Are Pulmonary Capillaries Susceptible to Mechanical ... - Journal

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Centripetal Tension and
Endothelial Retraction*
A/aim B. Moy, M.D.; Rebecca Site/don, BA.; Kntituj Liimd-’deuj. BA.;
Sandra Sima.sbm,, BA.; amid D. ,\ufcitael S/tathy. M. I).
I nflatusumsiatorv misolecumles suicim as histaumsuiuue incresuse
eumclothsehial permmseabihity by imsitiatimig retrstctioum of
ssdjsscemut eumdotluehial cells. We recemstly reported that ims
hmsummuamu umnubilic’al vein emidothueliash (I! UVE) cells huista-
mssimie imucresuseci phuosphorylatioms of thse light chmaimm tif
mssyosimu (MLC) by 0.18 ± 0.02 moles phsosphmsitc’ p’ mndile
MLC (ussolP/nmolMLC). This is consistemmt with time his’-
pothesis timsit Imistamimme initiates retrsicti(imi by increasimsg
ceistripetath temmsiomu within euidothmehial cells. However,
chselatiomi of extracehlular calcitumsi whelm interrumpts cell-
cell amid ceil-sul)strate hiiumding also increases endotimehial
permnestl)ility simmcl causes emmdothselistl cell retrstetioms hiothu
itt situ immperfumsed lummgs mudl iii vitro with cultmureei cells.
TIse effects of cstlc’iuummu elmc’lattioms sire’ coumsistemit ss’ithm tlue
hiy’potiuesis tlmaut retesuse of forces tetlmerimug emidothuelial
cells imi plaice atllows expressiuiui of’ at e(immstitultive centrip-
etal teumsioms. Ims our receumt report, we fouund commstitumtive
)lmospImorylsitiomm of M LC at 0.20 ± 0.02 msmolP/ummolMLC,
coumsistemit with si c’onstituutive’ atctommsy’osimi-mmsediatu’d teum-
siomm. \Vc’ asked if reclumctioum of Ni LC phmosphorvhaitioum
woumld prevemmt tile respomise to hmiststmmmimue or calciuumui
chmel5ution. aimscl conversely, if iuscrestsedi comistitustive, Ni LC
plmosphorylsitiomm wosmld cause cell retrsictioms.
1mmcommtrot amid huistsimimse-stuimiumlateel H UVE cells amid imm
comutreil porcimie puhmmiomuary arterv eutdothmelissh (PPAE)
cells tryptic peptide misaps indicated that M LC was phmos-
phmom’y’lamtecl by the csulcisumss calmimoduhimi -dlepemudemut myosimi
light clmsuin kinase. Pretreatm#{236}ment cif H UVE cells withs
cAMP pres’emmtsc! the huistamnimme-stimsiuulatech immcrease imm
MLC phsosphmorylation (-0.08 ± 0.02 mmuolP/mssoIMLC) ammcl
a huistsumuimme imuitiated imscreasse iii H UVE cell misonolaver
periuueal)ility (-12 ± 1 percemmt). Pretreatumiemut of IIUVE
cells withm tue cathciumui-csulmnodulims inhmihiitor, Ni L-9, also
prevented time huistsimisimse stimsmulated imicreutse its Ni LC
pluosphmorylation (-0.29 ± 0.04 muuolP/mmsolM LC) mmmc! tIme
iumcrease imu HUVE cell msuonolayer permeability (14 ± 4
percemmt of time coumtrol response). Simssihstrlv, pretreatmsmemmt
of PPAE cells with cAMP reduced bstssih MLC phsplm-
rylatiomm (-0.16 ± 0.O3molP/molM LC) amid reduced tIle
increase in mmsoncilayer permssesuhility fohlowimsg calciumms
chelatioum (21 ± 14 percemut of tIle c’ommtrol response). Pre-
treatmuuemst of PPAE cells witls ML-9 also reduced bausath
M LC phmosphmorvlation (-0.13 ± 0.02 mmsolP/miucil M LC) atnel
reduced the imseresise iii msmousolaver permuueahuhitv fohlosv-
imug calciumsu chielsttiomm (47 ± 5 percent of control re-
5l)onse).
TIse hstsai level of M LC phmosplmoryhsutiomm likely rehire-
sents comustituitive kiumatse stud pImsplmsutsise activity. Okadstic’
stcid iumcreaseei Ni LC )imosphmorylsstiomm ium i’PAE cells (1
j.tM, 0.06 ± 0.O4mmsolP/mmuo1MLC siumel 10 1.tM, 0.17 ± 0.05
uiuotP/umsolMLC ) iii su dose-depemsdemut muistumumer, simucl 10
f.LM (289 ± 32 1)ercemst) but hot I i.sM (4 ± 5 perce’mmt)
okssciatic atcid imscrestseci PPAE cell umueimmolsive’r permumesthil-
6Frouus thue Ummivc’rsity- of Iowa College of Mediciuue, Iowa City’.
CHEST / 105 / 3 / MARCH, 1994 / Supplement 107S