V. Ralevic et al., EFFECTS OF STREPTOZOTOCIN-DIABETES ON SYMPATHETIC-NERVE, ENDOTHELIAL AND SMOOTH-MUSCLE FUNCTION IN THE RAT MESENTERIC ARTERIAL BED, European journal of pharmacology, 286(2), 1995, pp. 193-199
Mesenteric arterial function was assessed in constantly perfused prepa
rations isolated from rats 12 weeks after treatment with streptozotoci
n (65 mg kg(-1), i.p.) to induce diabetes. Frequency-dependent vasocon
strictor responses to electrical field stimulation of sympathetic nerv
es (4-32 Hz, 0.1 ms, 90V, 30 s) were severely attenuated in preparatio
ns from streptozotocin-diabetic rats, although dose-dependent vasocons
trictions to the sympathetic cotransmitters noradrenaline and ATP, as
well as to potassium chloride, were not significantly changed. Dose-de
pendent relaxations to the endothelium-dependent vasodilators acetylch
oline and ATP were significantly impaired in preparations from strepto
zotocin-diabetic rats, although endothelium-independent vasodilatation
to sodium nitroprusside was unimpaired. These results suggest that 12
weeks after induction of streptozotocin-diabetes in rats there is pre
-junctional impairment of sympathetic neurotransmission and impaired e
ndothelial function of the mesenteric arteries. This is in contrast to
our previous findings that at 8 weeks after induction of streptozotoc
in-diabetes sympathetic nerve and endothelial function is normal, alth
ough sensory-motor vasodilatation is severely attenuated. It is sugges
ted that selective changes occur in mesenteric arterial function after
streptozotocin treatment depending on the duration of diabetes; senso
ry-motor nerves are affected first, followed by sympathetic nerves and
the endothelium, while the smooth muscle is relatively resistant to c
hange.