Ouabain-insensitive salt and water movements in duck red cells. II. Norepinephrine stimulation of sodium plus potassium cotransport.

Abstract

A B S T R A C T Catecholamines induce net salt and water movements in duck redGen. Physiol. 70:59-79. Otherwise, these two systems share a great many similarities. In both cases, net water and salt movements have a marked dependence on external cation concentrations, are sensitive to furosemide and insensitive to ouabain, and allow the substitution of rubidium for external potassium. In the presence of ouabain, but the absence of external potassium (or rubidium), a furosemide-sensitive net extrusion of sodium against a large electrochemical gradient can be demonstrated. When norepinephrine-treated cells are incubated with ouabain and sufficient external sodium, the furosemide-sensitive, unidirectional influxes of both sodium and rubidium are half-maximally saturated at similar rubidium concentrations; with saturating external rubidium, the same fluxes are half-maximal at comparable levels of external sodium. In the absence of sodium, a catecholamine-stimulated, furosemide-sensitive influx of rubidium persists. In the absence of rubidium, a similar but smaller component of sodium influx can be seen. We interpret these results in terms of a cotransport model for sodium plus potassium which is activated by hypertonicity or norepinephrine. When either ion is absent from the incubation medium, the system promotes an exchange-diffusion type of movement of the co-ion into the cells. In the absence of external potassium, net movement of potassium out of the cell leads to a coupled extrusion of sodium against its electrochemical gradient.

Ouabain-insensitive salt and water movements in duck red cells. III. The role of chloride in the volume response.

“…The following discussion is an attempt to explain these interactions by consideration of the thermodynamic driving forces acting on the putative carrier of the cotransport pathway. In the previous paper (Schmidt and McManus, 1977b), we presented a scheme which was helpful in explaining many of the findings reported there. Since the basic emphasis of this whole investigation has been on the study of net ion and water shifts rather than unidirectional fluxes, a detailed kinetic analysis of the model cannot be generated from these results.…”

“…(5), an re1 value of 3.79 (Eel ---+36.0 mV) is predicted as necessary to prevent net sodium change. The initial rcl of 4.89 (Eel = +42.8 mV) given by 20 mM [C1]o and pHo 6.55 led to a modest but measurable net loss of cell sodium (Table III) (Schmidt and McManus, 1977b). Net sodium is transported against its electrochemical gradient simply because the total forces acting on that ion favor extrusion.…”

“…Acetate (Ac) is an organic anion that rapidly penetrates red cell membranes, probably by nonionic diffusion of the undissociated form (Deuticke, 1973 (Schmidt and McManus, 1977b), was included to test the effect of this agent on a system which allows anion movement via a pathway separate from that of chloride. In spite of the low level of [Cl]o, the cells in [Ac]o still accumulate water in response to norepinephrine (Fig.…”

Beta-Adrenergic Receptors and Isoproterenol-stimulated Potassium Transport in Erythrocytes from Normal and Hypothyroid Turkeys

“…Detailed examination of these quantitative relationships has shown that, for a given absolute level of beta receptor occupancy, even though a greater concentration of isoproterenol is required in hypothyroidism, the stimulation ofpotassium influx by isoproterenol is identical in normal and hypothyroid cells. When [15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30] receptors are occupied by agonist in either normal or hypothyroid cells, the same maximal stimulation of potassium influx occurs. These observations suggest that the reduction in beta receptor number per se in the hypothyroid turkey erythrocyte can account for its decreased sensitivity to isoproterenol-stimulated potassium influx.…”

“…The turkey erythrocyte satisfies these criteria by having a well-defined beta-adrenergic receptor and by responding to beta-adrenergic agonists with increased adenylate cyclase activity, cyclic AMP generation, and a cyclic AMP-linked enhancement of monovalent cation transport (16,17). This latter enhancement of monovalent cation transport is resistant to ouabain and sensitive to furosemide and represents, most likely, an activation of a sodium-plus-potassium cotransport pathway (18).…”