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Introduction: Saccharina japonica (SJ) is one of brown algae. The extract of SJ (SJE) is often used for soup stock in Japanese cuisine. We recently observed the decreases in blood pressure (BP) by intake of SJ or SJE diet in 2-kidney, 1-clip renovascular hypertensive (2K1C) rats. SJ is rich in aspartate (Asp), which is the umami taste of amino acid. The intake of Asp was reported to reduce BP in Dahl salt sensitive rats. As well, the potassium Asp (AspK) intake was reported to improve BP in hypertensive patients. 70% (70 of 100) of amino acids such as Asp are eluted into the SJE from SJ. Therefore, we hypothesized that Asp in SJE contributes to the mechanism of BP reduced by dietary SJE in 2K1C rats. In this study, we observed BP in 2K1C rats fed a diet containing Asp or AspK and investigated whether those diets alleviate hypertension to the same extent of the diet containing SJE. Methods: Male Sprague-Dawley rats (6 wks) were treated with sham operation (SHAM) or clipping the left renal artery (2K1C). After surgery, the rats fed a control diet (C), a diet containing Asp, AspK or SJE for 6 weeks. The content of SJE was set to be the same as that in our previous study. The amount of Asp in diet was set to be the same as that in our previous study which showed the antihypertensive effect of SJ. The amount of AspK in diet was set to be equimolar to Asp. The systolic BP (SBP) was measured by a tail-cuff method every week. At the end of the procedure, mean arterial BP (MAP) was measured in each rat under anesthesia. Results: Six weeks after the surgery, 2K1C-C significantly increased in SBP compared with SHAM-C (126±2 vs 159±4 mmHg, p Conclusions: Asp and AspK may attenuate hypertension in 2K1C renovascular hypertension as much as SJE which contains similar quantities of Asp. It is possible that Asp and/or AspK eluted into SJE contributes to the mechanism of alleviating hypertension by SJE in 2K1C.

BACKGROUND Potassium aspartate (PA), as an electrolyte supplement, is widely used in clinical practice. In our previous study, we found PA had neuroprotective effects against apoptosis after cerebral ischemia/reperfusion in rats. In this study, we examine whether PA has protective effects on traumatic brain injury (TBI). MATERIAL AND METHODS TBI was induced by controlled cortical impact (CCI) in rats. Vehicle treatment (control) or PA treatment was administered intraperitoneally at 30 minutes after CCI. The modified neurological severity score (mNSS) and cortical lesion volume were examined. Brain edema and blood-brain barrier (BBB) integrity were measured, as well as brain ATP contents, lactic acid levels, and Na+/K+-ATPase activities. RESULTS We found that CCI induced cortical injury in rats. Acute PA treatment at the dose of 62.5 mg/kg and 125 mg/kg significantly improved neurological deficits (p

Potassium aspartate (PA), as an electrolyte supplement, is used widely in clinical practice. To test the idea that high extracellular K+ might attenuate neuronal apoptosis, male Sprague-Dawley rats were subjected to 2 h of middle cerebral artery occlusion (MCAo) and 22 h of reperfusion. Vehicle or PA was administrated intraperitoneally after 1 h MCAo. The neurological deficit and dose-responses of PA to MCAo were examined. Brain ATP and lactic acid levels, caspase-3 and caspase-9 activities and the apoptotic cell death were evaluated as well as western blot analysis for cytochrome c (cyt c) release and Poly(ADP-ribose) polymerase-1 (PARP-1) cleaved. Our results show that PA treatment at the dose of 62.5 mg/kg significantly improved neurological deficits (P

In this study, a new liquid chromatographic method with pre-column derivatization was developed and validated for the simultaneous quantification of acetylcarnitine taurinate, asparagine, potassium aspartate, asparagine and carnosine in new and commercial alimentary supplements. The effect of complex matrices was evaluated by the study of the amino acid derivatization reaction with 2,5-dimethyl-1H-pyrrole-3,4-dicarbaldehyde in placebo solutions (DPD). Experimental parameters affecting the derivatization and chromatographic separation were investigated. The reaction was carried out at room temperature for 10 min. The adducts were separated on a Synergi Hydro-RP 80 column using a mobile phase consisting of 11 mM aqueous tetrapropylammonium bromide (pH 3.5)/methanol by gradient elution conditions at a flow rate of 0.8 mL/min. UV absorbance detection was set at lambda = 320 nm. The validation parameters such as linearity, sensitivity, accuracy, precision, specificity and ruggedness were highly satisfactory. Linear responses were obtained by placebo solutions (determination coefficient a parts per thousand currency sign 0.9994). Intra-day precision (RSD) was a parts per thousand currency sign1.06 % for corrected peak area and a parts per thousand currency sign1.14 % for retention times (t (R)) without significant differences between intra- and inter-day data. Recovery studies showed good results for all the examined compounds (from 97.72 to 101.5 %) with RSD

A RP-HPLC method with pre-column derivatization was developed and validated for the simultaneous quantification of carnosine (Carn), acetylcarnitine taurinate (AC-Tau), asparagine (Asn), potassium aspartate (Asp) and for the determination of phosphoserine (p-Ser) in new and commercial alimentary supplements. The effect of complex matrices was evaluated by the study of the amino acid derivatization reaction with 2,4-dinitrofluorobenzene (DNFB) both in standard and placebo solutions. The reaction was carried out for 20 min at 70 ◦C in alkaline medium (pH10) for p-Ser analysis, whereas for 60 min in the case of Carn, AC-Tau, Asn and Asp analysis. The adducts have been separated on a Discovery RP Amide C16 (250 mm × 4.6 mm, i.d.) column using a mobile phase consisting of acetonitrile (ACN) and triethylammonium (TEA) phosphate buffer (pH 3, 0.05 M) under gradient elution conditions at a flow-rate of 0.8 mL/min. Detection was set at 360 nm. The validation parameters such as linearity, sensitivity, accuracy, precision and specificity were found to be highly satisfactory. Linear responses were observed by placebo solutions (determination coefficient ≤0.9996). Intra-day precision (relative standard deviation, RSD) was ≤1.06% for corrected peak area and ≤0.99% for retention times (tR) without significant differences between intra- and inter-day data. Recovery studies showed good results for all examined compounds (from 97.7% to 101.5%) with RSD ranging from 0.5% to 1.3%). The high stability of derivatized compound solutions at room temperature means an undoubted advantage of the method allowing the simultaneous preparation of a large number of samples and consecutive chromatographic analyses by the use of an autosampler. The developed method can be considered suitable for the quality control of new and commercial products.

The ergogenic effect of aspartate salts on performance during prolonged exercise is still controversial. Potential mechanisms of the suggested ergogenic effect of aspartate on exercise performance are a sparing of muscle glycogen stores or its faster resynthesis during exercise. The purpose of this study was to determine whether aspartate causes a sparing of muscle glycogen during exercise. Six groups of rats were studied: one group received a single injection of aspartate (1 g ·. kg −1 , IP) and was then sacrificed at rest, a second group of aspartate-treated rats was sacrificed after a 60-min swim. The third and fourth groups were given an injection of physiological saline and then sacrificed respectively at rest and after a 60-min swim. The fifth and sixth groups were given an aspartate or a saline injection and then sacrificed after swimming to exhaustion. The exhaustion times after saline (178.9 ± 38.2 min) and aspartate (174.4 ± 45.2 min) were not significantly different. Results did not confirm an ergogenic effect of a single dose of aspartate on swimming endurance in the rat. Aspartate-treated rats had a significantly lower plasma FFA concentration after swimming to exhaustion when compared to control rats (respectively, 0.70 ± 0.25 vs. 1.16 ± 0.45 m M ). Also, the results of the present study do not support the hypothesis of a sparing of muscle or liver glycogen with aspartate, because a similar content of glycogen remained in the muscles and liver of control rats after a 60-min min swim or after swimming to exhaustion.

The aim of this study was to determine if the potassium aspartate and magnesium (PAM) prevent reperfusion-induced ventricular arrhythmias (RIVA) in ischemia-reperfusion (IR) rabbit heart. Thirty rabbits were randomly divided into control, ischemia and PAM groups. Arterially-perfused rabbit left ventricular preparations were made, and transmural ECG as well as action potentials from both endocardium and epicardium were simultaneously recorded in the whole process of all experiments. In control group rabbit ventricular wedge preparations were continuously perfused with Tyrode’s solution, and in ischemia group and PAM groups the perfusion of Tyrode’s solution was stopped for 30 min. Then the ischemia group was reperfused with Tyrode’s solution and the PAM group with Tyrode’s solution containing 2.42 mg/L PAM, respectively. ECG, QT interval, transmural repolarization dispersion (TDR) and action potentials from epicardium and endocardium were simultaneously recorded, and the RIVA of the wedge preparation was observed. Compared with control group, TDR and incidence of RIVA were significantly increased in ischemia group (P

Plasma aspartate levels were measured after potassium aspartate administration through different routes to rats of various ages. The changes in plasma levels were most significant with intraperitoneal injection. Dose- and age-related responses to aspartate load were obtained. The present data suggest that a marked elevation of plasma aspartate levels may result in neuronal necrosis. By comparing the plasma aspartate levels with the results on hypothalamic lesion (Okaniwa et al., 1979), plasma peak value associated with the lesion was estimated in each case of various administration routes and rat ages.

Rats of various ages were treated orally or intraperitoneally with potassium aspartate. The dose required to induce hypothalamic lesion varied considerably by the age of animals and route of administration. Additional experiment, in which the animals were orally treated three times a day with potassium aspartate in dose levels between the maximum safety dose and minimum lesion-producing dose in the preceding single dose study, revealed no hypothalamic lesion at all in any animals of each age group. In this condition, the maximum safety dose was 3--5 times as large as that in single dosage administration experiment. Regarding the safety evaluation of potassium aspartate preparations, brief discussions on some points in extrapolation of the results of the present experimental study to the clinical use were made.