What began a quarter century ago as two separate threads in the fabric of our knowledge of cellular control mechanisms (193,212, 233) has merged today into a single dominant pattern: the synarchic regulation of cell function by the two messengers, calcium ion and cyclic AMP. It has become evident that these messengers are involved in coupling stimulus to response in a wide variety of differentiated cell types when these cells are called on to perform their specific function. In regulating cellular function, Ca2+ and CAMP nearly always function together. Their interactions are plastic rather than stereotyped in character. Although the molecular and cellular mechanisms involved in the initiation, propagation, reception, and termination of the CAMP message have 938

Oxygen uptake rates and microdistributions of 0, in sediment of Aarhus Bay, Denmark. were studied over a year. Oxygen uptake was determined in the laboratory by 3 methods: (a) total O2 uptake in closed cores, (b) O2 flux through the diffusive boundary layer and (c) O2 consumption within the oxic surface zone. The O2 consumption rates in the oxic surface layer, calculated from (b) and (C) using molecular diffusion coefficients of 02, closely agreed and accounted for 70 % of the total O2 uptake. The O2 uptake rates strongly depended on in situ O2 concentrations in the overlying seawater. which in the bay varied from 100 % air saturation during winter to 23 ' X, during summer. The potentially higher O2 respiration during the summer months was counteracted by a lower O2 concentration in the bottom water, which led to a small seasonal variation in 0, uptake. Depth of the oxic sediment zone reached 5.1 mm during winter, narrowed down rapidly to a few mm upon settling of a spring phytoplankton bloom, and was only 1.2 mm during summer. Modeling of O2 consumption from O2 microprofiles showed zero-order kinetics, i.e. constant 0, consumption rates throughout the oxic zone during winter. Enhanced O2 consumption was found at the oxic-anoxic interface during summer, presumably due to reducing solutes which diffused up from anoxic layers Sediment 0, uptake was impeded by 3 to 5 % during winter and by 12 to 16 "L during summer due to transport resistance through the 300 pm thick diffusive boundary layer. Results demonstrate the importance of the boundary layer for sediment O2 uptake and its regulation.

The hypothesis advanced in this article requires further validation. Undoubtedly it will require modification as our knowledge of biochemical control increases. Nevertheless, it should prove useful in focusing attention on the apparent similarity in the response of a large number of specific cell types to particular stimuli. Emphasis has been placed on a few common and apparently key elements in these responses. It is recognized that other factors are undoubtedly involved. Specifically, the changes in membrane potentials indicate the likelihood of widespread changes in the properties of the cell membrane, for example, changes in Na(+) and K(+) transport and distribution. These aspects of cellular responses may eventually prove to be of equal or greater importance than those common aspects of the system already identified.

No abstract

The cellular and molecular mechanisms underlying smooth muscle contraction are reviewed in the light of recent studies of smooth muscle ultrastructure and of the role of polyphosphoinositide turnover and protein kinase C function in smooth muscle contraction. A new model of smooth muscle contraction is proposed that differs radically from accepted views, particularly the latch bridge hypothesis, in terms of both Ca2+ messenger function and the molecular events underlying this process. A coordinate fibrillar domain model of contraction is proposed in which the initial and sustained phases of contraction are mediated by different cellular and molecular events. The initial phase of response is mediated by a rise in [Ca2+]c and the resulting calmodulin-dependent activation of both myosin light chain kinase and the dissociation of caldesmon from the actin-caldesmon-tropomyosin-myosin fibrillar domain. These events lead to an interaction between actin and the phosphorylated light chains of myosin just as in previous models. However, this initial phase is followed by a sustained phase in which a rise in [Ca2+]sm stimulates the plasma membrane-associated, Ca2+-sensitive form of protein kinase C that results in the phosphorylation of both structural and regulatory components of the filamin-actin-desmin fibrillar domain. These events underlie the tonic phase of contraction.