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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.

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.

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