Effect of norepinephrine and hypertonicity on K influx and cyclic AMP in duck erythrocytes.
Cyclic adenosine 3',5'-monophosphate (cAMP) accumulation and cation transport were measured in duck erythrocytes after stimulation by norepinephrine (NE) or shrinkage induced by exposure to hypertonic media (S). Previously both NE and S were shown to initiate a similar transport process in this cell. NE elicited a rapid rise in cellular cAMP and 42K influx. Both effects were eliminated by propranolol. At concentrations of NE below 3 X 10(-8) M (the concentration at which 42K influx saturates), there was good correlation between the magnitude of the permeability change and the increment in cAMP. In contrast, medium hypertonicity, at a level which stimulated K influx to the same extent as a near-maximal norepinephrine response, did not alter cAMP content. The data are discussed in terms of a model in which S and NE activate a final common transport pathway by different mechanisms, which in the case of S does not involve cAMP.
D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D000242:Cyclic AMP / Q000378:metabolism*; D004372:Ducks / Q000097:blood*; D004912:Erythrocytes / Q000378:metabolism*; D005665:Furosemide / Q000494:pharmacology; D006982:Hypertonic Solutions; D008954:Models, Biological; D009638:Norepinephrine / Q000494:pharmacology*; D011188:Potassium / Q000378:metabolism*; D011433:Propranolol / Q000494:pharmacology
D006982:Hypertonic Solutions; D005665:Furosemide; D011433:Propranolol; D000242:Cyclic AMP; D011188:Potassium; D009638:Norepinephrine