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Dysfunction of the endothelium and constriction of the isolated rat's middle cerebral artery in low sodium environment in the presence of vasopressin.
- Source :
-
Clinical and experimental pharmacology & physiology [Clin Exp Pharmacol Physiol] 2020 May; Vol. 47 (5), pp. 759-764. Date of Electronic Publication: 2020 Jan 22. - Publication Year :
- 2020
-
Abstract
- Hyponatraemia, a water-electrolyte 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-associated 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 <superscript>+</superscript>  = 144 mmol/L) buffer or low-sodium (Na <superscript>+</superscript>  = 121 mmol/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 <superscript>+</superscript> concentration, vasopressin (1.4 × 10 <superscript>-11</superscript>  mol/L) or angiotensin II (10 <superscript>-9</superscript>  mol/L) resulted in relaxation of the MCA. Substitution of low-sodium 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 <subscript>1</subscript> receptor antagonist or concomitant inhibition of endothelin-1 receptors and synthesis of thromboxane A <subscript>2.</subscript> In contrast, no constriction of the MCA in low-sodium 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-vasodilatory to pro-vasoconstrictory. This phenomenon may be an overlooked factor contributing to vasospasm in SAH patients with hyponatraemia caused by inappropriate antidiuretic hormone secretion (SIADH).<br /> (© 2019 John Wiley & Sons Australia, Ltd.)
- Subjects :
- Animals
Endothelin-1 metabolism
Endothelium, Vascular metabolism
Endothelium, Vascular physiopathology
Hyponatremia complications
Hyponatremia metabolism
In Vitro Techniques
Male
Middle Cerebral Artery metabolism
Middle Cerebral Artery physiopathology
Rats, Wistar
Receptors, Vasopressin agonists
Receptors, Vasopressin metabolism
Thromboxane A2 metabolism
Vasospasm, Intracranial etiology
Vasospasm, Intracranial metabolism
Endothelium, Vascular drug effects
Hyponatremia physiopathology
Middle Cerebral Artery drug effects
Sodium deficiency
Vasoconstriction drug effects
Vasoconstrictor Agents pharmacology
Vasopressins pharmacology
Vasospasm, Intracranial physiopathology
Subjects
Details
- Language :
- English
- ISSN :
- 1440-1681
- Volume :
- 47
- Issue :
- 5
- Database :
- MEDLINE
- Journal :
- Clinical and experimental pharmacology & physiology
- Publication Type :
- Academic Journal
- Accession number :
- 31876005
- Full Text :
- https://doi.org/10.1111/1440-1681.13242