Membrane damage and the Ca(2+)-paradox in the perfused rat kidney.
Lactate dehydrogenase (LDH) leaks from the perfused rat kidney under the artificial conditions of a Ca(2+)-paradox protocol, namely Ca(2+)-repletion following a 20 minute period of Ca(2+)-depletion. LDH leakage was markedly suppressed by perfusion at 25 degrees C or with 0.1 mM dibucaine or 2 mM lidocaine. Lidocaine inhibited leakage only during Ca(2+)-depletion. Lowering the perfusion rate significantly reduced LDH escape. No LDH loss occurred if the osmotic pressure of the perfusion fluid was raised by 420 mOsm during either Ca(2+)-depletion or Ca(2+)-repletion. Amiloride (2 mM) significantly reduced LDH leakage to 43%. Reduction of the pH of the perfusion fluid to 6.8 significantly inhibited LDH loss, and at pH 6.4 this leakage was almost completely suppressed. LDH loss was equally suppressed at pH 6.4 only during Ca(2+)-depletion, whereas pH 6.4 was markedly less effective when perfused only during Ca(2+)-repletion. Ouabain (5 x 10(-6) M) had only a limited effect in exacerbating LDH leakage. Raising [K+]o significantly protected against LDH leakage, which fell to 36% at 16 mM [K+]. These features correspond with the Ca(2+)-paradox of the perfused rat heart an it is suggested that: (i) a Ca(2+)-paradox can be produced in the rat kidney; (ii) a similar mechanism governs the release of cytosolic proteins in these two preparations; and (iii) the damage mechanism of the plasmalemma is a transmembrane oxidoreductase-diaphorase molecular complex which generates H+ when activated by Ca(2+)-depletion.
원문보기 무료다운로드 유료다운로드
- 원문이 없습니다.
유료 다운로드의 경우 해당 사이트의 정책에 따라 신규 회원가입, 로그인, 유료 구매 등이 필요할 수 있습니다. 해당 사이트에서 발생하는 귀하의 모든 정보활동은 NDSL의 서비스 정책과 무관합니다.
NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니 담기를 통하여 원문복사서비스 이용이 가능합니다.