Calcium fluxes in cardiac sarcolemma and sarcoplasmic reticulum isolated from endotoxin-shocked guinea pigs.

In vitro examination of cardiac tissues isolated from septic and endotoxin-shocked animals has demonstrated intrinsic decreased contractile function and has suggested calcium-related dysfunction. Both the sarcolemma (SL) and sarcoplasmic reticulum (SR) membranes have important roles in regulating cardiac free Ca2+ concentration. Therefore, calcium fluxes were examined in well-characterized SL and SR fractions isolated from hearts of control and endotoxin-shocked guinea pigs.

Contractile function of aortic smooth muscle in guinea pig endotoxin shock.

Contractile responsiveness of aortic rings from control and endotoxin-shocked guinea pigs was examined in vitro. Aortae were removed 16 h following intraperitoneal administration of 4 mg/kg of Escherichia coli endotoxin or sterile saline. Although no shift in the dose-response curve or maximal contraction to norepinephrine (10(-9)-10(-4) M) was observed, there was an enhanced contractile response to KCl in shock rings.

Ca2+-induced aortic contraction in normal K+ after exposure to Ca2+- and Mg2+ -free solution.

Guinea pig and rabbit aortic rings which have been incubated in a Ca2+- and Mg2+ -free solution containing ethylene glycol bis-(beta-aminoethyl ether) N,N,N'N'-tetraacetic acid (EGTA) responded to addition of Ca2+ in a similar Ca2+ - and Mg2+ -free solution without EGTA by increasing tension gradually at first and then more sharply at Ca2+ concentrations above 2 mM. Prior addition of D 600 (10 or 50 microM) inhibited contractions to low Ca2+ concentrations, but only partially attenuated those to high Ca2+ concentrations. The resulting contraction is thought to represent Ca2+ entry from both voltage-dependent (D 600-sensitive) Ca2+ channels and Na+ -Ca2+ exchange (D 600-insensitive).

Effects of manganese on 45Ca mobilization and contractile responses in rabbit aortic smooth muscle.

In rabbit aortic smooth muscle, 1.5 mM Mn2+ inhibits contractile responses to norepinephrine more than those to high K+. Other associated effects include decreases in the La3+-resistant high affinity Ca2+ fraction, the high affinity Ca2+ uptake component in the Scatchard-coordinate plot, and high affinity Ca2+ uptake and binding in canine aortic microsomes.

Potassium-induced contraction in smooth muscle.

High K-induced contractions in the smooth muscle of rabbit aorta and guinea pig taenia coli may be described as follows: High K depolarizes the smooth muscle cell membrane and opens voltage dependent Ca channels, resulting in an influx of extracellular Ca and an activation of contractile machinery. A part of the cellular Ca is taken up by mitochondria. Oxygen consumption of the muscle increases to compensate for the ATP consumed by contraction.