Role of Extracellular Ca
            <sup>2+</sup>
            in Subarachnoid Hemorrhage−Induced Spasm of the Rabbit Basilar Artery

Zuccarello, Mario; Boccaletti, Riccardo; Tosun, Metiner; Rapoport, Robert M.

doi:10.1161/01.str.27.10.1896

Cited by 40 publications

(27 citation statements)

References 31 publications

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“…The findings are also consistent with findings that ET-1-induced vasospasm in arteries of a two-haemorrhage rabbit model was due to Ca 2 þ influx through VOCs and SOCs (Zuccarello et al, 1996a).…”

Section: J Zhao and Df Van Heldensupporting

confidence: 91%

ET‐1‐associated vasomotion and vasospasm in lymphatic vessels of the guinea‐pig mesentery

Zhao

Helden

2003

British J Pharmacology

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1 In vitro experiments were performed to investigate the actions of endothelin-1 (ET-1) on vasomotion and vasospasm in guinea-pig mesenteric lymphatics. 2 ET-1 modulated lymphatic vasomotion independent of the endothelium, with lower concentrations (p10 nM) increasing lymphatic vasomotion and higher concentrations (X100 nM) causing vasospasm. 3 ET-1-induced increases in vasomotion were accompanied by an increase in tonic [Ca 2 þ ] i . 4 These actions were inhibited by the ET A receptor antagonist BQ-123 (1 mM), the phospholipase C (PLC) inhibitor U73122 (5 mM), removal of extracellular Ca 2 þ , chelation of intracellular Ca 2 þ with BAPTA/AM (10 mM), the store Ca 2 þ -ATPase inhibitor thapsigargin (1 mM), caffeine (10 mM) and the inositol 1,4,5-trisphosphate (IP 3 ) receptor blocker heparin and 2-APB (30 mM). In contrast, the ET B receptor antagonist BQ-788 (1 mM), ryanodine (1 & 20 mM), pertussis toxin (PTx) or Cs þ had no significant actions on vasomotion or the magnitude of increase in tonic [Ca 2 þ ] i . 5 ET-1-induced vasospasm was accompanied by a transient increase in smooth muscle [Ca 2 þ ] i followed by a sustained plateau, an action that was abolished by removal of extracellular Ca 2 þ , but only marginally inhibited by nifedipine (1 mM). 6 Caffeine (10 mM), SKF 96165 (30 mM) or U73122 (5 mM) together with nifedipine (1 mM) abolished ET-1-induced vasospasm and increase in [Ca 2 þ ] i . 7 These results indicate that ET-1 increases lymphatic vasomotion by acting on smooth muscle ET A receptors and activation of G-protein-PLC-IP 3 cascade, which is known to cause pacemaker Ca 2 þ release and resultant pacemaker potentials. High concentrations of ET-1 cause a failure in Ca 2 þ homeostasis causing vasospasm, triggered by excessive Ca 2 þ influx primarily through store-operated channels (SOCs) with L-Ca 2 þ voltage-operated channels (VOCs) also contributing, but to a much lesser extent.

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Section: J Zhao and Df Van Heldensupporting

confidence: 91%

ET‐1‐associated vasomotion and vasospasm in lymphatic vessels of the guinea‐pig mesentery

Zhao

Helden

2003

British J Pharmacology

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“…On the other hand, complete reversal of CPA-enhanced PE responses by the ␣-AR antagonist prazosin, suggested to us that CPA-induced Ca 2ϩ elevation may alter ET A receptor-mediated responses, which we earlier reported its predominant role in subarachnoid hemorrhage-induced basilar artery spasm (40).…”

Section: Discussionmentioning

confidence: 84%

“…Furthermore, ET-1-induced force generation was only partially sensitive to verapamil, whereas it was abolished by Ni 2ϩ addition in rat aorta (Fig. 4), rabbit basilar artery, and rat caudal artery (6,40), suggesting the predominant involvement of NSCCs in ET receptor activation. Verapamil sensitivity could be explained by the membrane depolarization induced by massive SOC entry and reverse activation of Na ϩ /Ca 2ϩ exchanger.…”

Section: Discussionmentioning

confidence: 93%

Sarcoplasmic-endoplasmic reticulum Ca²⁺-ATPase inhibition prevents endothelin A receptor antagonism in rat aorta

Tosun

Erac²,

Selli³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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This study tested whether sarcoplasmic-endoplasmic reticulum Ca 2ϩ -ATPase regulates the ability of endothelin receptor antagonist to inhibit the endothelin-1 constriction. The endothelin A receptor antagonist BQ-123 (1 M) completely relaxed constriction to 10 nM endothelin-1 in endothelium-denuded rat aorta. Challenge with cyclopiazonic acid (10 M), a sarcoplasmicendoplasmic reticulum Ca 2ϩ -ATPase inhibitor, during the plateau of endothelin-1 constriction enhanced the constriction by ϳ30%. BQ-123 relaxed the endothelin-1 plus cyclopiazonic acid constriction by only ϳ10%. In contrast, prazosin (1 M), an ␣-adrenergic receptor antagonist, still completely relaxed the 0.3 M phenylephrine constriction in the presence of cyclopiazonic acid. Verapamil relaxed the endothelin-1 plus cyclopiazonic acid constriction by ϳ30%, whereas Ni 2ϩ and 2-aminoethoxydiphenyl borate, nonselective cation channel and store-operated channel blockers, respectively, completely relaxed the constriction. These results suggest that lowered sarcoplasmicendoplasmic reticulum Ca 2ϩ -ATPase activity selectively decreases the ability of endothelin receptor antagonist to inhibit the endothelin A receptor. The decreased antagonism may be related to the opening of store-operated channels and subsequent greater internalization of endothelin A receptor.BQ-123; vascular smooth muscle; store-operated calcium; caveola THE ROLE OF STORE-OPERATED CALCIUM (SOC) in the regulation of receptor-operated vascular tone is somewhat controversial. The apparent complexity is partly due to the presence of SOC in both cell types found in blood vessels, endothelial cells and vascular smooth muscle cells. Depletion of agonist-sensitive Ca 2ϩ stores in either cell type results in elevation of cytosolic Ca 2ϩ concentration through SOC channels (SOCCs) (21). Elevation of Ca 2ϩ in endothelial cells activates endothelial nitric oxide synthase, yielding to endothelium-dependent vascular smooth muscle relaxation via nitric oxide (17,38,39). On the other hand, in the absence of intact endothelium, SOCCs also mediate Ca 2ϩ elevation in vascular smooth muscle (1,13,26,27,29,31,33). Store-operated channels may be responsible for nonselective cation entry during any inositol 1,4,5-trisphosphate (IP 3 )-producing receptor stimulation and coupled to vascular contraction in the presence of certain agonists, such as endothelin (ET) (see Ref. 16 for review).ET, one of the most potent vasoconstricting peptides released from endothelial cells (35), exerts its effects through two types of sarcolemmal G protein-coupled receptors, ET A and ET B (3, 25). ET A subtype is profoundly expressed in the vascular smooth muscle and is responsible for the constricting effects of ET-1. ET B , on the other hand, is also present at membranes of endothelial cell and vascular smooth muscle cell nucleus, counteracting the pressor effects of ET-1 and preventing nuclear Ca 2ϩ overload (7). More than a decade ago, ET A receptors were shown to be localized in caveolae in the absence of its ligand (8). A struct...

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“…A low flow rate or a short-term increase in flow would enhance ET-1 production, whereas a high flow rate or a long-term decrease in flow would diminish ET-1 production. 15 Endothelin-1 might be involved in several pathological situations such as preeclampsia, 18 renal dysfunction, 19,20 sepsis, 21 heart failure, 22 atherosclerosis, 16 cerebral vasospasm, 23,24 and aging. 25 In spontaneous hypertension, the role of ET-1 is still a matter of debate.…”

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confidence: 99%

Chronic Endothelin-1 Improves Nitric Oxide–Dependent Flow-Induced Dilation in Resistance Arteries From Normotensive and Hypertensive Rats

Henrion¹,

Iglarz²,

Lévy³

1999

ATVB

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Abstract-Endothelin-1 (ET-1) is released on stimulation by shear stress of the vascular wall. In several pathological situations, an involvement of ET-1 is suspected. Nevertheless, the effect of a chronic increase in circulating ET-1 on vascular tone in resistance arteries is not yet fully understood. We investigated the response to tensile stress (pressure-induced myogenic tone) and shear stress (flow-induced dilation, FD) of rat mesenteric resistance arteries cannulated in an arteriograph. Intraluminal diameter was measured continuously. Rats (normotensive Wistar-Kyoto rats [WKYs] and spontaneously hypertensive rats [SHRs]) were treated for 2 weeks with ET-1 (5 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 SC; nϭ8 to 16 per group). Systolic arterial blood pressure increased significantly in ET-1-treated rats (171Ϯ7 versus 196Ϯ6 mm Hg in WKYs and 216Ϯ8 versus 245Ϯ6 mm Hg in SHRs, PϽ0.05). Passive arterial diameter in isolated resistance arteries ranged from 78Ϯ9 to 169Ϯ4 m in WKYs and from 62Ϯ6 to 149Ϯ7 m in SHRs (pressure from 10 to 150 mm Hg). Myogenic tone was not significantly affected by chronic ET-1. Flow (9 to 150 L/min) significantly increased the arterial diameter by 2Ϯ0.5 to 22Ϯ2 m in WKYs and by 1.3Ϯ0.7 to 8.3Ϯ0.8 m in SHRs (PϽ0.001 versus WKYs). The NO synthesis blocker N G -nitro-L-arginine methyl ester (L-NAME; 100 mol/L) attenuated FD in WKYs (eg, 22Ϯ2 versus 15Ϯ3 m after L-NAME, flowϭ150 L/min) and, to a lesser extent, in SHRs (PϽ0.001 versus WKYs). The cyclooxygenase inhibitor indomethacin (3 mol/L) attenuated the remaining FD in WKYs (eg, 15Ϯ3 versus 8Ϯ3 m, flowϭ150 L/min) and in SHRs (eg, 7.5Ϯ0.5 versus 5.0Ϯ0.6 m). Chronic ET-1 significantly increased FD in SHRs but not in WKYs. In both strains, NO-dependent FD was significantly increased by chronic ET-1. Furthermore, indomethacin-sensitive FD was increased by chronic ET-1 in SHRs only. Thus, chronic ET-1 increased NO-dependent FD in resistance mesenteric arteries from both WKYs and SHRs and increased indomethacin-sensitive Key Words: myogenic tone Ⅲ shear stress Ⅲ resistance arteries Ⅲ endothelin Ⅲ hypertension P ressure-induced tone (myogenic tone) is a characteristic of small resistance arteries and of some veins. [1][2][3][4][5] It is opposed by flow-induced dilation in vitro as well as in vivo. 1,2,6 -8 These 2 mechanical stimuli determine a basal vascular tone in resistance arteries and allow a rapid adaptation to changes in flow and pressure. 1,8 Whereas myogenic tone is mainly independent of endothelial factors, 1,5 flow produces shear stress and triggers an endothelium-dependent dilation. 1,7,8 Flow-induced dilation depends in part on the production of NO 8 -11 and cyclooxygenase (COX) products 10 -13 by endothelial cells.Endothelial cells stimulated by hormonal 14 or mechanical 15-17 factors can produce endothelin-1 (ET-1). Mechanical factors such as pressure or wall stretch increase ET-1 gene expression and ET-1 production. 16,17 Flow, or shear stress, exerts a flow rate-dependent effect on the production of ET-1. A low flow rate or a short-term increas...

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Role of Extracellular Ca ²⁺ in Subarachnoid Hemorrhage−Induced Spasm of the Rabbit Basilar Artery

Cited by 40 publications

References 31 publications

ET‐1‐associated vasomotion and vasospasm in lymphatic vessels of the guinea‐pig mesentery

ET‐1‐associated vasomotion and vasospasm in lymphatic vessels of the guinea‐pig mesentery

Sarcoplasmic-endoplasmic reticulum Ca²⁺-ATPase inhibition prevents endothelin A receptor antagonism in rat aorta

Chronic Endothelin-1 Improves Nitric Oxide–Dependent Flow-Induced Dilation in Resistance Arteries From Normotensive and Hypertensive Rats

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Role of Extracellular Ca 2+ in Subarachnoid Hemorrhage−Induced Spasm of the Rabbit Basilar Artery

Cited by 40 publications

References 31 publications

ET‐1‐associated vasomotion and vasospasm in lymphatic vessels of the guinea‐pig mesentery

ET‐1‐associated vasomotion and vasospasm in lymphatic vessels of the guinea‐pig mesentery

Sarcoplasmic-endoplasmic reticulum Ca2+-ATPase inhibition prevents endothelin A receptor antagonism in rat aorta

Chronic Endothelin-1 Improves Nitric Oxide–Dependent Flow-Induced Dilation in Resistance Arteries From Normotensive and Hypertensive Rats

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Role of Extracellular Ca ²⁺ in Subarachnoid Hemorrhage−Induced Spasm of the Rabbit Basilar Artery

Sarcoplasmic-endoplasmic reticulum Ca²⁺-ATPase inhibition prevents endothelin A receptor antagonism in rat aorta