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Abstract:
The resting cell membrane potential varies from -40 to -70 mV according to type of gland cell and species. The RP depends mainly on the large transmembrane concentration gradient for K maintained by a pump mechanism extruding Na and accumulating K. Since the Na permeability (PNa) is much smaller than PK, the Na concentration gradient is less important. In addition to the dominant electrodiffusional control of RP the Na pump itself contributes since the active transport of Na (out) exceeds that of the active K uptake. Gland cells are generally electrically coupled--i.e., the junctional membrane resistance is much lower than the surface membrane resistance. The coupling may be widespread (e.g., liver) or confined to one acinus (e.g., salivary gland and pancreas). The specific surface cell membrane resistance may be about 2000 omega cm2. A number of neurotransmitters and hormones control cellular transport processes by their action on surface cell membrane receptors. Agonist-receptor interaction causes prominent changes in membrane potential and resistance, in many cases of a complex nature. Most gland cell membranes so far investigated in detail appear to be electrically inexcitable; i.e., stimulation does not cause the appearance of action potentials (e.g., salivary glands, exocrine pancreas, and liver) but prominent exceptions to this are the endocrine pancreas (beta-cells) and the adrenal cortex. The main importance of agonist-induced membrane permeability changes is to alter the intracellular ion activities. An increase in [Na+] seems to be important whenever stimulation results in fluid transport and an increase in [Ca2+] triggers exocytosis.