Cerebral vasospasm and vasoconstriction caused by endothelin

Kobayashi, Hidenori; Hayashi, Minoru; Kobayashi, Shogo; Kabuto, Masanori; Handa, Yuji; Kawano, Hirokazu; Ide, Hisashi

doi:10.1097/00006123-199105000-00006

Cited by 46 publications

(23 citation statements)

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“…This is felt to be the mecha nism by which subarachnoid hemorrhage induces vaso spasm [58], Subarachnoid hemorrhage is associated with increased cerebrospinal fluid levels of ET-1 [58], while ad ministration of ET-1 into cerebral ventricles can cause sub arachnoid hemorrhage and cerebral vasospasm [59,60]. In fact, pretreating rats with an ETA -receptor antagonist, prior to the experimental induction of subarachnoid hem orrhage, prevented the associated vasospasm [61].…”

Section: Receptorsmentioning

confidence: 99%

Endothelins as Cardiovascular Peptides

Levin¹

1996

Am J Nephrol

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The normal functional state of the vasculature and the events leading to the development of significant arterial disease involve the interaction of important vasoactive substances, which play important modulating or initiating roles in the development of hypertension and arteriosclerosis. Three endothelins have now been identified, of which ET-1 is the best characterized. ET-1 is produced by epithelial, mesangial, neuronal and glial, and liver cells, and is the most potent vasoconstrictor yet found. Each endothelin is derived from a different gene on separate chromosomes, and each binds to at least 2 types of receptor. The plasma half-life of ET-1 is about 7 min, and this provides a rapid mechanism for adjusting vascular resistance or blood pressure. The actions of endothelin are mediated through several pathways of postreceptor signaling, including activation of the mitogen-activated protein kinase cascade, which give rise to its growth-stimulating properties. Secretion of ET-1 from cultured endothelial cells is stimulated by a wide range of substances, and is inhibited by some prostaglandins. Endothelin in turn stimulates secretion of nitric oxide, arginine vasopressin and atrial natriuretic peptide, and participates in the hormonal control of salt and water balance. Hypoxia and ischemia augment ET-1 secretion, as does insulin, and this could play a role in the accelerated vascular disease of diabetes. ET-1 also causes bronchoconstriction and has been implicated in the development of acute asthma, primary pulmonary hypertension and pulmonary fibrosis. Its role in hypertension is still debatable, though most of the manifestations of congestive heart failure can theoretically be explained by the actions of ET-1. Endothelin also has extensive renovascular and parenchymal effects in the kidney. It is hoped that a fuller understanding of the role of endothelins in normal or pathologic vasculature will lead to effective therapy based on antagonism or augmentation of specific functions.

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Section: Receptorsmentioning

confidence: 99%

Endothelins as Cardiovascular Peptides

Levin¹

1996

Am J Nephrol

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“…Kobayashi et al [17] have reported, using light and electron microscopy and immunohistochemical techniques, that endothelial injuries such as vacuolization in the cytoplasm, disruption of tight junctions and denudation were observed in canine basilar arteries from two-hemorrhage dogs on day 7, and that no ir-ET-1 products were detected on the endothelial cells in these dogs. These observations were similar to the present results with regard to the reduction in endothelial ir-ET-1 products in SAH dogs on day 6 compared with day 2.…”

Section: Discussionmentioning

confidence: 99%

Localization and Alteration of Immunoreactive Endothelin-1 in Canine Basilar Arteries Following Subarachnoid Hemorrhage.

Kobayashi

Nishikibe

Maruyama

et al. 1995

Acta Histochem. Cytochem

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“…The levels remained constant over the interval investigated, which included the typical period for vasospasm. The ET-1 levels in the perivascular space and in the cisternal CSF were high enough to produce vasospasm; [3,25,47] however, the levels were unchanged by the development or resolution of vasospasm. These results indicate that the increase in CSF ET-1 levels observed by others [11,14,48,49] cannot be solely responsible for the development of vasospasm.…”

Section: Vasospasm and Et-1mentioning

confidence: 96%

“…[31,46] One of the potential oxyhemoglobin-related mechanisms of vasospasm is the release of endothelin-1 (ET-1), [3,33,37] a potent endothelium-derived vasoconstricting agent, [21,55] into the cerebrospinal fluid (CSF) after SAH. [3,11,14,15,19,21,25,33,[47][48][49] Not only are astrocytes, neurons, and pituitary cells a normal source of extraluminal ET-1, [10,17,26,29,56] but endothelial [9,24,40] and smooth-muscle [24] cells also release ET-1 when stimulated by oxyhemoglobin [9,24,40] or thrombin. [10 ] Because an increase in the levels of ET-1 in CSF has been described in patients with cerebral vasospasm and delayed ischemic neurological deficits after SAH, [11,14,48,49] the production of ET-1 may also be induced by ischemia.…”

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confidence: 99%

Source and cause of endothelin-1 release to cerebrospinal fluid after subarachnoid hemorrhage

Pagnanelli

Barrer²

1997

FOC

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Despite years of research, delayed cerebral vasospasm remains a serious complication of subarachnoid hemorrhage (SAH). Recently, it has been proposed that endothelin-1 (ET-1) mediates vasospasm. The authors examined this hypothesis in a series of experiments. In a primate model of SAH, serial ET-1 levels were measured in samples from the perivascular space by using a microdialysis technique and in cerebrospinal fluid (CSF) and plasma during the development and resolution of delayed vasospasm. To determine whether elevated ET-1 production was a direct cause of vasospasm or acted secondary to ischemia, the authors also measured ET-1 levels in plasma and CSF after transient cerebral ischemia. To elucidate the source of ET-1, they measured its production in cultures of endothelial cells and astrocytes exposed to oxyhemoglobin (10 μM), methemoglobin (10 μM), or hypoxia (11% oxygen). There was no correlation between the perivascular levels of ET-1 and the development of vasospasm or its resolution. Cerebrospinal fluid and plasma levels of ET-1 were not affected by vasospasm (CSF ET-1 levels were 9.3 ± 2.2 pg/ml and ET-1 plasma levels were 1.2 ± 0.6 pg/ml) before SAH and remained unchanged when vasospasm developed (7.1 ± 1.7 pg/ml in CSF and 2.7 ± 1.5 pg/ml in plasma). Transient cerebral ischemia evoked an increase of ET-1 levels in CSF (1 ± 0.4 pg/ml at the occlusion vs. 3.1 ± 0.6 pg/ml 4 hours after reperfusion; p < 0.05), which returned to normal (0.7 ± 0.3 pg/ml) after 24 hours. Endothelial cells and astrocytes in culture showed inhibition of ET-1 production 6 hours after exposure to hemoglobins. Hypoxia inhibited ET-1 release by endothelial cells at 24 hours (6.4 ± 0.8 pg/ml vs. 0.1 ± 0.1 pg/ml, control vs. hypoxic endothelial cells; p < 0.05) and at 48 hours (6.4 ± 0.6 pg/ml vs. 0 ± 0.1 pg/ml, control vs. hypoxic endothelial cells; p < 0.05), but in astrocytes hypoxia induced an increase of ET-1 at 6 hours (1.5 ± 0.6 vs. 6.4 ± 1.1 pg/ml, control vs. hypoxic astrocytes; p < 0.05). Endothelin-1 is released from astrocytes, but not endothelial cells, during hypoxia and is released from the brain after transient ischemia. There is no relationship between ET-1 and vasospasm in vivo or between ET-1 and oxyhemoglobin, a putative agent of vasospasm, in vitro. The increase in ET-1 levels in CSF after SAH from a ruptured intracranial aneurysm appears to be the result of cerebral ischemia rather than reflecting the cause of cerebral vasospasm.

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Cerebral vasospasm and vasoconstriction caused by endothelin

Cited by 46 publications

References 0 publications

Endothelins as Cardiovascular Peptides

Endothelins as Cardiovascular Peptides

Localization and Alteration of Immunoreactive Endothelin-1 in Canine Basilar Arteries Following Subarachnoid Hemorrhage.

Source and cause of endothelin-1 release to cerebrospinal fluid after subarachnoid hemorrhage

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