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  • ATP-Sensitive Potassium Channels in the Basilar Artery During Chronic Hypertension
    2016
    Co-Authors: T Kitazono, Donald D. Heistad, Frank M. Faraci
    Abstract:

    We examined the hypothesis that dilatation of the Basilar Artery in response to activation of ATP-sensitive potassium channels is impaired in stroke-prone spontaneously hypertensive rats (SHRSP). Changes in Basilar Artery diameter in response to aprikalim, a direct activator of ATP-sensitive potassium channels, were measured in anesthetized SHRSP and normotensive Wistar-Kyoto (WKY) rats through a cranial window. Topical application of aprikalim increased Basilar Artery diameter in WKY rats. Glibenclamide, a selective inhibitor of ATP-sensitive potassium channels, abolished aprikalim-induced vasodilatation. Thus, ATP-sensitive potassium channels are functional in the Basilar Artery of WKY rats in vivo. Aprikalim (10~6 mol/L) dilated the Basilar Artery by 31±5 % (mean + SEM) in WKY rats but only 5±1% in SHRSP. The concentration-response curve to aprikalim in SHRSP was significantly shifted to the right, but the response to the highest concentration of aprikalim (10~55 mol/L) was similar in SHRSP and WKY rats. Vasodilatation in response to norepinephrine was also impaired in SHRSP. Dilator responses of the Basilar Artery to forskolin, a direct activator of adenylate cyclase, and nitroprusside, a direct activator of guanylate cyclase, were normal in SHRSP. The findings suggest that dilatation of the Basilar Artery in response to direct activation of ATP-sensitive potassium channels is impaired in SHRSP compared with WKY rats in vivo. (Hypertension. 1993;22:677-681.

  • Role of ATP-sensitive potassium channels in the Basilar Artery
    American Journal of Physiology-Heart and Circulatory Physiology, 1993
    Co-Authors: Frank M. Faraci, Donald D. Heistad
    Abstract:

    This study examined the hypothesis that activation of ATP-sensitive potassium channels produces vasodilation and contributes to dilator responses of the Basilar Artery to acetylcholine in vivo. Diameter of the Basilar Artery (baseline diam = 245 +/- 14 microns, means +/- SE) was measured through a cranial window in anesthetized rats. RP52891 (1 microM), a direct activator of ATP-sensitive potassium channels, increased the diameter of the Basilar Artery by 33 +/- 5%. Glibenclamide (1 microM), an inhibitor of ATP-sensitive potassium channels, did not alter baseline diameter but abolished responses of the Basilar Artery to RP52891. Topical application of acetylcholine (10 microM) for 3 min produced peak dilatation of 33 +/- 6% at 30 s and produced a sustained increase in diameter of 17 +/- 4%. Glibenclamide did not inhibit dilator responses of the Basilar Artery to acetylcholine. Nitro-L-arginine methyl ester (10 and 100 microM), which inhibits synthesis of endothelium-derived relaxing factor (EDRF), produced concentration-dependent inhibition of dilatation of the Basilar Artery in response to acetylcholine. Thus ATP-sensitive potassium channels are functional but do not appear to influence basal tone of the Basilar Artery. Dilator responses of the Basilar Artery to acetylcholine are dependent on formation of EDRF but not dependent on activity of glibenclamide-sensitive potassium channels.

  • Effect of norepinephrine on rat Basilar Artery in vivo.
    The American journal of physiology, 1993
    Co-Authors: T Kitazono, Frank M. Faraci, D. D. Heistad
    Abstract:

    In anesthetized rats, we used a cranial window to examine effects of topical norepinephrine on diameter of the Basilar Artery in vivo. Topical application of norepinephrine increased the diameter of the Basilar Artery. NG-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthase, inhibited vasodilatation to acetylcholine but did not attenuate dilator responses to norepinephrine. Indomethacin also did not attenuate vasodilatation in response to norepinephrine. Dilatation of the Basilar Artery to norepinephrine was inhibited by propranolol and the beta 1-antagonist atenolol but not by the beta 2-antagonist butoxamine. Thus dilatation of the Basilar Artery in response to norepinephrine is produced by activation of beta 1-receptors and is not mediated by endothelium-derived relaxing factor or prostanoids. Glibenclamide, a selective inhibitor of ATP-sensitive K+ channels, partially inhibited vasodilatation in response to norepinephrine. Forskolin, a direct activator of adenylate cyclase, also increased the diameter of the Basilar Artery, and glibenclamide attenuated the dilatation. Thus dilatation of rat Basilar Artery in response to norepinephrine is mediated, in part, by activation of ATP-sensitive K+ channels, and activation of these K+ channels may be achieved by an adenosine 3',5'-cyclic monophosphate-dependent mechanism.

  • ATP-sensitive potassium channels in the Basilar Artery during chronic hypertension.
    Hypertension (Dallas Tex. : 1979), 1993
    Co-Authors: T Kitazono, Donald D. Heistad, Frank M. Faraci
    Abstract:

    We examined the hypothesis that dilatation of the Basilar Artery in response to activation of ATP-sensitive potassium channels is impaired in stroke-prone spontaneously hypertensive rats (SHRSP). Changes in Basilar Artery diameter in response to aprikalim, a direct activator of ATP-sensitive potassium channels, were measured in anesthetized SHRSP and normotensive Wistar-Kyoto (WKY) rats through a cranial window. Topical application of aprikalim increased Basilar Artery diameter in WKY rats. Glibenclamide, a selective inhibitor of ATP-sensitive potassium channels, abolished aprikalim-induced vasodilatation. Thus, ATP-sensitive potassium channels are functional in the Basilar Artery of WKY rats in vivo. Aprikalim (10(-6) mol/L) dilated the Basilar Artery by 31 +/- 5% (mean +/- SEM) in WKY rats but only 5 +/- 1% in SHRSP. The concentration-response curve to aprikalim in SHRSP was significantly shifted to the right, but the response to the highest concentration of aprikalim (10(-5.5) mol/L) was similar in SHRSP and WKY rats. Vasodilatation in response to norepinephrine was also impaired in SHRSP. Dilator responses of the Basilar Artery to forskolin, a direct activator of adenylate cyclase, and nitroprusside, a direct activator of guanylate cyclase, were normal in SHRSP. The findings suggest that dilatation of the Basilar Artery in response to direct activation of ATP-sensitive potassium channels is impaired in SHRSP compared with WKY rats in vivo.

  • Flow-mediated dilatation of the Basilar Artery in vivo.
    Circulation research, 1991
    Co-Authors: Kenichiro Fujii, D. D. Heistad, Frank M. Faraci
    Abstract:

    Flow-mediated dilatation has been described mainly in peripheral conduit arteries. The goal of this study was to examine mechanisms and functional implications of flow-mediated dilatation in large cerebral arteries in vivo. Vessel diameter and velocity of blood flow through the Basilar Artery were measured using a cranial window in 45 anesthetized rats. Mean blood flow velocity through the Basilar Artery increased by 94 +/- 8% during unilateral common carotid Artery occlusion and 203 +/- 13% during bilateral occlusion. Diameter of the Basilar Artery increased by 10 +/- 1% during unilateral common carotid Artery occlusion and 29 +/- 2% during bilateral occlusion from control diameter of 275 +/- 8 microns. Vasodilatation appeared with a delay of 13 +/- 1 seconds after the onset of the increase in flow velocity. With systemic arterial pressure maintained at baseline levels, pressure in the Basilar Artery (servonull) decreased initially during carotid occlusion, and during dilatation of the Basilar Artery, pressure was restored partially toward normal. Indomethacin (10 mg/kg i.v.), topical application of tetrodotoxin (10(-6) M), NG-monomethyl L-arginine (5 x 10(-6) M), tetraethylammonium chloride (10(-2) M), glibenclamide (10(-5) M), SKF 525A (3 x 10(-5) M), and ouabain (10(-5) M) had no effect on flow-mediated dilatation.(ABSTRACT TRUNCATED AT 250 WORDS)

Fana Alemseged - One of the best experts on this subject based on the ideXlab platform.

D. D. Heistad - One of the best experts on this subject based on the ideXlab platform.

  • Effect of norepinephrine on rat Basilar Artery in vivo.
    The American journal of physiology, 1993
    Co-Authors: T Kitazono, Frank M. Faraci, D. D. Heistad
    Abstract:

    In anesthetized rats, we used a cranial window to examine effects of topical norepinephrine on diameter of the Basilar Artery in vivo. Topical application of norepinephrine increased the diameter of the Basilar Artery. NG-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthase, inhibited vasodilatation to acetylcholine but did not attenuate dilator responses to norepinephrine. Indomethacin also did not attenuate vasodilatation in response to norepinephrine. Dilatation of the Basilar Artery to norepinephrine was inhibited by propranolol and the beta 1-antagonist atenolol but not by the beta 2-antagonist butoxamine. Thus dilatation of the Basilar Artery in response to norepinephrine is produced by activation of beta 1-receptors and is not mediated by endothelium-derived relaxing factor or prostanoids. Glibenclamide, a selective inhibitor of ATP-sensitive K+ channels, partially inhibited vasodilatation in response to norepinephrine. Forskolin, a direct activator of adenylate cyclase, also increased the diameter of the Basilar Artery, and glibenclamide attenuated the dilatation. Thus dilatation of rat Basilar Artery in response to norepinephrine is mediated, in part, by activation of ATP-sensitive K+ channels, and activation of these K+ channels may be achieved by an adenosine 3',5'-cyclic monophosphate-dependent mechanism.

  • Flow-mediated dilatation of the Basilar Artery in vivo.
    Circulation research, 1991
    Co-Authors: Kenichiro Fujii, D. D. Heistad, Frank M. Faraci
    Abstract:

    Flow-mediated dilatation has been described mainly in peripheral conduit arteries. The goal of this study was to examine mechanisms and functional implications of flow-mediated dilatation in large cerebral arteries in vivo. Vessel diameter and velocity of blood flow through the Basilar Artery were measured using a cranial window in 45 anesthetized rats. Mean blood flow velocity through the Basilar Artery increased by 94 +/- 8% during unilateral common carotid Artery occlusion and 203 +/- 13% during bilateral occlusion. Diameter of the Basilar Artery increased by 10 +/- 1% during unilateral common carotid Artery occlusion and 29 +/- 2% during bilateral occlusion from control diameter of 275 +/- 8 microns. Vasodilatation appeared with a delay of 13 +/- 1 seconds after the onset of the increase in flow velocity. With systemic arterial pressure maintained at baseline levels, pressure in the Basilar Artery (servonull) decreased initially during carotid occlusion, and during dilatation of the Basilar Artery, pressure was restored partially toward normal. Indomethacin (10 mg/kg i.v.), topical application of tetrodotoxin (10(-6) M), NG-monomethyl L-arginine (5 x 10(-6) M), tetraethylammonium chloride (10(-2) M), glibenclamide (10(-5) M), SKF 525A (3 x 10(-5) M), and ouabain (10(-5) M) had no effect on flow-mediated dilatation.(ABSTRACT TRUNCATED AT 250 WORDS)

  • Responses of rat Basilar Artery to acetylcholine and platelet products in vivo.
    Stroke, 1991
    Co-Authors: Frank M. Faraci, William G. Mayhan, D. D. Heistad
    Abstract:

    Studies in vitro suggest that the Basilar Artery has distinctive responses to endothelium-dependent stimuli. Our first goal was to examine the effects of acetylcholine on diameter of the Basilar Artery in vivo. Because aggregating platelets may have important effects on cerebral arteries, our second goal was to examine the effects on the Basilar Artery of products that are released by platelets (thromboxane, serotonin, and adenosine 5'-diphosphate). Diameter of the Basilar Artery was measured through a cranial window in anesthetized rats (n = 25). Baseline diameter of the Basilar Artery was 247 +/- 10 microns mean +/- SEM. Topical application of acetylcholine at 10(-6) and 10(-5) M dilated the Basilar Artery by 13 +/- 2% and 19 +/- 2%, respectively. The thromboxane analogue U46619 at 10(-8) and 10(-7) M reduced the diameter of the Basilar Artery by 18 +/- 5% and 29 +/- 4%, respectively. At 10(-8) and 10(-7) M, serotonin had little effect on pial arterioles on the cerebrum but constricted the Basilar Artery by 18 +/- 2% and 29 +/- 4%, respectively. At 10(-6) and 10(-5) M, adenosine 5'-diphosphate produced marked dilatation of pial arterioles on the cerebrum (9 +/- 2% and 20 +/- 3%, respectively) but had little effect on the Basilar Artery (increased diameter by 4 +/- 2% and 6 +/- 2%, respectively). Thus, in contrast to some studies of the Basilar Artery in vitro, acetylcholine produces dilatation of the Basilar Artery in vivo. Potent constrictor responses to thromboxane and serotonin, in combination with the minimal dilator effect of adenosine 5'-diphosphate, suggest that release of these products during platelet aggregation would favor constriction of the Basilar Artery.

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Paolo Stanzione - One of the best experts on this subject based on the ideXlab platform.