ABSTRACT
High extracellular potassium can induce spreading depression-like depolarizations, elevations of extracellular glutamate and even neuronal death in normal brain. To investigate the contribution of high potassium in vivo, a microelectrode arrays ( MEAs ) probe integrated with recording sites for glutamate concentration (50í150 μm) and local field potential ( LFP) ( diameter=15 μm) was fabricated by Micro-electro-mechanical-systems ( MEMS) technologies. We implanted the MEA probe acutely in the rat brain and exposed the brain to a high potassium solution. During these multi-modal recordings, it was observed that high potassium elevated extracellular glutamate while suppressing the LFP irreversibly. This is one of the first studies in which a dual mode MEA probes is applied in vivo for neuronal death, and it is concluded that our MEA probes are capable of examining specific spatiotemporal relationships between electrical and chemical signaling in the brain.
ABSTRACT
Objective To investigate the effect of commercial low-sodium and high-potassium salt substitutes on blood pressure in the rural community-based population in China.Methods We conducted a quasi-experiment on 411 adults, who were 30 to 60 years of age, in 2 rural communities from Laiwu city in Shandong province of China on data from blood pressure screening.The subjects were divided into 2 groups: high blood pressure (HBP) and non-HBP (NHBP). Both groups and their family members took a low-sodium and high-potassium salt substitute for 3 months to replace the normal salt in their bodies. Blood pressure (BP) and 24-hour urinary sodium and potassium were measured regularly in the 2 groups. Results There was a continuously decreasing trend for BP at the end of the first month. Three months later, the mean BP decreased by 7.4 mm Hg (1 mm Hg=0.133 kPa, t=10.096, P=0.000) for SBP and 3.8 mm Hg (t=8.017, P=0.000) for DBP in the HBP group,when compared to a 1.2 mm Hg(t=2.507,P=0.007) decrease on SBP and 1.0 nun Hg(t=2.987, P=0.002) on DBP in the NHBP group. The mean urinary sodium had a decrease of 15.5 mmol/24 h (t=1.803,P=0.037) ,but the urinary potassium increased by 4.2 mmol/24 h (t' =2.132, P=0.018). The result of urinary sodium appepared to be as follows:potassium ratio (Na+/K+ ) decreased by 1.2 (t=2.786,P=0.003) in the HBP group. However,in NHBP group,the mean urinary sodium decreased by 1.7 mmol/24 h (t=0.211, P=0.417) and urinary potassium increased by 3.7 mmol/24 h (t' =2.207,P=0.015) ,together with the decrease ofNa+/K+ by 0.7 (t=1.818, P=0.036). Conclusion Results from our study clearly demonstrated that the intake of low-sodium and high-potassium salt substitute could effectively reduce the BP with good compliance among adults in the rural community-based population in China. This was an effective but non-medical method to prevent and control the high blood pressure.
ABSTRACT
Aim To observe the effects of Breviscapine (Bre) on the contractions induced by noradrenaline (NA) and high potassium in rabbit aorta strips and to investigate the relationships of these effects to the changes of intracellular free calcium( i). Methods The effects of Bre on the concentration-response curves for NA and high potassium, and on the transient contractions induced by NA and caffeine in Ca 2+-free medium and the sustained contraction by NA after replenishing Ca 2+ were surveyed using rabbit aorta strips; the changes of i increased by NA and high potassium in the presence of Bre were determined using fura-2/AM loaded cultured smooth muscle cells of rabbit aorta. Results Bre shifted the concentration-response curve for NA to right in a dose-dependent manner , but shifted that for high potassium to left; it inhibited the transient contraction induced by NA and caffeine in the Ca 2+-free medium and the sustained contraction induced by NA after replenishing Ca 2+; Bre inhibited the i increased by NA, but enhanced that increased by high potassium in the smooth muscle cells of rabbit aorta. Conclusion Bre inhibits the contraction induced by NA through its inhibition effects on Ca 2+-influx and Ca 2+-release ; it enhances the Ca 2+-influx induced by high potassium, but the mechanism by which Bre enhances the high potassium inducing Ca 2+ -influx is not known.