Ooi BS, Papademetrious V, Cohen DJ
A novel mechanism for the pathogenesis of hypertension
Am Soc Nephrol
J Am Soc Nephrol (abstract)
(Sep) 7:1518 1996
Endothelial cells respond to humoral and paracrine stimuli as well as
physical forces to change their phenotype and to elaborate a variety
of endothelium-derived vasoactive substances. The authors reasoned that
sera from hypertensive patients might favor endothelial synthesis of
vasoconstrictor, rather than vasodilator, factors.
Cultured
endothelial cells were incubated with sera from 10 hypertensive and 11
normal subjects and then the medium was assayed for endothelin, thromboxane
B2,
and a stable metabolite of prostacyclin. Thromboxane synthesis was
markedly ( >3 fold) higher with hypertensive sera, endothelin was
slightly but significantly higher, and prostacylcin synthesis was
unchanged. The authors interpret these results to suggest the presence of
circulating
substances in hypertensive sera which favor endothelium
derived vasoconstrictor synthesis as a novel mechanism in the genesis
of hypertension.
Comment: The study has many limitations versus many previous
similar ones assessing endothelial response to serum components: 1)
small numbers of (possibly heterogenous) patients, 2) known
heterogeneity of endothelial cells derived from different vascular
beds, 3) known temporal variation in endothelial synthesis of
vasoactive substances following serum exposure, 4) modulation of such
responses by physiologic shear-stress in vivo, 5) lack of study of
endothelium-derived nitric oxide, 6) inability to distinguish
mechanisms which perpetuate hypertension from those which lead to its
"genesis", and 7) lack of insight into the identity of such serum-derived
factor(s) and their mechanism(s) of action. These preliminary data
should provide impetus for important studies which may address the
above concerns. (Jason G. Umans, M.D., University of Chicago)
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Am Soc Nephrol
H: Pathophysiology :
Endothelium, Nitric Oxide
H: Pathophysiology :
Vascular pathology