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Division of Nephrology and Hypertension and Center for Hypertension and Renal Disease Research, Georgetown University Medical Center, Washington, DC 20007
A TP receptor (TP-R) mimetic causes
salt-sensitive hypertension and renal afferent arteriolar
vasoconstriction. TP-Rs mediate effects of ANG II on renal vascular
resistance and drinking. Therefore, we investigated the hypothesis that
thromboxane A2 synthase (TxA2-S) and/or TP-R
expression is regulated by salt and/or ANG II. Rats (n = 6) received high-salt (HS) or low-salt (LS) diets. Additional HS-diet
rats received ANG II while other HS- and LS-diet rats received the
AT1 receptor (AT1-R) antagonist
losartan. Excretion of thromboxane B2 by conscious
rats was increased with the HS diet compared with the LS diet (126 ± 10 vs. 48 ± 5 pmol/24 h, respectively; P < 0.01). The mRNA abundance for TP-Rs (relative to 
-actin) in
the kidney cortex was enhanced 30% by the HS diet (P < 0.001) and was reduced 50% by the addition of ANG II
(P < 0.001). However, during losartan administration,
the effects of salt were reversed; mRNA more than doubled during the LS
diet (P < 0.001). Similarly, the mRNA abundance for
TP-Rs in the brain stem was reduced by 50% with the addition of ANG II
(P < 0.001) and during losartan administration was
almost doubled by the LS diet (P < 0.001). The mRNA
abundance for TxA2-S in the kidney cortex also was
increased many times with the HS diet (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 administration, TxA2-S increased modestly
in the brain stem with the LS diet. mRNA abundance for TP-Rs in the
kidney cortex and brain stem is suppressed by ANG II acting on
AT1-Rs. In the absence of AT1-Rs,
expression of TP-Rs at both sites is enhanced by LS intake. In
contrast, ANG II does not affect the mRNA abundance for
TxA2-S. Expression of TxA2-S is enhanced by HS
intake in the kidney cortex but by LS intake in the brain stem only
during losartan administration. Thus TP-Rs are strongly dependent on
ANG II acting on AT1-Rs, whereas TxA2-S is
regulated differentially in the kidney cortex and brain stem by salt intake.
thromboxane A2; prostaglandins; angiotensin II; losartan; angiotensin receptor blocker; thromboxane prostanoid receptor
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