Differential inhibition of functional dilation of small arterioles by indomethacin and glibenclamide.
Indomethacin or glibenclamide treatments attenuate functional dilation of larger-diameter "feed" arterioles paired with venules in hamster cremaster muscle. We tested the hypothesis that release of cyclooxygenase products from venules is important for functional dilation of third- and fourth-order arterioles. We also tested whether ATP-sensitive potassium channels are important during functional dilation of smaller arterioles. The microcirculation of hamster cremaster muscle was visualized with in vivo video microscopy. We measured diameter responses of third- and fourth-order arterioles paired and unpaired with venules in response to 2 minutes of muscle field stimulation (40 microseconds, 10 V, 1 Hz). Control diameters of vessels were 31+/-2 (n=19), 13+/-1 (n=12), 12+/-2 (n=12), and 10+/-1 (n=12) for paired and unpaired third-order and paired and unpaired fourth-order arterioles, respectively. In all groups, field stimulation resulted in increases in mean control diameter of >80%. Indomethacin (28 micromol/L) superfused on the preparation was used to inhibit cyclooxygenase metabolism, or glibenclamide (10 micromol/L) was used to block ATP-sensitive potassium channels. Indomethacin attenuated arteriolar vasodilations to electrical stimulation in paired third-order vessels only, whereas glibenclamide attenuated this vasodilation in all 4 groups. These results support a role for ATP-sensitive potassium channels in functional dilation of arterioles of all sizes regardless of whether or not they are paired with venules. Conversely, a role for cyclooxygenase products is limited to larger "feed arterioles" paired with venules. This study provides further evidence that venules may be the source of prostaglandin release during functional hyperemia.
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, USA. lhammer@physiology.umsmed.edu
L W
LW
Hammer
A L
AL
Ligon
R L
RL
Hester
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001160:Arterioles / Q000187:drug effects* / Q000502:physiology; D006224:Cricetinae; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004558:Electric Stimulation; D005905:Glyburide / Q000494:pharmacology*; D007213:Indomethacin / Q000494:pharmacology*; D008297:Male; D008647:Mesocricetus; D018715:Microscopy, Video; D009132:Muscles / Q000098:blood supply* / Q000378:metabolism; D009599:Nitroprusside; D026902:Potassium Channel Blockers; D014664:Vasodilation / Q000187:drug effects; D014699:Venules / Q000187:drug effects / Q000502:physiology
D016861:Cyclooxygenase Inhibitors; D026902:Potassium Channel Blockers; D009599:Nitroprusside; D000255:Adenosine Triphosphate; D005905:Glyburide; D007213:Indomethacin