H. Suzuki et al., GLUCOCORTICOID MODULATES VASODILATOR RESPONSE OF MESENTERIC ARTERIOLES IN SPONTANEOUSLY HYPERTENSIVE RATS, Hypertension, 27(1), 1996, pp. 114-118
We previously reported that the response of the arterioles in spontane
ously hypertensive rats (SHR) to histamine is blunted compared with th
at in normotensive control rats (Wistar-Kyoto rats [WKY]). The present
study was designed to analyze the extent to which this blunted arteri
olar response may be attributed in SHR to the concurrent elevation of
circulating glucocorticoids through the use of adrenalectomy with and
without dexamethasone supplementation. Mesenteric arterioles were obse
rved by intravital microscopy under general anesthesia, and their lume
n diameters were measured after histamine superfusion. The concentrati
on-response curve with histamine was compared with that of an endothel
ium-independent vasodilator, sodium nitroprusside. At the end of each
experiment, papaverine was applied topically to determine the maximal
diameter for each vessel, from which a measure of arteriolar tone coul
d be computed. The arteriolar tone in sham-operated SHR is set at a hi
gher steady-stare level than in sham-operated WKY. The concentration r
equired for a 50% dilator response (EC(50)) of histamine in adrenalect
omized SHR was restored to the level of WKY. Adrenalectomy did not sig
nificantly affect the EC(50) of histamine in WKY. When adrenalectomize
d SHR received a supplement of dexamethasone, the arteriolar response
was found to show the same refractory pattern to histamine as sham-ope
rated SHR. In contrast, the EC(50) of sodium nitroprusside in sham-ope
rated and adrenalectomized SHR was similar to that in sham-operated WK
Y. Our results indicate that the impaired dilator response to histamin
e in SHR is related to an enhanced adrenal glucocorticoid secretion.