| Title: |
Endogenous and exogenous NO attenuates conduction of vasoconstrictions along arterioles in the microcirculation. |
| Authors: |
Rodenwaldt, Barbara, Pohi, Ulrich, Cor De Wit |
| Source: |
American Journal of Physiology: Heart & Circulatory Physiology; May2007, Vol. 292 Issue 5, pH2341-H2348, 8p, 1 Chart, 7 Graphs |
| Subject Terms: |
MICROCIRCULATION, NITRIC oxide, VASOMOTOR system, CONNEXINS, ACETYLCHOLINE, VASOCONSTRICTION |
| Abstract: |
Vascular coordination in the microcirculation depends on gap junctional intercellular communication (GJIC), which is reflected by the conduction of locally initiated vasomotor responses. However, little is known about the regulation of GJIC in vivo. We hypothesized that endothelial NO regulates GJIC and therefore studied whether conduction of constrictions and dilations along the vessel wall is modulated by modifying the level of microcirculatory NO. Arterioles were focally stimulated using high K+ or acetylcholine in the cremaster muscle in situ, and diameter changes were assessed at the local and remote upstream sites by intravital microscopy. Local stimulation with K+ initiated a constriction that conducted along the arteriole with diminishing amplitude (length constant λ: 371 ± 42 µm). After Nω-nitro-L-arginine (L-NNA), λ increased to 507 ± 30 µm, indicating that GJIC is attenuated by endogenous NO. Exogenous NO, but not adenosine, reduced λ after L-NNA in a reversible, concentration-dependent, and mainly cGMP-dependent manner as assessed by inhibition of soluble guanylate cyclase. In endothelial NO synthase-deficient mice, λ was 530 ± 80 µm and thus similar to that in wild-type mice after L-NNA. Exogenous NO likewise reduced λ in these mice. The effects of NO were comparable to those of wild-type animals in Cx40-deficient mice, which excludes Cx40 as a specific target of NO. In contrast to constrictions, the amplitude of conducted dilations on acetylcholine did not diminish up to 1,300 µm and were not altered by L-NNA or exogenous NO. We conclude that endogenously released NO attenuates the conduction of vasoconstrictions most likely due to a modulation of gap junctional conductivity. We suggest that this effect is specific for smooth muscle cells, which probably transmit constricting signals, and involves connexins other than Cx40. This mechanism may support the dilatory potency of NO by preventing the conduction of remote vasoconstrictions into areas with basal or activated NO release. [ABSTRACT FROM AUTHOR] |
|
Copyright of American Journal of Physiology: Heart & Circulatory Physiology is the property of American Physiological Society and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) |
| Database: |
Complementary Index |
