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Effect of a fibrin-derived vasoactive peptide on pulmonary angiotensin converting enzyme activity and on pressure responses to bradykinin.
J Pharmacol Exp Ther. 1987 Dec; 243(3):897-900.JP

Abstract

Decreased angiotensin converting enzyme (ACE) activity is a common finding in patients with adult respiratory distress syndrome and in animal models of lung injury. The nature of this effect is unknown. Intravascular fibrin, also a common finding in lung injury, is degraded to small peptides by proteolytic enzymes. Peptide 6A, corresponding to amino acid residues 43 to 47 of the B beta chain of fibrin(ogen), is produced by plasmin degradation of fibrin and has been shown to inhibit ACE in vitro. We investigated the effect of this peptide on the pulmonary hydrolysis of a synthetic ACE substrate, benzoyl-phenylalanyl-alanyl-proline, in anesthetized rabbits and in isolated, perfused rabbit lungs. Peptide 6A caused a reversible, dose-dependent inhibition of benzoyl-phenylalanyl-alanyl-proline hydrolysis. It also potentiated the increase in pulmonary arterial pressure and the decrease in systemic arterial pressure due to bradykinin (BK), as well as the increase in pulmonary artery pressure due to BK in isolated lungs. The amount of BK needed to increase pulmonary arterial pressure was about 1000-fold larger in the isolated lung than in the intact animal. Peptides of this type might contribute to decreased ACE activity in patients with adult respiratory distress syndrome and may potentiate BK-mediated hemodynamic changes in these patients.

Authors+Show Affiliations

Department of Medicine, Rhode Island Hospital, Providence.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

3694536

Citation

Moalli, R, et al. "Effect of a Fibrin-derived Vasoactive Peptide On Pulmonary Angiotensin Converting Enzyme Activity and On Pressure Responses to Bradykinin." The Journal of Pharmacology and Experimental Therapeutics, vol. 243, no. 3, 1987, pp. 897-900.
Moalli R, Saldeen K, Saldeen T. Effect of a fibrin-derived vasoactive peptide on pulmonary angiotensin converting enzyme activity and on pressure responses to bradykinin. J Pharmacol Exp Ther. 1987;243(3):897-900.
Moalli, R., Saldeen, K., & Saldeen, T. (1987). Effect of a fibrin-derived vasoactive peptide on pulmonary angiotensin converting enzyme activity and on pressure responses to bradykinin. The Journal of Pharmacology and Experimental Therapeutics, 243(3), 897-900.
Moalli R, Saldeen K, Saldeen T. Effect of a Fibrin-derived Vasoactive Peptide On Pulmonary Angiotensin Converting Enzyme Activity and On Pressure Responses to Bradykinin. J Pharmacol Exp Ther. 1987;243(3):897-900. PubMed PMID: 3694536.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effect of a fibrin-derived vasoactive peptide on pulmonary angiotensin converting enzyme activity and on pressure responses to bradykinin. AU - Moalli,R, AU - Saldeen,K, AU - Saldeen,T, PY - 1987/12/1/pubmed PY - 1987/12/1/medline PY - 1987/12/1/entrez SP - 897 EP - 900 JF - The Journal of pharmacology and experimental therapeutics JO - J Pharmacol Exp Ther VL - 243 IS - 3 N2 - Decreased angiotensin converting enzyme (ACE) activity is a common finding in patients with adult respiratory distress syndrome and in animal models of lung injury. The nature of this effect is unknown. Intravascular fibrin, also a common finding in lung injury, is degraded to small peptides by proteolytic enzymes. Peptide 6A, corresponding to amino acid residues 43 to 47 of the B beta chain of fibrin(ogen), is produced by plasmin degradation of fibrin and has been shown to inhibit ACE in vitro. We investigated the effect of this peptide on the pulmonary hydrolysis of a synthetic ACE substrate, benzoyl-phenylalanyl-alanyl-proline, in anesthetized rabbits and in isolated, perfused rabbit lungs. Peptide 6A caused a reversible, dose-dependent inhibition of benzoyl-phenylalanyl-alanyl-proline hydrolysis. It also potentiated the increase in pulmonary arterial pressure and the decrease in systemic arterial pressure due to bradykinin (BK), as well as the increase in pulmonary artery pressure due to BK in isolated lungs. The amount of BK needed to increase pulmonary arterial pressure was about 1000-fold larger in the isolated lung than in the intact animal. Peptides of this type might contribute to decreased ACE activity in patients with adult respiratory distress syndrome and may potentiate BK-mediated hemodynamic changes in these patients. SN - 0022-3565 UR - https://www.unboundmedicine.com/medline/citation/3694536/Effect_of_a_fibrin_derived_vasoactive_peptide_on_pulmonary_angiotensin_converting_enzyme_activity_and_on_pressure_responses_to_bradykinin_ L2 - https://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=3694536 DB - PRIME DP - Unbound Medicine ER -