Wg. Mayhan et Fm. Faraci, RESPONSES OF CEREBRAL ARTERIOLES IN DIABETIC RATS TO ACTIVATION OF ATP-SENSITIVE POTASSIUM CHANNELS, The American journal of physiology, 265(1), 1993, pp. 80000152-80000157
The goal of this study was to determine whether responses of pial arte
rioles to activation of ATP-sensitive potassium channels are altered d
uring diabetes mellitus. We measured changes in diameter of pial arter
ioles in vivo in nondiabetic and diabetic rats (streptozotocin; 50-60
mg/kg ip; studied 3-4 mo after streptozotocin) in response to RP52891,
an activator of ATP-sensitive potassium channels. RP52891 (1.0 muM) d
ilated pial arterioles in nondiabetic rats by 16 +/- 1% but constricte
d pial arterioles in diabetic rats by 2 +/- 2% (means +/- SE; P < 0.05
vs. response in nondiabetic rats). Dilatation of pial arterioles in n
ondiabetic rats in response to RP52891 was inhibited by glibenclamide
(1.0 muM) but was not altered by N(G)-monomethyl-L-arginine (1.0 muM),
apamin (0.1 muM), or charybdotoxin (50 nM). Thus dilatation of pial a
rterioles in response to RP52891 appears to be due to activation of AT
P-sensitive potassium channels and does not involve nitric oxide or ca
lcium-activated potassium channels. To determine whether impaired dila
tation of pial arterioles in response to RP52891 in diabetic rats was
related to a nonspecific effect of diabetes mellitus on vasodilatation
, we measured diameter of pial arterioles in nondiabetic and diabetic
rats in response to nitroglycerin. Nitroglycerin (1.0 muM) dilated pia
l arterioles by 12 +/- 1 % in nondiabetic rats and 16 +/- 2 % in diabe
tic rats (P > 0.05). Thus impaired dilatation of pial arterioles in di
abetic rats in response to RP52891 also is not related to a nonspecifi
c effect of diabetes mellitus on vasodilatation. The findings of the p
resent study suggest that ATP-sensitive potassium channels are functio
nal in cerebral arterioles in vivo and are impaired during diabetes me
llitus.