{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T02:16:05Z","timestamp":1788315365798,"version":"build-2803163510"},"reference-count":41,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2020,1,22]],"date-time":"2020-01-22T00:00:00Z","timestamp":1579651200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clin Exp Pharma Physio"],"published-print":{"date-parts":[[2020,5]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Hyponatraemia, a water\u2013electrolyte disorder diagnosed in patients with subarachnoid haemorrhage (SAH), increases a risk of persistent vasospasm. In majority of cases, hyponatraemia results from inappropriate secretion of vasopressin (AVP). The effect of AVP\u2010associated hyponatraemia on cerebral vasculature is unknown. The present study aimed to elucidate the role of AVP in the response of the middle cerebral artery (MCA) of the rat to hyponatraemia. Isolated, cannulated, and pressurized rat MCAs were perfused\/superfused with physiological (Na\n                    <jats:sup>+<\/jats:sup>\n                    \u00a0=\u00a0144\u00a0mmol\/L) buffer or low\u2010sodium (Na\n                    <jats:sup>+<\/jats:sup>\n                    \u00a0=\u00a0121\u00a0mmol\/L) buffer containing either AVP or angiotensin II (ANG II). ANG II was used to check if the effect of low plasma sodium concentration combined with AVP on the MCA tone is unique to vasopressin. At physiological Na\n                    <jats:sup>+<\/jats:sup>\n                    concentration, vasopressin (1.4\u00a0\u00d7\u00a010\n                    <jats:sup>\u221211<\/jats:sup>\n                    \u00a0mol\/L) or angiotensin II (10\n                    <jats:sup>\u22129<\/jats:sup>\n                    \u00a0mol\/L) resulted in relaxation of the MCA. Substitution of low\u2010sodium for the normal sodium buffer with the same concentration of AVP, resulted in the constriction of the MCA. This effect was absent after removal of the endothelium, administration of vasopressin V\n                    <jats:sub>1<\/jats:sub>\n                    receptor antagonist or concomitant inhibition of endothelin\u20101 receptors and synthesis of thromboxane A\n                    <jats:sub>2.<\/jats:sub>\n                    In contrast, no constriction of the MCA in low\u2010sodium buffer was observed when AVP was replaced with ANG II. Our data suggest that presence of vasopressin and low sodium ion concentration results in the change of endothelium phenotype from pro\u2010vasodilatory to pro\u2010vasoconstrictory. This phenomenon may be an overlooked factor contributing to vasospasm in SAH patients with hyponatraemia caused by inappropriate antidiuretic hormone secretion (SIADH).\n                  <\/jats:p>","DOI":"10.1111\/1440-1681.13242","type":"journal-article","created":{"date-parts":[[2019,12,26]],"date-time":"2019-12-26T01:34:12Z","timestamp":1577324052000},"page":"759-764","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Dysfunction of the endothelium and constriction of the isolated rat's middle cerebral artery in low sodium environment in the presence of vasopressin"],"prefix":"10.1111","volume":"47","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1922-7662","authenticated-orcid":false,"given":"Marta","family":"Aleksandrowicz","sequence":"first","affiliation":[{"name":"Laboratory of Experimental and Clinical Neurosurgery Mossakowski Medical Research Centre Polish Academy of Sciences Warsaw 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