PMID- 20083858
OWN - NLM
STAT- MEDLINE
DCOM- 20100407
LR  - 20131121
IS  - 1899-1505 (Electronic)
IS  - 0867-5910 (Linking)
VI  - 60 Suppl 4
DP  - 2009 Oct
TI  - Caveolae, caveolin and control of vascular tone: nitric oxide (NO) and 
      endothelium derived hyperpolarizing factor (EDHF) regulation.
PG  - 105-9
AB  - Endothelium plays a crucial role in the regulation of cardiovascular homeostasis 
      through the release of vasoactive factors. Nitric oxide (NO) and 
      endothelium-derived hyperpolarizing factors (EDHF) are the two major actors 
      controlling the vasomotor tone. The endothelial nitric oxide synthase (eNOS) was 
      reported in the mid 90ies to be under the control of caveolin, the structural 
      protein of caveolae. Nowadays, a large body of evidence has confirmed that the 
      caveolin/eNOS interaction was needed to prevent inadequate NO production under 
      basal conditions but also to facilitate the integration of extracellular stimuli 
      to intracellular NO signals. Compartmentation of key actors in the EDHF signaling 
      pathway is now also proposed to take place into caveolae. Accordingly, 
      caveolin-deficient animals revealed both an unopposed NO production promoting 
      vessel dilation and a lack of EDHF-driven vasorelaxation. The transient receptor 
      potential (TRP) channels are the link between caveolae and EDHF. Different TRP 
      channels involved in the capacitative calcium entry were found to directly 
      interact with caveolin-1 in endothelial cells. TRPC1 and TRPC4 form a complex 
      with the endoplasmic reticulum IP3 receptor thereby optimizing calcium signaling. 
      EDHF-driven vasodilation was documented to be altered in a TRPV4-deficient mouse 
      model. The close vicinity between TRPV4 and SKCa channels in caveolae together 
      with the gap-junctions subunits connexins support a role of these microdomains in 
      the generation and propagation of EDHF to vascular smooth muscle cells. In 
      conclusion, caveolae and caveolin are important control points in the control of 
      blood pressure by the endothelium. This also highlights how any alteration in the 
      caveolae integrity or caveolin abundance may lead to and/or exacerbate 
      endothelial dysfunction and associated cardiovascular diseases.
FAU - Rath, G
AU  - Rath G
AD  - Unit of Pharmacology and Therapeutics, Universite Catholique de Louvain, UCL-FATH 
      5349, 52 Avenue E. Mounier, B-1200 Brussels, Belgium.
FAU - Dessy, C
AU  - Dessy C
FAU - Feron, O
AU  - Feron O
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Poland
TA  - J Physiol Pharmacol
JT  - Journal of physiology and pharmacology : an official journal of the Polish 
      Physiological Society
JID - 9114501
RN  - 0 (Biological Factors)
RN  - 0 (Caveolins)
RN  - 0 (endothelium-dependent hyperpolarization factor)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
SB  - IM
MH  - Animals
MH  - Biological Factors/metabolism/*physiology
MH  - Caveolae/*physiology
MH  - Caveolins/*physiology
MH  - Humans
MH  - Mice
MH  - Muscle Tonus/physiology
MH  - Muscle, Smooth, Vascular/*physiology
MH  - Nitric Oxide/metabolism/*physiology
MH  - Nitric Oxide Synthase Type III/physiology
MH  - Signal Transduction/physiology
RF  - 55
EDAT- 2010/01/30 06:00
MHDA- 2010/04/08 06:00
CRDT- 2010/01/20 06:00
PHST- 2009/08/05 00:00 [received]
PHST- 2009/09/10 00:00 [accepted]
PHST- 2010/01/20 06:00 [entrez]
PHST- 2010/01/30 06:00 [pubmed]
PHST- 2010/04/08 06:00 [medline]
PST - ppublish
SO  - J Physiol Pharmacol. 2009 Oct;60 Suppl 4:105-9.