Protein kinase C modulates microvascular permeability through nitric oxide synthase

María M. Ramírez, David D. Kim, Walter Duran

Research output: Contribution to journalArticle

Abstract

Protein kinase C (PKC) serves important functions in signal transduction. We hypothesized that PKC modulation of microvascular permeability to macromolecules is mediated by nitric oxide (NO). To test this hypothesis, we stimulated PKC topically with 10-7 M phorbol 12,13- dibutyrate (PDBu) in the hamster cheek pouch microcirculation. N(G)- monomethyl-L-arginine (L-NMMA) at 10-4 M was superfused in a bicarbonate buffer solution throughout the experiment to inhibit the activity of NO synthase. We evaluated changes in transport of fluorescein isothiocyanate- labeled 150,000 mol wt dextran by integrated optical intensity (IOI) using intravital fluorometry and computer-assisted digital image analysis. Postcapillary areas were recorded, PDBu increased IOI from baseline to a value of 46.8 ± 6.3 units (±SE). Pretreatment with L-NMMA decreased the PDBu-stimulated increment to 10.8 ± 0.9 units. These results demonstrate that PKC-activated modulation of macromolecular transport operates through a mechanism involving the production of NO.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume271
Issue number4 40-4
StatePublished - Oct 1 1996

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Capillary Permeability
Phorbol 12,13-Dibutyrate
Nitric Oxide Synthase
Protein Kinase C
omega-N-Methylarginine
Nitric Oxide
Fluorometry
Computer-Assisted Image Processing
Cheek
Microcirculation
Bicarbonates
Dextrans
Fluorescein
Cricetinae
Arginine
Signal Transduction
Buffers

All Science Journal Classification (ASJC) codes

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

Cite this

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Protein kinase C modulates microvascular permeability through nitric oxide synthase. / Ramírez, María M.; Kim, David D.; Duran, Walter.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 271, No. 4 40-4, 01.10.1996.

Research output: Contribution to journalArticle

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