Logo image
Back
Neuronal NO mediates cerebral vasodilator responses to K+ in hypertensive rats
Journal article   Open access   Peer reviewed

Neuronal NO mediates cerebral vasodilator responses to K+ in hypertensive rats

Sophocles Chrissobolis, James Ziogas, Colin R Anderson, Yi Chu, Frank M Faraci and Christopher G Sobey
Hypertension (Dallas, Tex. 1979), Vol.39(4), pp.880-885
04/2002
DOI: 10.1161/01.HYP.0000013056.74554.CE
PMID: 11967243
url
https://doi.org/10.1161/01.HYP.0000013056.74554.CEView
Published (Version of record) Open Access

Abstract

Potassium ion (K+) normally causes cerebral vasodilatation by activating inwardly rectifying K+ (K(IR)) channels. We tested whether chronic hypertension affects the magnitude and/or mechanism of K+-induced cerebral vasodilatation in vivo. Basilar artery responses were examined in anesthetized Wistar-Kyoto (WKY; mean arterial pressure, 114+/-4 mm Hg) and spontaneously hypertensive (SHR; 176+/-3 mm Hg) rats. In WKY, elevating cerebrospinal fluid K+ concentration from 3 mmol/L to 5 and 10 mmol/L caused vasodilatation (percent maximum, 12+/-1 and 48+/-7, respectively). The response to 5 mmol/L K+ was greater in SHR (percent maximum, 17+/-2 [P<0.05 versus WKY] and 49+/-4). The K(IR) channel inhibitor, barium ion (Ba2+, 100 micromol/L) selectively inhibited dilator responses to 5 and 10 mmol/L K+ by approximately 75% in WKY. In SHR, Ba2+ had no effect on the response to 5 mmol/L K+, and only partially inhibited (by approximately 40%) the response to 10 mmol/L K+. The nonselective NO synthase (NOS) inhibitor N(omega)-nitro-L-arginine methyl ester, the neuronal NOS (nNOS) inhibitor 1-(2-trifluromethyl-phenyl)imidazole, and the N-type calcium channel inhibitor omega-conotoxin GVIA, were all without effect in WKY, but markedly inhibited the response to 5 mmol/L K+ in SHR. When applied together with Ba2+, each of these inhibitors also profoundly reduced responses to 10 mmol/L K+ in SHR. Immunostaining of basilar arteries revealed that the perivascular nNOS-containing nerve plexus was denser in SHR. Thus, K+ dilates the normotensive basilar artery predominantly via K(IR) channel activation. During chronic hypertension, small physiological elevations in K+ dilate the basilar artery by an nNOS-dependent mechanism that appears to be upregulated in a compensatory manner.
 Potassium Channels - biosynthesis Nitric Oxide Synthase - antagonists & inhibitors Nitric Oxide Synthase - physiology Rats, Inbred WKY Male Basilar Artery - physiopathology Nitric Oxide Synthase Type I Neurons - physiology Hypertension - enzymology Neurons - drug effects Potassium Channel Blockers - pharmacology NG-Nitroarginine Methyl Ester - pharmacology Rats, Inbred SHR Basilar Artery - enzymology Basilar Artery - drug effects Sodium-Potassium-Exchanging ATPase - antagonists & inhibitors Enzyme Inhibitors - pharmacology Rats Cerebral Arteries - physiopathology Imidazoles - pharmacology Barium - pharmacology Potassium - pharmacology Hypertension - physiopathology Hypertension - metabolism Animals Cerebral Arteries - enzymology Neurons - enzymology Vasodilation - drug effects Chronic Disease

Details

Metrics

17 Record Views
17 Times Cited - Web of Science
Logo image