Hyperthermia-Induced Vasoconstriction of the Carotid Artery and the Role of Potassium Channels

Mustafa, Seham; Thulesius, Olav

doi:10.1016/j.jstrokecerebrovasdis.2004.12.006

Cited by 7 publications

(5 citation statements)

References 20 publications

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“…By blocking them with BaCl 2 , the cell was prevented from returning to the rest state by a greater extent than during ultrasound exposure alone. These findings are consistent with evidence presented by Mustafa and Thulesius (2005) who observed that vasoconstriction induced by mild hyperthermia was mediated by potassium channel activity in the smooth muscle cell membrane. Several types of potassium ion channel were implicated in vasoconstriction due to hyperthermia (Mustafa and Thulesius 2005) and further work is required to establish exactly which are involved in this response.…”

Section: Discussionsupporting

confidence: 93%

“…In our previous paper, we hypothesised that a similar process occurs in the vascular wall. Further, we suggested that this change was a result of very slight heating of the smooth muscle cell membrane, which has previously been reported to induce changes in vascular tone (Mustafa et al 2004), through changes in potassium ion channel activity (Mustafa and Thulesius 2005). We now directly confirm this hypothesis by experiments on the effects of specific channel inhibitors on the response to ultrasound and by fluorescence-probe measurements of thermally-induced changes.…”

Section: Introductionsupporting

confidence: 75%

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Thermally-Mediated Ultrasound-Induced Contraction of Equine Muscular Arteries In Vitro and an Investigation of the Associated Cellular Mechanisms

Martin

Duck

Winlove

2012

Ultrasound in Medicine & Biology

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We have previously shown that MHz frequency ultrasound causes contraction of the carotid artery in vitro. We now extend this investigation to equine mesenteric arteries and investigate the cellular mechanisms. In vitro exposure of the large lateral cecal mesenteric artery to 4-min periods of 3.2 MHz continuous wave ultrasound at acoustic powers up to 145 mW induced reversible repeatable contraction. The magnitude of the response was linearly dependent on acoustic power and, at 145 mW, the mean increase in wall stress was 0.020 ± 0.017 mN/mm(2) (n = 34). These results are consistent with our previous study and the effect was hypothesised to be thermally mediated. A 2°C temperature rise produced an increase in intracellular calcium, measured by Fluo-4 fluorescence. Inhibition of the inward-rectifier potassium ion channel with BaCl(2) (4 μM) increased the response to ultrasound by 55% ± 49%, indicating a similar electrophysiologic basis to the response to mild hyperthermia. In small mesenteric arteries (0.5-1.0 mm diameter) mounted in a perfusion myograph, neither ultrasound exposure nor heating produced measureable vasoconstriction or a rise in intracellular calcium and we conclude that temperature-sensitive channels are absent or inactive in these small vessels. It, therefore, appears that response of blood vessels to ultrasound depends not only on the thermal properties of the vessels and surrounding tissues but also on the electrophysiology of the smooth muscle cells.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionsupporting

confidence: 75%

Thermally-Mediated Ultrasound-Induced Contraction of Equine Muscular Arteries In Vitro and an Investigation of the Associated Cellular Mechanisms

Martin

Duck

Winlove

2012

Ultrasound in Medicine & Biology

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“…β-adrenoceptor-induced relaxation is mediated by the increase of the intracellular cAMP concentration and/ or activation of K + channels [36] . Opening of K + channels leads to membrane potential hyperpolarization and closure of voltage-dependent channels, which decreases Ca 2+ entry and causes vasodilation [37] . In our experiments, propranolol, glibenclamide, tetraethylammonium and BaCl 2 did not affect the endothelium-independent relaxant response to formononetin in rat mesenteric arteries, suggesting that the K + channels and β-adrenoceptors are not involved in the vascular relaxation processes, which is in accordance with the previous findings that K + channel inhibitors did not affect the relaxation of genistein and zearalanone, two phytoestrogens, in rabbit coronary arteries [38] .…”

Section: Discussionmentioning

confidence: 99%

Vasorelaxant and antihypertensive effects of formononetin through endothelium-dependent and -independent mechanisms

Sun

Cao

2011

Acta Pharmacol Sin

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Aim: To investigate the mechanisms underlying the vasorelaxant effect of formononetin, an O-methylated isoflavone, in isolated arteries, and its antihypertensive activity in vivo. Methods: Arterial rings of superior mesenteric arteries, renal arteries, cerebral basilar arteries, coronary arteries and abdominal aortas were prepared from SD rats. Isometric tension of the arterial rings was recorded using a myograph system. Arterial pressure was measured using tail-cuff method in spontaneously hypertensive rats. Results: Formononetin (1-300 μmol/L) elicited relaxation in arteries of the five regions that were pre-contracted by KCl (60 mmol/L), U46619 (1 μmol/L) or phenylephrine (10 μmol/L). The formononetin-induced relaxation was reduced by removal of endothelium or by pretreatment with L-NAME (100 μmol/L). Under conditions of endothelium denudation, formononetin (10, 30, and 100 μmol/L) inhibited the contraction induced by KCl and that induced by CaCl 2 in Ca 2+ -free depolarized medium. In the absence of extracellular Ca 2+ , formononetin (10, 30, and 100 μmol/L) depressed the constriction caused by phenylephrine (10 μmol/L), but did not inhibit the tonic contraction in response to the addition of CaCl 2 (2 mmol/L). The contraction caused by caffeine (30 mmol/L) was not inhibited by formononetin (100 μmol/L). Formononetin (10 and 100 μmol/L) reduced the change rate of Ca 2+ -fluorescence intensity in response to KCl (50 mmol/L). In spontaneously hypertensive rats, formononetin (5, 10, and 20 mg/kg) slowly lowered the systolic, diastolic and mean arterial pressure. Conclusion: Formononetin causes vasodilatation via two pathways: (1) endothelium-independent pathway, probably due to inhibition of voltage-dependent Ca 2+ channels and intracellular Ca 2+ release; and (2) endothelium-dependent pathway by releasing NO. Both the pathways may contribute to its antihypertensive effect.

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“…It was found that heating-induced contractions were potentiated by the K-channel inhibitors tetraethylammonium, BaCl 2 , charybdotoxin and the Na + /K + ATPase inhibitor ouabain. On the other hand, levcromakalim, a K + channel activator, reduced heating-induced contractions [18] . Consequently, K + channel openers like levcromakalim may be useful drug candidates to treat delayed cerebral vasospasm after cerebral hemorrhage, as recently shown [19] .…”

Section: Carotid Arterymentioning

confidence: 99%

Thermal Reactions of Blood Vessels in Vascular Stroke and Heatstroke

Thulesius¹

2006

Med Princ Pract

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Research on the pathophysiology and treatment of brain damage with special focus on thermal vascular responses is the subject of this minireview. Interruption of cerebral blood supply by vascular obstruction, temporary cardiac arrest or hyperthermia causes a sudden attack of vascular stroke or heatstroke with serious consequences. It may not induce immediate cell death, but can precipitate a complex biochemical cascade leading to a delayed neuronal loss. When testing thermal vasomotor responses by stepwise cooling of isolated carotid arteries, a temperature-proportional dilatation was observed while heating induced the opposite response: a marked vasoconstriction. General hyperthermia with an increased oxygen demand combined with a reduction of blood supply therefore is a serious consequence. At the cellular level an important mechanism involving hyperthermia is the temperature-dependent regulation of K⁺ channel tone of vascular smooth muscle. Further, their inhibition through temperature elevation causes vasoconstriction. In heatstroke, which can induce platelet aggregation and the release of the vasoconstrictor serotonin, arterial cooling attenuates this response. General hypothermia is induced to prevent or attenuate neurological damage in stroke. The procedure is not without serious side effects. Therefore, rapid institution of selective brain cooling has been considered in adults and in infants with postpartum encephalopathy.

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Hyperthermia-Induced Vasoconstriction of the Carotid Artery and the Role of Potassium Channels

Cited by 7 publications

References 20 publications

Thermally-Mediated Ultrasound-Induced Contraction of Equine Muscular Arteries In Vitro and an Investigation of the Associated Cellular Mechanisms

Thermally-Mediated Ultrasound-Induced Contraction of Equine Muscular Arteries In Vitro and an Investigation of the Associated Cellular Mechanisms

Vasorelaxant and antihypertensive effects of formononetin through endothelium-dependent and -independent mechanisms

Thermal Reactions of Blood Vessels in Vascular Stroke and Heatstroke

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