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At confluency, LLC-PK1 monolayers develop a transepithelial electrical resistance of 127 omega X cm2 and a spontaneous electrical potential that very seldom exceeds 1 mV. The monolayer shows a linear current-voltage relation in symmetrical solutions. The total conductance increases linearly with increases in the electrolyte concentration of the bathing solution. These characteristics indicate that the membrane that controls the permeability properties of the monolayer is a single membrane that it does not contain very weakly charged sites and it is sufficiently thick to obey the principle of microscopic electroneutrality. The sodium-to-chloride permeability determined from dilution potentials or from direct measurements of unidirectional Na+ and Cl- flux are 0.30 and 0.38, respectively, almost identical to the ratio obtained in the straight segment of the renal proximal tubule. The steady-state value of the electrical resistance depends on the Ca2+ concentration in the incubation medium with an apparent Km of 0.1 mM. A transitory opening of the occluding junctions results in a more uniform distribution of the Na+-dependent sugar transport system, which is normally confined to the apical membrane of the epithelial cell. This result indicates that the occluding junctions in LLC-PK1 monolayers act as a mechanical barrier, preventing the intermixing of extrinsic as well as intrinsic membrane proteins.

The distribution of pyruvate, phosphate, malate, citrate, K+, aspartate, glutamate, ADP, and ATP between the mitochondrial and cytosolic compartments was studied in isolated rat hepatocytes exposed to 30 min anoxia. The results show that pyruvate and citrate gradients are comparable to aerobic values, indicating that the pH gradient across the membrane under anaerobic conditions is comparable to that under normal aerobic conditions. In contrast, the distribution of phosphate, malate, ATP, ADP, aspartate, and glutamate suggests that transport of these species may be inhibited during anoxia. The results are discussed in terms of potential regulation of mitochondrial function to provide a quiescent anoxic state that is capable of recovering normal function on reoxygenation.

Carotid body chemoreceptors are activated by low PO2, high PCO2, acidity, increased temperature, and tonicity. These receptors are important in homeostasis and mediate their reflex effects on the CNS through sensory discharges of the carotid (sinus) nerve. The receptor complex is formed by glomus (type I) cells and carotid nerve endings, which, morphologically, appear to form a sensory synapse. The junction between glomus cells and nerve endings is enveloped by processes of sustentacular (type II) cells. The mechanisms of chemoreceptor transduction are complex; there is no agreement about the identity of the primary receptor element (glomus cell or nerve terminal) or what mechanisms are responsible for the onset of the sensory discharge in the carotid nerve. There is increasing evidence that integrity of the glomus cell is essential for normal transduction and that the receptor synapse described by morphologists may be functionally active. There is no conclusive evidence, however, that the glomus cell is the primary site of sensory transduction. Stimuli act on the glomus cell to release "transmitter" and/or "modulator" substances; but it is unknown if the released chemicals are directly responsible for the accompanying change in sensory impulse frequency or merely modify an already ongoing discharge. Interactions between glomus cells and nerves may be complicated enough to make it very difficult to resolve this question.