Affiliation:
1. Mossakowski Medical Research Institute, Polish Academy of Sciences
Abstract
Abstract
The decrease in serum sodium ions concentration below 135 mmol L− 1 is usually accompanied by a decrease in plasma osmolality (hypoosmotic hyponatremia) and leads to the disorder of intracranial homeostasis mainly due to the cellular swelling. Recently, using in vitro model of hypoosmotic hyponatremia, we have found that a decrease in sodium ions concentration in the perfusate to 121 mmol L− 1 relaxes the isolated rat middle cerebral artery (MCA). The aim of present study was to explore the mechanism responsible for this relaxation. Isolated, pressurized and perfused MCAs placed in a vessel chamber were subjected to a decrease of sodium ions concentration to 121 mmol L− 1. The changes in the diameter of the vessels were monitored with a video camera. The removal of the endothelium, inhibition of nitric oxide-dependent signaling or reverse mode sodium-calcium exchanger (NCX) were used to study the mechanism of the dilation of the vessel during hyponatremia. The dilation of the MCA (19 ± 5%, p < 0.005) in low sodium buffer was absent after removal of the endothelium or administration of the inhibitor of the reverse mode of sodium-calcium exchange, and was reversed to constriction after the inhibition of nitric oxide (NO)/cGMP signaling. The dilation of the middle cerebral artery of the rat in 121 mM Na+ buffer depends on the endothelium, NO signaling and reverse mode of sodium-calcium exchange. Hyponatremia may constrict large cerebral arteries with impaired NO-dependent signaling and add to vascular spasm such as the one observed in the late phase after subarachnoid hemorrhage.
Publisher
Research Square Platform LLC