PMID- 9314417
OWN - NLM
STAT- MEDLINE
DCOM- 19971030
LR  - 20190722
IS  - 0194-911X (Print)
IS  - 0194-911X (Linking)
VI  - 30
IP  - 3 Pt 1
DP  - 1997 Sep
TI  - Growth-dependent induction of angiotensin II type 2 receptor in rat mesangial 
      cells.
PG  - 358-62
AB  - Angiotensin II acts on at least two receptor subtypes, AT1 and AT2. Although the 
      physiological role of the AT2 receptor is still poorly defined, it may be 
      implicated in inhibition of cell growth, vasorelaxation, and apoptosis. In the 
      present study, to investigate the role of the AT2 receptor in the kidney and its 
      implication in hypertensive states, we examined its expression using cultured 
      mesangial cells (MC) from normotensive Wistar-Kyoto rats (WKY) and from 
      stroke-prone spontaneously hypertensive rats (SHRSP). Receptor binding assays 
      were performed using a nonselective ligand, [Sar1,Ile8]angiotensin II, or 
      AT2-selective CGP42112A. Binding assays revealed that MC from WKY exhibited both 
      AT1 and AT2 receptors, the ratio of which was confluence-dependent. In contrast, 
      MC from SHRSP, whose proliferation activity was much higher than those from WKY, 
      showed only the AT1 subtype. In receptor binding and Northern blot analyses, 
      expression of the AT2 receptor of WKY-MC was low in the growing state but 
      significantly induced upon confluence to become abundant in the post-confluent 
      state, whereas that of SHRSP-MC was undetectable in either state. Gene 
      expressions of AT1A and AT1B receptors were not significantly altered in either 
      strain during the time in culture. These results indicate that the mesangial 
      AT2-receptor expression is growth-dependent and suggest a role in the inhibition 
      of MC growth in WKY. Much lower expression of the AT2 receptor in MC from SHRSP 
      may suggest involvement in their higher proliferation activity and possibly in 
      consequent renal disorders.
FAU - Goto, M
AU  - Goto M
AD  - Department of Medicine and Clinical Science, Kyoto University Graduate School of 
      Medicine, Japan.
FAU - Mukoyama, M
AU  - Mukoyama M
FAU - Suga, S
AU  - Suga S
FAU - Matsumoto, T
AU  - Matsumoto T
FAU - Nakagawa, M
AU  - Nakagawa M
FAU - Ishibashi, R
AU  - Ishibashi R
FAU - Kasahara, M
AU  - Kasahara M
FAU - Sugawara, A
AU  - Sugawara A
FAU - Tanaka, I
AU  - Tanaka I
FAU - Nakao, K
AU  - Nakao K
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 (Receptors, Angiotensin)
SB  - IM
MH  - Animals
MH  - Cell Division/physiology
MH  - Cells, Cultured
MH  - Cerebrovascular Disorders/genetics
MH  - Gene Expression
MH  - Genetic Predisposition to Disease
MH  - Glomerular Mesangium/*cytology/*metabolism
MH  - Male
MH  - Rats
MH  - Rats, Inbred SHR/genetics
MH  - Rats, Inbred WKY
MH  - Receptors, Angiotensin/classification/genetics/*metabolism
EDAT- 1997/10/06 00:00
MHDA- 1997/10/06 00:01
CRDT- 1997/10/06 00:00
PHST- 1997/10/06 00:00 [pubmed]
PHST- 1997/10/06 00:01 [medline]
PHST- 1997/10/06 00:00 [entrez]
AID - 10.1161/01.hyp.30.3.358 [doi]
PST - ppublish
SO  - Hypertension. 1997 Sep;30(3 Pt 1):358-62. doi: 10.1161/01.hyp.30.3.358.