Canine pulmonary vasoreactivity to serotonin: Role of protein kinase C and tyrosine kinase

Scott A. Barman, James R. Pauly, Carlos M. Isales

Research output: Contribution to journalArticlepeer-review

15 Scopus citations


The role of protein kinase C- and protein tyrosine kinase-mediated signal transduction in the canine pulmonary vascular response to serotonin (5-HT) was determined in the isolated blood-perfused dog lung. Pulmonary vascular resistances and compliances were measured with vascular occlusion techniques. 5-HT (10-5 M) significantly increased precapillary resistance by ~150% and postcapillary resistance twofold and significantly decreased total vascular compliance to ~50% of control values by decreasing large- vessel compliance and middle-compartment compliance. The 5-HT2-receptor blocker ketanserin (10-7 M), the protein kinase C inhibitor staurosporine (10-7 M), the voltage-dependent Ca2+-channel blocker verapamil (10-5 M), and the specific protein tyrosine kinase inhibitors genistein (5 x 10- 4 M) and tyrphostin 25 (5 x 10-4 M) completely inhibited the pressor response to 5-HT, whereas the 5-HT1-receptor antagonist (-)pindolol (10-7 M) had no significant effect on the serotonergic response. These results indicate that the canine pulmonary vascular response to 5-HT involves activation of 5-HT2 receptors and suggests that this receptor signal transduction pathway involves protein kinase C and tyrosine kinase and the activation of voltage-dependent Ca2+ channels.

Original languageEnglish
Pages (from-to)H740-H747
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number2 41-2
StatePublished - Feb 1997


  • genistein
  • ketanserin
  • pulmonary capillary pressure
  • pulmonary vascular compliance
  • pulmonary vascular resistance
  • staurosporine
  • tyrphostin 25
  • vasoconstriction
  • verapamil
  • voltage-dependent calcium channels

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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