The cerebrovascular response to elevated potassium – role of nitric oxide in the in vitro model of isolated rat middle cerebral arteries

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Abstract

We investigated the role of nitric oxide (NO) in the vascular response to high extraluminal K+-concentrations in the in vitro model of isolated rat middle cerebral arteries (MCA). Under control conditions, rat MCA dilated at 20, 30, 40 and 60 mM K+. At 80 mM K+, a slight vasoconstriction occurred. The unspecific NO synthase (NOS)-inhibitor Lω-nitro-L-arginine (L-NNA) increased the resting tone at 3 mM K+ by 31±5% (P<0.01). While the vasodilatative effect of 20 mM K+ was unaffected by L-NNA, NOS-inhibition resulted in vasoconstriction at ≥ 40 mM K+ (P<0.01). In presence of L-NNA, the basal vessel diameter was restored by either the NO-donor S-nitroso-N-acetylpenicillamine (SNAP) or the cell-permeable guanosine-3′,5′-cyclic monophosphate (cGMP) analogue 8-Br-cGMP. Co-application of L-NNA with either SNAP or 8-Br-cGMP resulted in partial restitution of the vasodilatative effect of 40 mM K+, respectively. In presence of the soluble guanylyl cyclase inhibitor 1 H-[l,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), the vascular response to 40 mM K+ was abolished. Our findings together with findings from the literature indicate a modulator role of NO at K+ ≥ 40 mM K+, involving a cGMP-dependent mechanism.

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Acknowledgements

This research was supported by the Deutsche Forschungsgemeinschaft (DFG) and the Hermann and Lilly Schilling Stiftung.

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