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Viral infection potentiates the increase in airway blood flow produced by substance P
I Yamawaki1, P Geppetti, C Bertrand
1Cardiovascular Research Institute, University of California, San Francisco 94143-0130, USA.
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.
Insights
Respiratory tract infection with Sendai virus exaggerates airway blood flow responses to substance P (SP) in rats. This effect may be due to decreased activity of angiotensin-converting enzyme (ACE) and neutral endopeptidase (NEP).
Area of Science:
- Respiratory physiology
- Immunology
- Pharmacology
Background:
- Respiratory tract infections can alter physiological responses.
- Substance P (SP) plays a role in regulating airway blood flow.
- The impact of viral infections on SP-mediated vascular responses is not fully understood.
Purpose of the Study:
- To investigate the effect of Sendai virus infection on airway blood flow responsiveness to SP in rats.
- To explore the role of neutral endopeptidase (NEP) and angiotensin-converting enzyme (ACE) in SP-induced airway hyperemia during viral infection.
Main Methods:
- Rats were inoculated with Sendai virus or a control medium.
- Airway and esophageal blood flows were measured using the microsphere technique.
- Responses to SP and histamine were assessed before and after viral inoculation.
- The effects of NEP and ACE inhibitors (phosphoramidon and captopril) were evaluated.
Main Results:
- Sendai virus infection potentiated the increase in airway blood flow induced by SP, but not by histamine.
- NEP and ACE inhibitors potentiated SP-induced airway hyperemia in pathogen-free rats.
- Combined inhibition of NEP and ACE normalized the SP-induced blood flow increase in infected rats to levels seen in pathogen-free rats.
Conclusions:
- Sendai virus infection enhances airway blood flow responses to SP.
- Reduced activity of ACE and NEP likely contributes to the exaggerated SP-mediated hyperemia in virus-infected rats.
- These findings suggest a mechanism for altered airway vascular regulation during respiratory viral infections.