Key result
High concentrations of BNP acted as a partial agonist in small human pulmonary arteries and inhibited relaxation to ANP.
Why the study?
Increasing levels of circulating ANP and BNP are associated with worsening heart failure and poor prognosis, leading investigators to test whether high BNP concentrations inhibit relaxation to ANP.
Does a high concentration of BNP inhibit relaxation to ANP in small human pulmonary arteries?
Does a high concentration of BNP inhibit relaxation to ANP in small human pulmonary arteries?
High concentrations of BNP may inhibit ANP-mediated relaxation in human pulmonary arteries, potentially contributing to decompensated heart failure and explaining the disappointing results of natriuretic peptide analogues in clinical trials.
Answers are grounded in this paper and cite their sources.
May blunt ANP-mediated pulmonary relaxation in decompensated HF; hypothesis-generating for natriuretic peptide analogue trial failures.
BACKGROUND: The prevalence of cardiovascular diseases, especially heart failure, continues to rise worldwide. In heart failure, increasing levels of circulating atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are associated with a worsening of heart failure and a poor prognosis. AIM: To test whether a high concentration of BNP would inhibit relaxation to ANP. METHODS: ), and concentration response curves were constructed to vasodilators by cumulative addition to the myograph chambers. CONCLUSION: BNP could be acting as a partial agonist in small human pulmonary arteries, and inhibits relaxation to ANP. Elevated levels of circulating BNP could be responsible for the worsening of decompensated heart failure. This finding could also explain the disappointing results seen in clinical trials of ANP and BNP analogues for the treatment of heart failure.
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Hussain et al. (2019) studied Heart failure. Brain natriuretic peptide (BNP) was evaluated on Relaxation to ANP (p=0.28). High concentrations of BNP acted as a partial agonist in small human pulmonary arteries and inhibited relaxation to ANP.
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