This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science 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 Web of Science (7) Citing Articles via Google Scholar Google Scholar Articles by Nakahata, K. Articles by Hatano, Y. Search for Related Content PubMed PubMed Citation Articles by Nakahata, K. Articles by Hatano, Y.

---

NEUROSURGICAL ANESTHESIA

Vasodilation Mediated by Inward Rectifier K⁺ Channels in Cerebral Microvessels of Hypertensive and Normotensive Rats

Katsutoshi Nakahata, MD, PhD^*, Hiroyuki Kinoshita, MD, PhD^*, Yasuyuki Tokinaga, MD^*, Yuko Ishida, PhD^*, Yoshiki Kimoto, MD, PhD^*, Mayuko Dojo, MD, PhD^*, Kazuhiro Mizumoto, MD, PhD^*, Koji Ogawa, MD, PhD^*, and Yoshio Hatano, MD, PhD^*

Departments of *Anesthesiology and Forensic Medicine, Wakayama Medical University, Wakayama, Japan

Address correspondence and reprint requests to Hiroyuki Kinoshita, MD, PhD, Department of Anesthesiology, Wakayama Medical University, 811-1 Kimiidera, Wakayama 641-0012, Japan. Address e-mail to hkinoshi{at}pd5.so-net.ne.jp.

Although inward rectifier K⁺ channels contribute to the regulation of cerebral circulation, dilation of cerebral microvasculature mediated by these channels has not been demonstrated in chronic hypertension. We designed the present study to examine the roles of inward rectifier K⁺ channels in the vasodilation produced by increased levels of extracellular K⁺ in cerebral parenchymal arterioles from hypertensive and normotensive rats. During constriction to prostaglandin F₂ (5 x 10^–7 M), the arterioles within brain slices were evaluated using computer-assisted microscopy. Potassium chloride (KCl) induced vasodilation in cerebral arterioles from normotensive (5–10 mM) and hypertensive (5–15 mM) rats, whereas an inward rectifier K⁺ channel antagonist barium chloride (BaCl₂; 10^–5 M) completely abolished the vasodilation in both strains. In arterioles of hypertensive rats, vasodilator responses to KCl were augmented compared with those in normotensive rats. In contrast, the vasodilator responses induced by sodium nitroprusside (3 x 10^–8 to 3 x 10^–6 M) in these two strains were similar. These results suggest that in cerebral cortex parenchymal microvessels, inward rectifier K⁺ channels play a crucial role in vasodilation produced by extracellular K⁺ and that the dilation of cerebral arterioles via these channels is augmented in chronic hypertension.

This article has been cited by other articles:

				K. Hama-Tomioka, H. Kinoshita, T. Azma, K. Nakahata, N. Matsuda, N. Hatakeyama, H. Kikuchi, and Y. Hatano The Role of 20-Hydroxyeicosatetraenoic Acid in Cerebral Arteriolar Constriction and the Inhibitory Effect of Propofol Anesth. Analg., December 1, 2009; 109(6): 1935 - 1942. [Abstract] [Full Text] [PDF]

				A. A. Tobin, B. K. Joseph, H. N. Al-Kindi, S. Albarwani, J. A. Madden, L. T. Nemetz, N. J. Rusch, and S. W. Rhee Loss of cerebrovascular Shaker-type K+ channels: a shared vasodilator defect of genetic and renal hypertensive rats Am J Physiol Heart Circ Physiol, July 1, 2009; 297(1): H293 - H303. [Abstract] [Full Text] [PDF]

				X.-L. Shi, G.-L. Wang, Z. Zhang, Y.-J. Liu, J.-H. Chen, J.-G. Zhou, Q.-Y. Qiu, and Y.-Y. Guan Alteration of Volume-Regulated Chloride Movement in Rat Cerebrovascular Smooth Muscle Cells During Hypertension Hypertension, June 1, 2007; 49(6): 1371 - 1377. [Abstract] [Full Text] [PDF]