This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Hammer, L. W. Articles by Hester, R. L. Search for Related Content PubMed PubMed Citation Articles by Hammer, L. W. Articles by Hester, R. L. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB INDOMETHACIN

(Hypertension. 2001;37:599.)
© 2001 American Heart Association, Inc.

Scientific Contributions

Differential Inhibition of Functional Dilation of Small Arterioles by Indomethacin and Glibenclamide

Leah W. Hammer; Alison L. Ligon; Robert L. Hester

From the Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson.

Correspondence to Leah Hammer, PhD, Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 N State St, Jackson, MS 39216-4505. E-mail lhammer{at}physiology.umsmed.edu

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 µs, 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 µmol/L) superfused on the preparation was used to inhibit cyclooxygenase metabolism, or glibenclamide (10 µmol/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.

Key Words: indomethacin • microcirculation • arterioles • potassium channels • cyclooxygenase

This article has been cited by other articles:

				L. Xiang and R. L. Hester Adipocyte-derived factor reduces vasodilatory capability in ob-/ob- mice Am J Physiol Heart Circ Physiol, August 1, 2009; 297(2): H689 - H695. [Abstract] [Full Text] [PDF]

				B. L. Hodnett, J. A. Dearman, C. B. Carter, and R. L. Hester Attenuated PGI2 synthesis in obese Zucker rats Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2009; 296(3): R715 - R721. [Abstract] [Full Text] [PDF]

				A. G. Goodwill, M. E. James, and J. C. Frisbee Increased vascular thromboxane generation impairs dilation of skeletal muscle arterioles of obese Zucker rats with reduced oxygen tension Am J Physiol Heart Circ Physiol, October 1, 2008; 295(4): H1522 - H1528. [Abstract] [Full Text] [PDF]

				L. Xiang, J. S. Naik, S. R. Abram, and R. L. Hester Chronic hyperglycemia impairs functional vasodilation via increasing thromboxane-receptor-mediated vasoconstriction Am J Physiol Heart Circ Physiol, January 1, 2007; 292(1): H231 - H236. [Abstract] [Full Text] [PDF]

				M.-h. Kim and N. R. Harris Leukocyte adherence inhibits adenosine-dependent venular control of arteriolar diameter and nitric oxide Am J Physiol Heart Circ Physiol, August 1, 2006; 291(2): H724 - H731. [Abstract] [Full Text] [PDF]

				W. G. Schrage, N. M. Dietz, and M. J. Joyner Effects of combined inhibition of ATP-sensitive potassium channels, nitric oxide, and prostaglandins on hyperemia during moderate exercise J Appl Physiol, May 1, 2006; 100(5): 1506 - 1512. [Abstract] [Full Text] [PDF]

				L. Xiang, J. S. Naik, B. L. Hodnett, and R. L. Hester Altered arachidonic acid metabolism impairs functional vasodilation in metabolic syndrome Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2006; 290(1): R134 - R138. [Abstract] [Full Text] [PDF]

				L. W. Hammer, C. R. Overstreet, J. Choi, and R. L. Hester ATP stimulates the release of prostacyclin from perfused veins isolated from the hamster hindlimb Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2003; 285(1): R193 - R199. [Abstract] [Full Text] [PDF]

				N. R. Harris Arteriovenous Pairing: a Determinant of Capillary Exchange Physiology, April 1, 2003; 18(2): 83 - 87. [Abstract] [Full Text] [PDF]

				R. L. Hester and L. W. Hammer Venular-arteriolar communication in the regulation of blood flow Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2002; 282(5): R1280 - R1285. [Abstract] [Full Text] [PDF]

				K. D Cohen and I. H Sarelius Muscle contraction under capillaries in hamster muscle induces arteriolar dilatation via KATP channels and nitric oxide J. Physiol., March 1, 2002; 539(2): 547 - 555. [Abstract] [Full Text] [PDF]

				K. D Cohen and I. H Sarelius Muscle contraction under capillaries in hamster muscle induces arteriolar dilatation via KATP channels and nitric oxide J. Physiol., March 1, 2002; 539(2): 547 - 555. [Abstract] [Full Text] [PDF]