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Biomedical subjects

C Ren

Publications and source records attributed to C Ren.

61 records · Page 4Linked to original sources
PubMed1992

Hypovolemia induces Fos-like immunoreactivity in neurons of the rat supraoptic and paraventricular nuclei.

Immunoreactivities to Fos proteins were detected in numerous neurons in the supraoptic, paraventricular and accessory neurosecretory nuclei 1 h following withdrawal of 4-5 cc of blood from the rat femoral arteries. Few or no positive cells were observed in the same nuclei in sham-operated or control animals. It is concluded that hypovolemia induces c-fos expression in hypothalamic neurons known to be associated with blood volume/pressure regulation.

Animals↗
PubMed1992

Synaptic mechanisms in sympathetic preganglionic neurons.

Intracellular recordings from sympathetic preganglionic neurons (SPNs) in adult cat and neonatal rat spinal cord slices reveal four types of synaptic potentials, namely, excitatory postsynaptic potentials (EPSPs), inhibitory postsynaptic potentials (IPSPs), and slow EPSPs in both preparations, and a slow IPSP in cat SPNs. Pharmacological studies show that glutamate or a related excitatory amino acid and glycine are the probable mediators of EPSPs and IPSPs. There may be heterogenous mediators of slow EPSPs; substance P, serotonin, norepinephrine, and epinephrine are all probable mediators of slow EPSPs in subpopulations of SPNs. In the case of slow IPSPs, norepinephrine appears to be the likely transmitter. Finally, stimulation of ventral roots elicits a synaptic potential that appears to be caused by glutamate released from afferent fibers in the ventral roots. Our results indicate that a multitude of synaptic mechanisms exist in the rat SPNs by means of which inputs arising from sensory and supraspinal neurons are processed in a timely and orderly manner, thus ensuring highly organized but differentiated outputs to multiple peripheral target cells.

Animals↗
PubMed1988

Effect of membrane potential and cellular ATP on glutathione efflux from isolated rat hepatocytes.

total glutathione (GSH) efflux was studied in isolated rat hepatocyte suspensions at repleted GSH content (45-55 nmol/10(6) cells). The increase in concentrations of medium K+ in place of Na+ caused a parallel fall in membrane potential and total GSH efflux. Ouabain (1 mM) and replacement of Na+ with choline caused a gradual fall in membrane potential and GSH efflux. Hyperpolarization of hepatocytes with lipophilic anions, thiocyanate, and nitrate was associated with significantly increased efflux. Total GSH efflux was inhibited by increasing concentrations of fructose, antimycin A, and carbonyl cyanide p-trifluoromethoxyphenylhydrazone, and there was a direct relationship between the rate of efflux and cellular ATP. Changes in total GSH efflux were paralleled by changes in GSH determined by high-performance liquid chromatography. Vanadate markedly inhibited efflux but caused only a modest decrease in cellular ATP. Fructose, antimycin A, and vanadate did not affect membrane potential or cell volume under the conditions at which efflux was inhibited. These results suggest independent requirements for both membrane potential and ATP in the transport of GSH.

Adenosine Triphosphate↗
PubMed1986

Kinetics of glutathione efflux from isolated rat hepatocytes.

The characteristics and kinetics of glutathione (GSH) efflux were examined in homogeneous suspensions of freshly isolated rat hepatocytes. GSH efflux was measured as its linear accumulation in the suspension medium. Appearance of GSH extracellularly was reflected in a quantitative loss in cellular GSH. However, the total GSH remained essentially unchanged, indicating minimal net synthesis of GSH under these experimental conditions. GSH efflux was sensitive to temperature, with a calculated Q10 value of 2.3. A wide range of cellular GSH concentration ranging from near complete and moderate depletion to severalfold the control values was achieved by treatment of animals or cells with various GSH depletors or inducers. At physiological (fed) and elevated (3-methylcholanthrene- and CoCl2-induced) cellular GSH, the rate of GSH efflux was near maximum. The rate fell dramatically to 50% maximum at a GSH concentration equaling 35 nmol/10(6) cells. A 48-h fast resulted in a 40% loss of cellular GSH, with a corresponding decrease in efflux rates. Addition of GSH to the incubation medium had no effect on efflux rates. The relationship of GSH efflux to cellular GSH concentration was characterized by apparent sigmoidal saturation kinetics. The data were fitted well by the Hill model with the following kinetic parameters: Vmax = 0.25 nmol X 10(6) cells-1 X min-1, Km = 3.5 mM, and n = 3. These results correspond very closely to our previous findings in the perfused liver.

Animals↗