title: Viral infection potentiates the increase in airway blood flow produced by substance P.
abstract: We examined the effect of respiratory tract infection with Sendai virus on the responsiveness of airway blood flow to substance P (SP) in rats. Pathogen-free rats were inoculated with either Sendai virus suspension or sterile viral growth medium into each nostril. Five days later, we measured airway and esophageal blood flows before and immediately after injection of SP or histamine into the left ventricle of rats in both groups using a modification of the reference-sample microsphere technique. Viral infection potentiated the increase in airway blood flow evoked by SP but not by histamine. We also examined the effect of neutral endopeptidase (NEP) and angiotensin-converting enzyme (ACE) on the SP-induced increase in airway blood flow. Both phosphoramidon (NEP inhibitor) and captopril (ACE inhibitor) potentiated the increase in airway blood flow produced by SP in pathogen-free rats. In the presence of both peptidase inhibitors, a submaximal dose of SP increased blood flow to a similar level in infected and pathogen-free rats. Thus decreased activity of both ACE and NEP may be involved in the exaggerated increase in airway blood flow evoked by SP in virus-infected rats.
authors.affiliation: Cardiovascular Research Institute, University of California, San Francisco 94143-0130, USA.
authors.forename: I
authors.initials: I
authors.lastname: Yamawaki
authors.forename: P
authors.initials: P
authors.lastname: Geppetti
authors.forename: C
authors.initials: C
authors.lastname: Bertrand
authors.forename: B
authors.initials: B
authors.lastname: Chan
authors.forename: P
authors.initials: P
authors.lastname: Massion
authors.forename: G
authors.initials: G
authors.lastname: Piedimonte
authors.forename: J A
authors.initials: JA
authors.lastname: Nadel
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D002216:Captopril / Q000494:pharmacology; D015536:Down-Regulation / Q000502:physiology; D006020:Glycopeptides / Q000494:pharmacology; D006632:Histamine / Q000494:pharmacology; D008297:Male; D008863:Microspheres; D015260:Neprilysin / Q000037:antagonists & inhibitors / Q000378:metabolism; D010222:Parainfluenza Virus 1, Human; D018184:Paramyxoviridae Infections / Q000503:physiopathology*; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D011480:Protease Inhibitors / Q000494:pharmacology; D051381:Rats; D011916:Rats, Inbred F344; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D012137:Respiratory System / Q000098:blood supply* / Q000187:drug effects / Q000503:physiopathology; D013373:Substance P / Q000494:pharmacology*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D006020:Glycopeptides; D011480:Protease Inhibitors; D013373:Substance P; D006632:Histamine; D002216:Captopril; D007703:Peptidyl-Dipeptidase A; D015260:Neprilysin; C008890:phosphoramidon