PMID- 1592476
OWN - NLM
STAT- MEDLINE
DCOM- 19920630
LR  - 20190722
IS  - 0194-911X (Print)
IS  - 0194-911X (Linking)
VI  - 19
IP  - 6 Pt 2
DP  - 1992 Jun
TI  - High potassium diets greatly increase growth-inhibiting agents in aortas of 
      hypertensive rats.
PG  - 749-52
AB  - High potassium diets greatly reduce intimal and medial thickening in stroke-prone 
      spontaneously hypertensive rats (SHRSP). In vascular smooth muscle cells, 
      transforming growth factor-beta (TGF-beta) inhibits proliferation. To test 
      whether high potassium diets decrease aortic thickening through TGF-beta, we 
      measured TGF-beta-like activity in medium bathing aortas from rats fed either 
      normal potassium or high potassium diets. Five-week-old SHRSP were fed 6% high 
      NaCl diets containing either normal (0.5%) potassium (11 rats) or high (2.1%) 
      potassium (14 rats) for 7 weeks. Aortas were freshly excised and perfused for 3 
      hours with tissue culture medium at ordinary arterial pressures. TGF-beta-like 
      activity in the acid-activated perfusing medium was assessed using the growth 
      inhibitory action on mink lung cells. Growth inhibition was assessed by 
      [3H]thymidine incorporation. In the medium perfusing the outside of the aorta, 
      the growth inhibitory rates were 2.5 times higher in high potassium SHRSP than in 
      normal potassium SHRSP (-49% versus -20%, p less than 0.03). Antibodies to 
      TGF-beta 1 and TGF-beta 2 were added to other aliquots and did not alter the 
      results whatsoever. Thus, the difference in growth inhibition was not due to 
      differences in TGF-beta. The high potassium aortas released 2.5 times more 
      growth-inhibiting agents than the normal potassium aortas. The same pattern of 
      growth inhibition was also seen using vascular smooth muscle cells rather than 
      mink lung cells (r = +0.818, p less than 0.001, n = 13). The increased growth 
      inhibition of high potassium aortas was not due to an increased release of 
      heparin.(ABSTRACT TRUNCATED AT 250 WORDS)
FAU - Sugimoto, K
AU  - Sugimoto K
AD  - Department of Medicine, University of Minnesota Medical School, Minneapolis.
FAU - Tobian, L
AU  - Tobian L
FAU - Ishimitsu, T
AU  - Ishimitsu T
FAU - Lange, J M
AU  - Lange JM
LA  - eng
GR  - HL-17871/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Hypertension
JT  - Hypertension (Dallas, Tex. : 1979)
JID - 7906255
RN  - 0 (Antibodies)
RN  - 0 (Growth Inhibitors)
RN  - 0 (Transforming Growth Factor beta)
RN  - RWP5GA015D (Potassium)
SB  - IM
MH  - Animals
MH  - Antibodies/immunology
MH  - Aorta/drug effects/*metabolism
MH  - Blood Pressure
MH  - Cell Division
MH  - Diet
MH  - Growth Inhibitors/*metabolism
MH  - Hypertension/*metabolism/physiopathology
MH  - In Vitro Techniques
MH  - Male
MH  - Muscle, Smooth, Vascular/cytology
MH  - Perfusion
MH  - Potassium/*administration & dosage/pharmacology
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Transforming Growth Factor beta/immunology/metabolism
EDAT- 1992/06/01 00:00
MHDA- 1992/06/01 00:01
CRDT- 1992/06/01 00:00
PHST- 1992/06/01 00:00 [pubmed]
PHST- 1992/06/01 00:01 [medline]
PHST- 1992/06/01 00:00 [entrez]
AID - 10.1161/01.hyp.19.6.749 [doi]
PST - ppublish
SO  - Hypertension. 1992 Jun;19(6 Pt 2):749-52. doi: 10.1161/01.hyp.19.6.749.