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1 Division of Nephrology and Hypertension and Center for Hypertension and Renal Disease Research, Georgetown University Medical Center, Washington, DC, USA
* To whom correspondence should be addressed. E-mail: wilcoxch{at}georgetown.edu.
A TP receptor mimetic causes salt-sensitive hypertension and renal afferent arteriolar vasoconstriction. TP-R mediate effects of Ang II on renal vascular resistance and drinking. Therefore, we investigated the hypothesis that TxA2 synthase (TxA2-S) and/or TP-R expression is regulated by salt and/or Ang II. Methods: Rats (n=6) received high salt (HS) or low salt (LS) diets. Additional HS received Ang II and additional HS and LS received the AT1 receptor (AT1-R) antagonist, losartan. Results: Excretion of TxB2 by conscious rats was increased by HS, compared to LS (LS, 48 ± 5 vs. 126 ± 10 pmol.24h-1; p<0.01). The mRNA abundance for TP-R (relative to 
-actin) in kidney cortex was enhanced 30% by HS (p<0.001) and was reduced 30% by Ang II (p<0.001). However, during losartan, the effects of salt were reversed; mRNA more than doubled during LS (p<0.001). Likewise, the mRNA abundance for TP-R in the brain stem was reduced by 50% by Ang II (p<0.001) and, during losartan, was was almost doubled by LS (p<0.001). The mRNA abundance for TxA2-S in the kidney cortex also was increased many fold by HS (p<0.001). In contrast, the mRNA for TxA2-S in the brain was unaffected by salt. Ang II did not affect TxA2-S at either site. During losartan, TxA2-S increased modestly with LS in the brain stem. Conclusions: mRNA for TP-R in kidney cortex and brain stem are suppressed by Ang II acting on AT1-R. In the absence of AT1-R, expression of TP-R at both sites is enhanced by LS. In contrast, Ang II does not affect the mRNA abundance for TxA2-S. Expression of TxA2-S is enhanced by HS in the kidney cortex, but by LS in the brain stem only during losartan. Thus TP-R is strongly dependent on Ang II acting on AT1-R, whereas TxA2-S is regulated differentially in the kidney cortex and brain stem by salt intake.
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