Enhancement of the Na, K-ATPase Activity of the Brain Microvessel by Arachidonic Acid and Its Hydroperoxide, 15-HPAA

In the prepared brain microvessel (MV), it has been shown that the endothelial cells of the brain capillary play a vital role in the transport function of the blood-brain barrier (BBB) [3, 6, 20, 22]. It was also shown that there is a unipolar transport mechanism of sodium across the BBB, which is due to the anteluminal localization of the Na, K-ATPase in the endothelium [2, 3]. This mechanism may be important in the regulation of ion homeostasis as well as the volume control of the extracellular fluid (ECF) in the physiological state [2, 4] it may also be relevant to the mechanism of ischemic brain edema, since the sodium influx across the BBB was shown to correlate closely with the edema formation [2, 11]. In this regard, we have shown that production of hydroxy acids in the MVis enhanced following regional ischemia in rats [1], and that some radical scavengers, such as AVS, suppress both the lipoxygenase activity of the MVand edema formation [10, 15]. These results suggest that the production of hydroperoxides by the MV lipoxygenase is related to edema formation following ischemia. In this respect, lipid peroxides are known to reduce the activity of the Na, K-ATPase activity of the synaptosomes [17, 23]. However, since their effects on the Na, K-ATPase of the MV are unknown, the present study was carried out to study the effect of AA and its hydroperoxide, 15-HPAA, on the activity of the Na, K-ATPase of the MV.