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Department of Pharmacology, University of Aarhus, 8000 Aarhus C, Denmark
A possible role for a metabolite of cytochrome
P-450 
-hydroxylase in the initial and sustained phases of
the myogenic response in cannulated rat mesenteric small arteries was
studied. With slight preconstriction (norepinephrine and neuropeptide
Y), pressure was raised from 60 to 100 mmHg, and both initial (within 2 min) and sustained phases (at 10 min) of the myogenic response were quantified. The myogenic response was fully inhibited by D600 (methoxyverapamil). Ketoconazole and 17-octadecanoic acid did not
affect the initial phase but inhibited the sustained phase. In
contrast, miconazole did not affect either phase. Charybdotoxin and
iberiotoxin potentiated the initial phase but eliminated the sustained
phase. Apamin, glibenclamide, 4-aminopyridine, and barium had no effect
on either phase. The results demonstrate different mechanisms for the
initial and sustained phases of the myogenic response of rat mesenteric
small arteries. Only the sustained phase appears mediated through a
cytochrome P-450 -hydroxylase metabolite and
calcium-activated K+ channels. However, both phases of the
response are dependent on calcium influx through voltage-dependent
calcium channels.
calcium-activated potassium channels; autoregulation
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