PMID- 6311735
OWN - NLM
STAT- MEDLINE
DCOM- 19831123
LR  - 20190722
IS  - 0194-911X (Print)
IS  - 0194-911X (Linking)
VI  - 5
IP  - 5
DP  - 1983 Sep-Oct
TI  - Sodium and potassium ion transport accelerations in erythrocytes of DOC, 
      DOC-salt, two-kidney, one clip, and spontaneously hypertensive rats. Role of 
      hypokalemia and cell volume.
PG  - 642-52
AB  - Sodium (Na+) and potassium (K+) transport by the furosemide-sensitive Na+-K+ 
      transport system, the Na+-K+ pump, and the cation leak(s) were studied in 
      erythrocytes from DOC-water, DOC-salt, two-kidney, one clip (Sprague-Dawley), and 
      spontaneously hypertensive rats (Wistar-Kyoto). Rubidium (Rb+) was used as a 
      tracer for K+. After 4 weeks of DOC-salt hypertension, inward K+ (Rb+) transport 
      by the furosemide-sensitive system was increased threefold, and the inward Na+ 
      leak and the red cell Na+ content were elevated by about 50%. The rise in cell 
      Na+ accelerated K+ inward and Na+ outward transport by the Na+-K4 pump, DOC-water 
      hypertension caused similar but less pronounced changes. In two-kidney, one clip 
      hypertension, the Na+ leak and the Na+-K+ pump rates were slightly elevated, and 
      furosemide-sensitive Rb+ uptake tended to be increased. In spontaneously 
      hypertensive rats, furosemide-sensitive Rb+ uptake was accelerated by 50%. The 
      marked hypokalemia in DOC-water and DOC-salt hypertension was associated with a 
      slight loss of red cell K+ and an increase in mean cellular hemoglobin content 
      (MCHC), indicative of cell shrinkage. Hypokalemia induced by dietary K+ 
      deficiency caused alterations in red cell cation transport, content, and cell 
      volume which were qualitatively similar but more pronounced than those seen in 
      DOC-salt hypertension. Osmotic shrinkage in vitro induced a severalfold 
      acceleration of furosemide-sensitive Rb+ uptake, similar to that observed in rat 
      erythrocytes shrunken in vivo in K+-deficient states. It is concluded that the 
      acceleration of furosemide-sensitive K+ (Rb+) transport in erythrocytes of 
      mineralocorticoid hypertensive rats is largely caused by the hypokalemia and 
      consecutive red cell K+ loss and shrinkage, respectively. Mean cellular 
      hemoglobin content (MCHC) is thus a parameter that must be considered in studies 
      on Na+ and K+ transport across the membrane of rat erythrocytes.
FAU - Duhm, J
AU  - Duhm J
FAU - Gobel, B O
AU  - Gobel BO
FAU - Beck, F X
AU  - Beck FX
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Hypertension
JT  - Hypertension (Dallas, Tex. : 1979)
JID - 7906255
RN  - 0 (Hemoglobins)
RN  - 0 (Ion Channels)
RN  - 40GP35YQ49 (Desoxycorticosterone)
RN  - 7LXU5N7ZO5 (Furosemide)
RN  - 9NEZ333N27 (Sodium)
RN  - RWP5GA015D (Potassium)
SB  - IM
MH  - Animals
MH  - Biological Transport
MH  - Blood Pressure
MH  - Desoxycorticosterone/*physiology
MH  - Erythrocyte Volume
MH  - Erythrocytes
MH  - Furosemide/pharmacology
MH  - Hemoglobins/analysis
MH  - Hypertension, Renovascular/*metabolism
MH  - Hypokalemia/*physiopathology
MH  - Ion Channels
MH  - Male
MH  - Potassium/blood/*metabolism
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Sodium/*metabolism
EDAT- 1983/09/01 00:00
MHDA- 1983/09/01 00:01
CRDT- 1983/09/01 00:00
PHST- 1983/09/01 00:00 [pubmed]
PHST- 1983/09/01 00:01 [medline]
PHST- 1983/09/01 00:00 [entrez]
AID - 10.1161/01.hyp.5.5.642 [doi]
PST - ppublish
SO  - Hypertension. 1983 Sep-Oct;5(5):642-52. doi: 10.1161/01.hyp.5.5.642.