You should seek the advice of your veterinarian if your pet is ill as only he or she can correctly advise on the diagnosis and recommend the treatment that is most appropriate for your pet.

BNP is a peptide hormone produced by the heart. A commercial assay for canine and Feline BNP has been developed

Brain natriuretic peptide (BNP) is produced mainly by the ventricles of the heart, although much higher concentrations (x100) are found in the atria. The plasma half-life of atrial natriuretic peptide (ANP) is only about 3 minutes, whereas the half-life of BNP is 22 minutes.

BNP secretion is increased in response to stretching of the cardiac wall, and this hormone stimulates the kidneys to excrete salt and water. So, BNP has the opposite action to angiotensin II.

Circulating plasma BMP concentrations are increased in human patients with a variety of asymptomatic cardiac disorders including

Canine Interpretation

NT-pro-BNP levels less than 900 pmol/L are found in normal healthy dogs and it is unlikely that the clinical signs are related to cardiac failure.

NT-pro-BNP levels between 900 and 1800 pmol/L are in the suspect range and in the absence of a murmur or common clinical signs, heart disease is unlikely.

NT-pro-BNP levels greater than 1800 pmol/L Heart disease is likely.
Further investigation and other tests should be performed to confirm this.

Feline Interpretation

NT-pro-BNP levels less than 100 pmol/L are found in normal healthy cats and it is unlikely that the clinical signs are related to cardiac failure.

NT-pro-BNP levels between 100 and 270 pmol/L are in the suspect range and in the absence of a murmur or common clinical signs, heart disease is unlikely.

2003 Mar-Apr;17(2):172-7.

Brain natriuretic peptide concentration in dogs with heart disease and congestive heart failure.

MacDonald KA¹, Kittleson MD, Munro C, Kass P.

Author information

Abstract

Plasma brain natriuretic peptide concentration ([BNP]) is high in humans with cardiac disease and is further increased with congestive heart failure (CHF). The hypotheses of this study were that dogs with moderate to severe mitral regurgitation due to myxomatous mitral valve disease (MVD) would have increased plasma [BNP] compared to normal dogs, that plasma [BNP] would be higher in dogs with CHP, and that plasma [BNP] would predict premature death from cardiovascular disease. The study population consisted of 34 dogs: 9 normal dogs and 25 dogs with MVD. Patients were divided into 4 groups: group 1-10 dogs with moderate to severe MVD and no radiographic evidence of CHF; group II--6 dogs with severe MVD and mild CHF; group III--7 dogs with severe MVD and moderate CHF; and group IV--2 dogs with severe MVD and severe CHF. Diagnostic tests included thoracic radiographs, an echocardiogram, a serum chemistry profile, and the measurement of plasma [BNP] by a canine-specific radioimmunoassay. There was a significant positive correlation between the plasma [BNP] and heart disease/failure groups (P = .0036). Plasma [BNP] increased with progressively increasing severity of MVD and CHE Group I dogs had higher plasma [BNP] than did control dogs (P < .0001), and plasma [BNP] was higher in dogs with CHF (groups II-IV versus group I; P = .012). Plasma [BNP] was also weakly positively correlated with left atrial size (r = 0.43, P = .04). For every 10-pg/mL increase in plasma [BNP], the mortality rate over 4 months' time increased approximately 44%.