Background: The basic and clinical implications of evaluating plasma atrial natriuretic peptide (ANP) concentration in calves are unknown.
Objective: To investigate the relationship between the plasma ANP concentration and left ventricular end-diastolic pressure (LVEDP) in healthy calves subjected to volume overload (Study 1), and to compare the plasma ANP concentration in calves with or without heart disease (Study 2).
Animals: Six healthy calves were used in Study 1; disease calves and sick calves with (n = 9) and without congenital heart disease (CHD) (n = 9) were used in Study 2.
Methods: In Study 1, LVEDP in anesthetized calves was manipulated by IV administration of acetated Ringer's solution (rate of 100 mL/kg/h for 20 minutes) and furosemide. In Study 2, disease calves were identified by blood examination and echocardiography or pathological examination. The plasma ANP concentration was determined by a chemiluminescence enzyme immunoassay for human alpha-ANP.
Results: In Study 1, preloading significantly increased the plasma ANP concentration (36 +/- 20-185 +/- 156, P < .01) and LVEDP (-11 +/- 7-2 +/- 12, P < .01) from the baseline. Furthermore, plasma ANP concentrations were strongly correlated with LVEDP (r= 0.61). In Study 2, the plasma ANP concentration was significantly higher in the calves with CHD than in the calves without heart disease (220 [67-970] versus 31 [10-86]; mean [range], P < .001).
Conclusions And Clinical Importance: Measurement of plasma ANP concentrations in calves can provide additional information useful for predicting hemodynamic abnormalities.
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http://dx.doi.org/10.1111/j.1939-1676.2009.0293.x | DOI Listing |
J Cell Mol Med
December 2024
Inserm, CHU Lille, Institut Pasteur de Lille, U1167-RID-AGE, Université de Lille, Lille, France.
Chronic pressure overload induces adverse cardiac remodelling characterised by left ventricular (LV) hypertrophy and fibrosis, leading to heart failure (HF). Identification of new biomarkers for adverse cardiac remodelling enables us to better understand this process and, consequently, to prevent HF. We recently identified clusterin (CLU) as a biomarker of cardiac remodelling and HF after myocardial infarction.
View Article and Find Full Text PDFCoron Artery Dis
December 2024
Department of Cardiology.
Cardiovasc Toxicol
December 2024
Department of Cardiology, First Affiliated Hospital, Harbin Medical University, No. 23 YouZheng Street, NanGang District, Harbin, 150001, Heilongjiang, China.
Sci Adv
October 2024
Institute of Metabolic and Cardiovascular Diseases, INSERM/Paul Sabatier University, UMR1297, Team MetaDiab, Toulouse, France.
Am J Physiol Renal Physiol
December 2024
Tulane Hypertension and Renal Center of Excellence and Department of Physiology, Tulane University School of Medicine, New Orleans, Louisiana, United States.
In the proximal tubules of the kidney, angiotensin II (ANG II) binds and activates ANG II type 1 (AT) receptors to stimulate proximal tubule Na reabsorption, whereas atrial natriuretic peptide (ANP) binds and activates natriuretic peptide receptors (NPR) to inhibit ANG II-induced proximal tubule Na reabsorption. These two vasoactive systems play important counteracting roles to control Na reabsorption in the proximal tubules and help maintain blood pressure homeostasis. However, how AT and NPR receptors interact in the proximal tubules and whether natriuretic effects of NPR receptor activation by ANP may be potentiated by deletion of AT (AT) receptors selectively in the proximal tubules have not been studied previously.
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