Ten serwis zostanie wyłączony 2025-02-11.
Nowa wersja platformy, zawierająca wyłącznie zasoby pełnotekstowe, jest już dostępna.
Przejdź na https://bibliotekanauki.pl
Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 10

Liczba wyników na stronie
first rewind previous Strona / 1 next fast forward last
Wyniki wyszukiwania
Wyszukiwano:
w słowach kluczowych:  extracellular calcium
help Sortuj według:

help Ogranicz wyniki do:
first rewind previous Strona / 1 next fast forward last
EN
The effects of extracellular K⁺ in relation to extracellular Ca²⁺ on acid production were studied. Studies were performed in vitro using isolated cells from rat stomachs, and acid production was indirectly determined by ¹⁴C-aminopyrine (AP) accumulation. In the absence of K⁺ in the incubation medium histamine-stimulated AP accumulation ratios were significantly decreased independently in the presence or absence of extracellular Ca²⁺. Under basal conditions, in the absence of extracellular Ca²⁺ , increasing concentrations of extracellular K⁺ enhanced AP accumulation ratios to significantly higher than those found in the presence of Ca²⁺. In histamine-, cAMP-, and carbachol-stimulated parietal cells, high K⁺ concentrations increased AP accumulation significantly less in Ca²⁺-free than in Ca²⁺-containing media. High K⁺ also induced significantly both an increase in cytosolic free Ca²⁺ concentration and ⁴⁵ Ca²⁺ uptake. The present results confirmed the importance of K⁺ in gastric acid production and suggested a role for Ca²⁺ as a modulator of mechanisms of parietal cell stimulation.
2
100%
EN
Under the condition of rapid perfusion, the time course of contractile response of single ventricular cells to extracellular calcium (Ca) depletion and repletion identifies „fast” and „slow” cellular Ca pools. ⁴⁵Ca exchange was studied in these cells under the same conditions of on-line rapid perfusion. Four kinetically-defined compartments were distinguished: (1) A „rapid” compartment containing 2.6mmoles Ca/kg dry wt of lanthanum (La) displaceable Ca, t½ < 1 sec.; (2) An „intermediate” compartments) containing 2.1 mmoles, t½ = 3 and 19 sec. Caffeine displaced significant amounts of Ca from this compartment whereas La displaced none; (3) A „slow” compartment containing 1.6 mmoles, t½ = 3.6 min. Addition of inorganic phosphate to the perfusate adds significant amounts of Ca to this compartment; (4) An „inexchangeable” compartment, containing 1.2 mmoles. The „rapid” compartment’s flux is > 300 µmoles Ca/kg wet wt/sec. Its exchange rate indicates that it is the kinetic counterpart of the functionally-defined „fast” pool. Its subcellular locus is undefined. The „intermediate” compartment is best correlated with the „slow” pool and represents Ca in the sarcoplasmic reticulum. The „slow” compartment contains a significant fraction from the mitochondria. The results indicate that > 40% of cellular Ca can turn over within the period of one contraction cycle. These results are consistent with the following sequence: (1) Upon sarcolemmal depolarization, Ca moves through the Ca channel to arrive at the SR and at the myofilaments. (2) Ca induced Ca release occurs via the „feet” at the SR-inner SL region. The Ca diffuses to the myofilaments or is transported across the SL via the Na-Ca exchanger. (3) Ca is pumped into the free or longitudinal SR and diffuses to the cistemae. Ca is pumped across the SL by the SL Ca pump and by the Na-Ca exchanger. (4) Mitochondrial Ca exchange via the Na-Ca exchanger and/or SL Ca pump. (Supported by NHLBI and the Laubisch and Castera Endowments.)
EN
The "remodelling" of cardiac sarcolemma in diabetes is believed to underlie the reduced sensitivity of diabetic hearts due to their overload with extracellular calcium. Along with a non-enzymatic glycosylation and the free radical-derived glycoxidation of sarcolemmal proteins there is ongoing reduction in cardiomyocyte membrane fluidity, the modulator of cardiac sarcolemmal functioning. Aminoguanidine derivatives, that inhibit glycation and glycoxidation, might suppress myocardium "remodelling" occurring in diabetic heart. To verify this hypothesis, we studied physical parameters of cardiac sarcolemma from the streptozotocin-induced diabetic rats (45 mg.kg-1 i.m.) treated with resorcylidene aminoguanidine (RAG, 4 or 8 mg.kg-1 i.m.). The treatment with RAG not only completely abolished protein glycation and a generation of free oxygen species (p<0.001) in treated diabetic animals, but also considerably attenuated the decrease in sarcolemmal membrane fluidity (p<0.001). In diabetic animals the "normalizatio". of the sarcolemmal membrane fluidity was accompanied by the vastly increased susceptibility of diabetic hearts to be overload with external calcium. We concluded that the decreased fluidity of the sarcolemmal membrane, apparently linked to the excessive glycation of sarcolemmal membrane proteins, might be intimately connected with the adaptation mechanism(s) that are likely to develop in diabetic heart to protect it against the overload with external calcium.
first rewind previous Strona / 1 next fast forward last
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.