Effects of nifedipine and captopril on cisplatin induced nephrotoxity in rats / 대한신장학회잡지

No abstract available.

The Study on the Na(+), K(+)-ATPase Activities of the Spontaneously Hypertensive Rats

Although the mechanism of the development of hypertension has not been fully elucidated, abnormal ion transport across the cardiovascular musle membrance may play some role in this mechanism. The elevation of intraceular sodium by inhibition of the Na(+), K(+)-ATPase diminshes the sodium gradient for calcium extrusion and/or increase Na(+)/Ca(++) exchange across the cell membrance. In any event, contractility and vascular tone of cardiovascular system can be incresed as reslut of an increase of intracellular calcium. Recently it is reported that the defects of Na(+), K(+)-ATPase occur in spontaneously hypertensive rat(SHR) hearts, compared to control normotensive Spargue Dawley(SD) rat hearts. However, one missing, unresolved question arose in the previous reports in whether the reduced Na(+)-pump activity in the heart of SHR is associated with the development of hypertension itself in these animals or is a consequence of inhertied pathological features that later reslut in a reduced pump activity. In order to clearify this question it is attempted to measured to measure the change of the Na(+), K(+)-ATPase activities in cardiac sarcolemma purified from both the normotensive SD rats and SHR rats during growth ; Simultaneously the charge of cation concentration in both intracellular space(RBC) and extracelluar space(ECF) are measured to the erythrocyte test(Garay and Meyer) applied to the clinical investiation of hypertension. The results obtained are summarized as follows ; 1) The systolic blood pressure of 7 week old SHR was 120-130mmHg, which was not significantly different from that of the age-matched SD rats. However, the blood pressure was elevated to 160-170mmHg in 13-15 week old SHR, even elevated to 190mmHg in one of 19 week old SHR. On the other hand, SHR, in which hypertension was well established had pronounced cardiac hypertrophy. 2) The Na(+), K(+)-ATPase activities in cardiac sarcolemma of the SHR rats were decreased gradually as hypertension established.The decrease of Na(+), K(+)-ATPase was well associated with the increase of intracellular potassium concentration.By contrast, thr Na(+), K(+)-ATPase activities and cation transports og the normotensive SD rats were not significanlty chaged during growth. 3) The charges of Na(+), K(+)-ATPase activities in SHR were specific because the activities of Ca(++)-ATPase which is one of the membrance bound enzyme were not changed during growth appeared to be a major fator which generated hypertension in SHR rats. However, question on how the Na(+), K(+)-ATPase activities are decreased and which event is initiative between reduction of Na(+), K(+)-ATPase and development of hypertension are still remained unclear. Recent literature suggests the there might be a genetic factor, so-called Na(+)-pump inhibitor, involved in the meachanism.

Effects of Bupivacaine on Calcium Transport Across Biological Membranes and Its Cardiotoxicity / 대한마취과학회지

A new local anesthetic, bupivacaine, is widely used for regional anesthesia because of its high potency and long duration of action. However, bupivacaine is reported to result in cardiovascular collapse associated with convulsion at a plasma concentration above the normal one, while other local anesthetics do not. Also resuscitation is very difficult. Although the mechanism of this action is not known, bupivacaine seems to have an influence on Ca2+ transport across cell membranes via various pathways. The present study was designed to evaluate the effects of bupivacaine on Ca2+ transport across cell membranes. The results are as follows: 1) Bupivacaine inhibites Ca2+ uptake by SR of skeletal muscle. 2) Bupivacaine suppressed the Bowditch and Woodworth staircase phenomena in a guines pig's left auricle, however this was reversible even at convulsant doses. 3) Bupivacaine also suppressed the Na+-Ca2+ exchange pump on guines pig's left auricle. 4) Bupivacaine increased the Ca2+-ATPase activity by SR of skeletal muscle. 5) At concentrations above 3ug/ml, bupivacaine induced cardiac arrhythmia. These findings suggest that bupivacaine-induced cardiotoxicity is possibly due to a Ca2+- channel blockade, depression of the Na+-Ca2+ pump, inhibition of Ca2+ uptake by SR and subsequent decrease of intracellular Ca2+ concentration.