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PubMed1989

Anisosmotic cell volume regulation: a comparative view.

A variety of organisms and cell types spanning the five taxonomic kingdoms are exposed, either naturally or through experimental means, to osmotic stresses. A common physiological response to these challenges is maintenance of cell volume through changes in the concentration of intracellular inorganic and organic solutes, collectively termed osmolytes. Research on the mechanisms by which the concentration of these solutes is regulated has proceeded along several experimental lines. Extensive studies on osmotically activated ion transport pathways have been carried out in vertebrate cells and tissues. Much of our knowledge on organic osmolytes has come from investigations on invertebrates, bacteria, and protists. The relative simplicity of bacterial genetics has provided a powerful and elegant tool to explore the modifications of gene expression during volume regulation. An implication of this diverse experimental approach is that phylogenetically divergent organisms employ uniquely adapted mechanisms of cell volume regulation. Given the probability that changes in extracellular osmolality were physiological stresses faced by the earliest organisms, it is more likely that cell volume regulation proceeds by highly conserved physiological processes. We review volume regulation from a comparative perspective, drawing examples from all five taxonomic kingdoms. Specifically, we discuss the role of inorganic and organic solutes in volume maintenance and the mechanisms by which the concentrations of these osmolytes are regulated. In addition, the processes that may transduce volume perturbations into regulatory responses, such as stretch activation of ion channels, intracellular signaling, and genomic regulation, are discussed. Throughout this review we emphasize areas we feel are important for future research.

Animals↗
PubMed1984

Vasopressin in plasma and cerebrospinal fluid of hydrated and dehydrated steers.

Levels of arginine-vasopressin (AVP), the antidiuretic hormone, have been concurrently measured by radioimmunoassay (RIA) in plasma (p) and cerebrospinal fluid (CSF) from conscious, unrestrained steers. During 4 days of dehydration, plasma osmolarity (posm) rose progressively from control hydrated levels of 301.3 +/- 0.632 mosm/1(mean +/- SE) to 338.5 +/- 3.090 mosm/1(p less than 0.001). Packed cell volume also rose from 39.9 +/- 0.64% to 44.7 +/- 1.24% (p less than 0.001). Associated with these changes was a progressive increase in pAVP from control levels of 1.3 +/- 0.19 microU/ml to 16.9 +/- 1.88 microU/ml(p less than 0.001) after 4 days without water. Log pAVP was linearly related to posm (r = 0.82, p less than 0.001). Mean level of CSF-AVP in control animals was 5.4 +/- 0.97 microU/ml. During dehydration, CSF-AVP levels also rose, becoming significantly greater than control levels (p less than 0.01) after 3 days without water and further increasing to reach 15.2 +/- 1.83 microU/ml after 4 days without water (p less than 0.001). Log CSF-AVP could also be linearly related to posm (r = 0.62, p less than 0.01). Termination of dehydration by restoration of ad libitum water supply was accompanied by return of pAVP and CSF-AVP to pre-dehydration levels. Regression analysis of concurrent levels of pAVP an CSF-AVP indicates that CSF-AVP levels are linearly correlated to pAVP levels in hydrated and dehydrated animals (r = 0.70, p less than 0.001). These experiments suggest that neurosecretory neurons secreting AVP at sites accessible to CSF respond to similar stimuli during dehydration as those neurons secreting AVP into blood.

Animals↗
PubMed1992

The effect of age on motor and cognitive deficits after traumatic brain injury in rats.

Age is one of the most important predictors of outcome after human traumatic brain injury. This study used fluid percussion brain injury to investigate the effects of aging on outcome after brain injury in rats. Three-month-old (n = 8) and 20-month-old (n = 11) rats were injured at a low level (1.7-1.8 atm) of fluid percussion brain injury or received a sham injury (n = 6 for both age groups). Body weight and motor function (beam balance and beam walking) were assessed before injury and for the first 5 days after injury. Cognitive outcome was assessed with the Morris water maze on Days 11 to 15 after injury. Injury did not produce significant weight loss in either age group. At the low level of brain injury used in this study, the 3-month-old rats did not demonstrate any significant motor deficits on the beam-balance or beam-walking tasks. However, the 20-month-old rats displayed significant beam-balance deficits on each of the 5 postinjury test days and significant beam-walking deficits for the first 3 postinjury days. Although Morris water maze performance was impaired in both age groups, the magnitude of impairment was greater in the aged animals. These data demonstrate that traumatic brain injury in the aged animal is marked by increased motor and cognitive deficits, in the absence of pronounced compromise of the animal's general health.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗