Urea alters set point volume for K-Cl cotransport, Na-H exchange, and Ca-Na exchange in dog red blood cells

1993 ◽  
Vol 265 (2) ◽  
pp. C447-C452 ◽  
Author(s):  
J. C. Parker
Keyword(s):  
Red Blood Cells ◽  
Cell Volume ◽  
Okadaic Acid ◽  
Blood Cells ◽  
Regulatory System ◽  
Set Point ◽  
Volume Sensor

Urea equilibrates rapidly across the red blood cells of mammals. It was speculated that urea might affect the cell volume sensor by virtue of its properties as a protein perturbant. At concentrations of 0.1-0.6 M, urea caused a decrease in the set points for shrinkage-induced Na-H exchange, swelling-induced K-Cl cotransport, and swelling-induced Ca-Na exchange of dog red blood cells. Okadaic acid opposed the action of urea on all three pathways. The effects were reversible and not due to cyanate. Formamide and acetamide had actions similar to urea but not as potent. Equimolar concentrations of methanol had no effect. The coordinated influence of urea on three separate volume-activated transporters suggests that it acts on a mutual regulatory system that senses and transduces volume stimuli.

scholarly journals pH regulatory Na/H exchange by Amphiuma red blood cells.

1994 ◽  
Vol 103 (6) ◽  
pp. 1035-1053 ◽  
Author(s):  
P M Cala ◽  
H M Maldonado
Keyword(s):  
Blood Cell ◽  
Red Blood Cells ◽  
Cell Volume ◽  
Red Blood Cell ◽  
Blood Cells ◽  
Ph Sensing ◽  
Cell Shrinkage ◽  
Set Point ◽  
Degree Of Acidification ◽  
Regulatory Functions

In Amphiuma red blood cells, the Na/H exchanger has been shown to play a central role in the regulation of cell volume following cell shrinkage (Cala, P. M. 1980. Journal of General Physiology. 76:683-708.) The present study was designed to evaluate the existence of pH regulatory Na/H exchange in the Amphiuma red blood cell. The data illustrate that when the intracellular pHi was decreased below the normal value of 7.00, Na/H exchange was activated in proportion to the degree of acidification. Once activated, net Na/H exchange flux persisted until normal intracellular pH (6.9-7.0) was restored, with a half time of approximately 5 min. These observations established a pHi set point of 7.00 for the pH-activated Na/H exchange of Amphiuma red blood cell. This is in contrast to the behavior of osmotically shrunken Amphiuma red blood cells in which no pHi set point could be demonstrated. That is, when activated by cell shrinkage the Na/H exchange mediated net Na flux persisted until normal volume was restored regardless of pHi. In contrast, when activated by cell acidification, the Na/H exchanger functioned until pHi was restored to normal and cell volume appeared to have no effect on pH-activated Na/H exchange. Studies evaluating the kinetic and inferentially, the molecular equivalence of the volume and pHi-induced Amphiuma erythrocyte Na/H exchanger(s), indicated that the apparent Na affinity of the pH activated cells is four times greater than that of shrunken cells. The apparent Vmax is also higher (two times) in the pH activated cells, suggesting the involvement of two distinct populations of the transporter in pH and volume regulation. However, when analyzed in terms of a bisubstrate model, the same data are consistent with the conclusion that both pH and volume regulatory functions are mediated by the same transport protein. Taken together, these data support the conclusion that volume and pH are regulated by the same effector (Na/H exchanger) under the control of as yet unidentified, distinct and cross inhibitory volume and pH sensing mechanisms.

Colloid osmotic pressure changes of dog's blood exposed to different mixtures of CO2 and air

1978 ◽  
Vol 44 (2) ◽  
pp. 254-257 ◽  
Author(s):  
Y. Kakiuchi ◽  
A. B. DuBois ◽  
D. Gorenberg
Keyword(s):  
Red Blood Cells ◽  
Osmotic Pressure ◽  
Cell Volume ◽  
Blood Cells ◽  
Freezing Point ◽  
Colloid Osmotic Pressure ◽  
Red Cell ◽  
Freezing Point Depression ◽  
Pressure Changes ◽  
Different Levels

Hansen's membrane manometer method for measuring plasma colloid osmotic pressure was used to obtain the osmolality changes of dogs breathing different levels of CO2. Osmotic pressure was converted to osmolality by calibration of the manometer with saline and plasma, using freezing point depression osmometry. The addition of 10 vol% of CO2 to tonometered blood caused about a 2.0 mosmol/kg H2O increase of osmolality, or 1.2% increase of red blood cell volume. The swelling of the red blood cells was probably due to osmosis caused by Cl- exchanged for the HCO3- which was produced rapidly by carbonic anhydrase present in the red blood cells. The change in colloid osmotic pressure accompanying a change in co2 tension was measured on blood obtained from dogs breathing different CO2 mixtures. It was approximately 0.14 mosmol/kg H2O per Torr Pco2. The corresponding change in red cell volume could not be calculated from this because water can exchange between the plasma and tissues.

scholarly journals Volume regulation by flounder red blood cells in anisotonic media

1977 ◽  
Vol 69 (5) ◽  
pp. 537-552 ◽  
Author(s):  
PM Cala
Keyword(s):  
Red Blood Cells ◽  
Cell Volume ◽  
Water Flow ◽  
Blood Cells ◽  
Volume Regulation ◽  
Control Cell ◽  
Regulatory Volume Decrease ◽  
Electrochemical Gradient ◽  
Osmotic Swelling ◽  
Inorganic Cation

The nucleated high K, low Na red blood cells of the winter flounder demonstrated a volume regulatory response subsequent to osmotic swelling or shrinkage. During volume regulation the net water flow was secondary to net inorganic cation flux. Volume regulation the net water flow was secondary to net inorganic cation flux. Volume regulation after osmotic swelling is referred to as regulatory volume decrease (RVD) and was characterized by net K and water loss. Since the electrochemical gradient for K is directed out of the cell there is no need to invoke active processes to explain RVD. When osmotically shrunken, the flounder erythrocyte demonstrated a regulatory volume increase (RVI) back toward control cell volume. The water movements characteristic of RVI were a consequence of net cellular NaCl and KCl uptake with Na accounting for 75 percent of the increase in intracellular cation content. Since the Na electrochemical gradient is directed into the cell, net Na uptake was the result of Na flux via dissipative pathways. The addition of 10(-4)M ouabain to suspensions of flounder erythrocytes was without effect upon net water movements during volume regulation. The presence of ouabain did however lead to a decreased ration of intracellular K:Na. Analysis of net Na and K fluxes in the presence and absence of ouabain led to the conclusion that Na and K fluxes via both conservative and dissipative pathways are increased in response to osmotic swelling or shrinkage. In addition, the Na and K flux rate through both pump and leak pathways decreased in a parallel fashion as cell volume was regulated. Taken as a whole, the Na and K movements through the flounder erythrocyte membrane demonstrated a functional dependence during volume regulation.

scholarly journals Impact of parity and gestational age of mothers with hypertension on birth weight, red blood cells and mode of delivery of their babies

1970 ◽  
Vol 19 (4) ◽  
pp. 3038-3044
Author(s):  
Helen Chioma Okoye ◽  
Chilota Chibuife Efobi ◽  
Josephat Maduabuchi Chinawa ◽  
Odutola Israel Odetunde ◽  
Awoere Tamunosiki Chinawa ◽  
...  
Keyword(s):  
Birth Weight ◽  
Red Blood Cells ◽  
Cell Volume ◽  
Gestational Age ◽  
Packed Cell Volume ◽  
Blood Cells ◽  
Mode Of Delivery ◽  
Poor Correlation ◽  
Hypertensive Group ◽  
The Impact

Background: Maternal factors are determinants of birth outcome which includes birth weight, haematological indices and mode of delivery of their babies.Objectives: To determine the impact of parity and gestational age of hypertensive mothers on some neonatal variables.Methods: A hospital based cross-sectional study of measurement of neonatal variables (birth weight, red blood cells and mode of delivery) among hypertensive mothers and their controls was conducted over a period of six months. Data were analyzed using the Statistical Package for Social Sciences program (SPSS), version 20.Results: There were statistically significant differences in means between the neonates of the hypertensive group and non-hypertensive group for maternal age (t =1.61, p = 0.002), baby weight (t =2.87, p < 0.001), haemoglobin (Hb) (t =4.65, p = 0.010) and packed cell volume (PCV) (t =4.75, p = 0.009), but none for gravidity (t =1.95, p = 0.927)For all subjects, there was poor correlation between gestational age and variables; birth weight , haemoglobin (Hb), packed cell volume (PCV), nucleated red blood cell (nRBC) and parity. Likewise, parity poorly correlated with variables; age, birth weight, Hb, PCV, and nRBC. There was a statistically significant association between mode of delivery and hypertension (χ2 =53.082, p <0.001) but none with having a family history of hypertension (χ2 =1.13, p = 0.287).Conclusion: Parity and gestational age of mothers with hypertension have no impact on birth weight and red cells when compared with their non-hypertensive counterparts. However, mothers of babies delivered by elective and emergency caesarean section were about 2-3 times more likely to be hypertensive than those that delivered through spontaneous vertex delivery.Keywords: Hypertension; neonate; gestational age; parity.

Splenic red cell sequestration and blood volume measurements in conscious pigs

1985 ◽  
Vol 248 (3) ◽  
pp. R293-R301 ◽  
Author(s):  
J. P. Hannon ◽  
C. A. Bossone ◽  
W. G. Rodkey
Keyword(s):  
Red Blood Cells ◽  
Cell Volume ◽  
Blood Volume ◽  
Plasma Volume ◽  
Blood Cells ◽  
Physical Restraint ◽  
Red Cell ◽  
Red Cell Volume ◽  
Epinephrine Injection ◽  
Volume Measurements

When estimated by the dilution of 51Cr-labeled red blood cells under nearly basal conditions, immature splenectomized pigs (n = 20) had a circulating red cell volume of 17.8 +/- 1.64 (SD) ml/kg. At an assumed body-to-large vessel hematocrit (BH:LH) ratio of 0.9, plasma volume was 49.6 +/- 3.12 ml/kg and blood volume 67.3 +/- 3.67 ml/kg. Sham-operated pigs (n = 20) had a circulating red cell volume of 16.2 +/- 1.39 ml/kg, a plasma volume of 51.1 +/- 3.42 ml/kg, and blood volume of 67.2 +/- 4.12 ml/kg. Kinetic analysis of early 51Cr loss from the circulating blood of the sham-operated pigs indicated a splenic red cell sequestration of 4.5 +/- 0.89 ml/kg and a t1/2 of 9.76 +/- 1.93 min for splenic red cell turnover. Epinephrine injection (n = 6) and physical restraint (n = 8) caused rapid mobilization of splenic red blood cells in sham-operated pigs. Volume estimates in splenectomized pigs (n = 7) based on simultaneous dilutions of 51Cr-labeled red blood cells and 125I-labeled bovine albumin gave circulating red cell, plasma, and blood volumes of 18.4 +/- 2.46, 60.7 +/- 4.01, and 79.0 +/- 3.51 ml/kg, respectively, and a BH:LH ratio of 0.756 +/- 0.029. The latter value may have reflected an overestimation of plasma volume by the 125I-labeled albumin procedure.

Cell volume and metabolic dependence of NEM-activated K+-Cl- flux in human red blood cells

1985 ◽  
Vol 249 (1) ◽  
pp. C124-C128 ◽  
Author(s):  
P. K. Lauf ◽  
C. M. Perkins ◽  
N. C. Adragna
Keyword(s):  
Red Blood Cells ◽  
Cell Volume ◽  
Blood Cells ◽  
Time Course ◽  
Transport Activity ◽  
Human Red Blood Cells ◽  
Atp Breakdown ◽  
The Difference ◽  
Metabolic Dependence ◽  
K Transport

The effects of incubation in anisosmotic media and of metabolic depletion on ouabain-resistant (OR) Cl--dependent K+ influxes stimulated by N-ethylmaleimide (NEM) were studied in human red blood cells using Rb+ as K+ analogue. The NEM-stimulated but not the basal Rb+-Cl- influx measured in phosphate-buffered anisosmotic media was found to be cell volume dependent. When cellular ATP, [ATP]c, was lowered to less than 0.10 of its initial level by exposure to nonmetabolizable 2-deoxy-D-glucose, the NEM-stimulated but not the basal Cl--dependent Rb+ influxes were abolished. Metabolically depleted red blood cells subsequently repleted by incubation in glucose plus inosine regained the NEM-inducible Rb+ (K+) transport activity. The difference in the time course of ATP breakdown and Rb+ influx inhibition suggests that energization of the NEM-stimulated Rb+ flux by metabolism may involve factors additional to ATP.

scholarly journals The role of ATP in swelling-stimulated K-Cl cotransport in human red cell ghosts. Phosphorylation-dephosphorylation events are not in the signal transduction pathway.

1993 ◽  
Vol 102 (3) ◽  
pp. 551-573 ◽  
Author(s):  
J R Sachs ◽  
D W Martin
Keyword(s):  
Signal Transduction ◽  
Red Blood Cells ◽  
Okadaic Acid ◽  
Blood Cells ◽  
Kinase Inhibitor ◽  
Signal Transduction Pathway ◽  
Maximal Activity ◽  
Cell Protein ◽  
Intact Cells ◽  
Human Red Blood Cells

Volume-sensitive K-Cl cotransport occurs in red blood cells of many species. In intact cells, activation of K-Cl cotransport by swelling requires dephosphorylation of some cell protein, but maximal activity requires the presence of intracellular ATP. We have examined the relation between K-Cl cotransport activity and ATP in ghosts prepared from human red blood cells. K-Cl cotransport activity in swollen ghosts increased by ATP, and the increase requires Mg so that it almost certainly results from the phosphorylation of some membrane component. However, even in ATP-free ghosts residual volume-sensitive K-Cl cotransport can be demonstrated. This residual cotransport in ATP-free ghosts is greater in the presence of vanadate, a tyrosyl phosphatase inhibitor, and in ghosts that contain ATP cotransport is reduced by genistein, a tyrosyl kinase inhibitor. Okadaic acid, an inhibitor of serine and threonine phosphatases, inhibits K-Cl cotransport in ghosts as it does in intact cells. Experiments in which ghosts were preexposed to okadaic acid showed that the protein dephosphorylation that permits K-Cl cotransport can proceed to completion before the ghosts are swollen and K transport measured and therefore dephosphorylation is not a response to ghost swelling. In experiments with ATP-free ghosts we found that phosphorylation is not necessary to increase the cotransport rate when shrunken ghosts are swollen, nor is rephosphorylation necessary to decrease the cotransport rate when swollen ghosts are shrunken. Cotransport is greater in swollen than in shrunken ghosts even when the swollen and shrunken ghosts have the same concentration of cytoplasmic solutes. We conclude that, although phosphorylation and dephosphorylation modify the activity of the cotransporter in swollen and in shrunken ghosts, neither of these processes nor any other known messenger is involved in signal transduction between the cell volume sensor and the cotransporter as originally proposed by Jennings and Al-Rohil (Jennings, M. L., and N. Al-Rohil. 1990. Journal of General Physiology. 95: 1021-1040).

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