Microvascular permeability and number of tight junctions are modulated by cAMP

R. H. Adamson, B. Liu, G. Nilson Fry, L. L. Rubin, F. E. Curry

Research output: Contribution to journalArticlepeer-review


We tested the hypothesis that increased endothelial cell adenosine 3',5'-cyclic monophosphate (cAMP) decreases microvascular permeability in vivo. The effects of cAMP-specific phosphodiesterase type IV inhibition and adenylate cyclase activation on microvascular hydraulic conductivity (L(p)) were investigated in intact individual capillaries and postcapillary venules in mesentery of pithed frogs (Rana pipiens). Treatment with rolipram (10 μM) and forskolin (5 μM) for 25 min decreased L(p) to 37% of control. Rolipram alone also significantly decreased L(p). Isoproterenol (10 μM) decreased L(p) to 27% of control within 20 min. A subgroup of eight vessels treated with rolipram and forskolin, in which mean L(p) fell to 25% of control, was examined with transmission electron microscopy. The mean number of tight junctions in the treated vessels was 2.2 per cleft (303 clefts), significantly higher than in a matched control group (192 clefts), which was 1.7 per cleft. The results indicate that microvascular L(p) can be modulated by intracellular cAMP and that one of the structural end points of stimulated cAMP levels is an increase in the mean number of tight-junction strands between endothelial cells.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number6 43-6
StatePublished - 1998
Externally publishedYes


  • Capillary permeability
  • Intercellular adhesion
  • Intercellular junctions
  • Vascular endothelium

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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