/mL increase; odds ratioϭ1.1 [95% CIϭ0.8 to 1.4], Pϭ0.73), was independently associated with coronary artery stenosis after adjusting for clinical and demographic variables. Furthermore, we measured these natriuretic peptides before and 3 to 6 months after percutaneous coronary intervention in patients with myocardial infarction of recent onset (nϭ58). Plasma levels of ANP, N-ANP, and BNP significantly decreased in patients without restenosis (nϭ46) (ANP, 91Ϯ15 to 39Ϯ7 pg/mL; BNP, 134Ϯ28.9 to 41Ϯ9 pg/mL; N-ANP, 688Ϯ81 to 407Ϯ52 fmol/mL; all PϽ0.05).In contrast, these natriuretic peptide levels did not change after coronary intervention in patients with restenosis (nϭ12) (ANP, 57Ϯ19 to 50Ϯ20; BNP, 102Ϯ35 to 57Ϯ13; N-ANP, 567Ϯ178 to 508Ϯ126; all NS). Our results support the findings of Bibbins-Domingo et al 1 ; however, we propose that N-ANP may be more useful for the discrimination of clinically significant coronary artery stenosis than BNP because of its different sites of production, mechanisms of release, and metabolic characteristics. To the Editor:We read the correspondence 1 about the article by BibbinsDomingo et al 2 with great interest. The report by BibbinsDomingo et al 2 demonstrated elevated plasma concentrations of B-type natriuretic peptide (BNP) associated with inducible ischemia in patients with stable coronary artery disease. In contrast, Nishikimi and Matsuoka 1 suggested that N-terminal proANP (atrial natriuretic peptide) might be a more sensitive plasma marker of stable coronary artery disease than are...

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Section: To the Editormentioning

confidence: 87%

mentioning

confidence: 84%

Section: To the Editormentioning

confidence: 99%

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Letters Regarding Article by Bibbons-Domingo et al, “B-Type Natriuretic Peptide and Ischemia in Patients With Stable Coronary Disease: Data From the Heart and Soul Study”

Nishikimi

Matsuoka

2005

Circulation

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“…High levels of circulating ANF have been described during percutaneous transluminal coro nary angioplasty [10,11], as well as following dipyrida mole-dependent myocardial ischemia associated with a marked rise in ischemic regional wall stress [13]. In the latter study ANF was measured in a single blood sample at 'peak dipyridamole', and the patients were not studied under placebo infusion.…”

Section: Discussionmentioning

confidence: 99%

“…Atrial natriuretic factor (ANF) promotes diuresis and natriuresis, and interacts with the renin-angiotensin sys tem in experimental animal models and in man [1,2] whereas its role in the regulation of the peripheral vascu culating ANF was reported to rise after moycardial infarc tion [9] while little information is available on its levels during transient myocardial ischemia [10,11]. The dipy ridamole echocardiography test (DET) is used as screen ing procedure in patients with coronary artery disease (CAD): it causes an ischemia-induced reduction of region al left ventricular (LV) function with dyssynergy detect able by ultrasound [12].…”

Section: Introductionmentioning

confidence: 99%

Atrial Natriuretic Factor Release during Transient Myocardial Ischemia: A Placebo-Controlled Study in Man

Cassisa¹,

Tonolo²,

Glorioso³

et al. 1993

Am J Noninvas Cardiol

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Atrial natriuretic factor (ANF) exerts a vasodilatory effect on the coronary bed in myocardial ischemia. Besides wall stretch, ANF release can also be triggered by endothelin in experimental models. We studied the time course of ANF release and its relationship with endothelin during transient myocardial ischemia in man. Twelve patients subjected to the dipyridamole echocardiography test (DET) in a single-blind, randomly balanced, placebo-controlled setting were studied. Circulating ANF and endothelin were monitored during both dipyridamole and placebo. Dipyridamole caused left ventricular (LV) dyssynergy in 6 patients (group 1: multiple or isolated coronary artery stenosis) and acute left atrial dilation in 5 out of 6. In these 5 patients, a progressive rise of circulating ANF was found soon after LY dyssynergy, starting from time +8 min (55 ± 12 vs. 40 ± 7 at time 0 and 42 ± 8 pmol/1 time-matched placebo, p < 0.05 for both), becoming highly significantly different from + 10 min (72 ± 13 vs. 40 ± 7 at time 0 and vs. 47 ± 5 pmol/1 time-matched placebo, p < 0.01 for both) up to the end of the study (+40 min). Circulating ANF and echocardiographie parameters did not vary in the other 6 patients undergoing the DET (group 2) as well as during placebo in both groups. The DET caused heart rate and the rate-pressure products to increase to the same extent in both groups (+12 and +13%; +13 and +15%, respectively). Circulating endothelin did not vary. The consistent and long-lasting rise of circulating ANF in patients with coronary artery disease during transient myocardial ischemia indicate that ANF measurements during chest pain may be an important marker of the reduction in myocardial perfusion and LV dysfunction. Further studies will indicate if ANF may play a physiological role to attenuate anginal attacks.

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Intracoronary and systemic release of the atrial natriuretic factor and cyclic-guanosine monophosphate during coronary angioplasty

et al. 1996

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This study was undertaken to investigate intracoronary production and systemic release of the atrial natriuretic factor (ANF) and cyclic-guanosine monophosphate (c-GMP) during coronary angioplasty (PTCA). Three coronary blood samples were collected, through a balloon catheter, from the area distal to the lesion: before balloon inflation, at maximum inflation and 5 min later. Four additional venous samples were collected: before PTCA, and 5 min, 2 h and 24 h after the procedure. Local intracoronary c-GMP production increased from the baseline level of 7.5 + 0.9 pmol/ml to 11.1 + 1.3 pmol/ml at maximum balloon inflation (p < 0.01) and decreased 5 min later to 9.5 + 1.0 pmol/ml (p = NS). In contrast, intracoronary ANF production failed to show any significant change at any time during the procedure. Peripheral venous ANF levels increased from 79.1 + 11.1 pmol/ml to 99.9 + 16.6 pmol/ml 5 min after balloon inflation (p < 0.05) and gradually decreased 2 h (91.9 + 13.6 pmol/ml) and 24 h (85.6 + 10.4 pmol/ml) after the procedure. Similarly, peripheral venous c-GMP levels increased from 11.3 + 1.7 pmol/ml before PTCA to 14.9 + 1.9 pmol/ml 5 min after balloon inflation (p < 0.05), and then gradually decreased 2 h (10.8 + 1.4 pmol/ml) and 24 h (8.2 + 1.4 pmol/ml) after the procedure (p < 0.01 and < 0.0001 compared to the peak value, respectively). In conclusion, acute vessel occlusion and distension during balloon inflation stimulates intracoronary c-GMP production without affecting ANF release.

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Transient myocardial ischemia stimulates atrial natriuretic factor release

Cited by 26 publications

References 18 publications

Letters Regarding Article by Bibbons-Domingo et al, “B-Type Natriuretic Peptide and Ischemia in Patients With Stable Coronary Disease: Data From the Heart and Soul Study”

Letters Regarding Article by Bibbons-Domingo et al, “B-Type Natriuretic Peptide and Ischemia in Patients With Stable Coronary Disease: Data From the Heart and Soul Study”

Atrial Natriuretic Factor Release during Transient Myocardial Ischemia: A Placebo-Controlled Study in Man

Intracoronary and systemic release of the atrial natriuretic factor and cyclic-guanosine monophosphate during coronary angioplasty

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