The tubuloglomerular feedback (TGF) response is potentiated by
thromboxane A2 (TxA2) and/or
prostaglandin endoperoxide (
PGH2) acting on specific receptors. Infusion of the TxA2/
PGH2 mimetic, U-46,619, into conscious rats leads to
hypertension that is potentiated by a high-
salt intake. Therefore, we tested the hypothesis that a high-
salt intake enhances the expression of transcripts for
TxA2/PGH2 receptors in the kidney and glomeruli and enhances the response of TGF to TxA2/
PGH2 receptor stimulation. Groups of rats were accommodated to a low-
salt (LS), normal
salt (NS), or high-
salt (HS) diet for 8-10 days. TxA2/
PGH2 receptor
mRNA was detected by reverse transcription-polymerase chain reaction in kidney cortex, isolated glomeruli, and abdominal aorta. TxA2/
PGH2 mRNA abundance was significantly (P < 0.001) increased during intake of high-
salt compared with
low-salt diets in the kidney cortex (1.34 +/- 0.10 vs. 0.84 +/- 0.04 arbitrary units) and isolated outer cortical glomeruli (0.68 +/- 0.04 vs. 0.32 +/- 0.03 arbitrary units), but there was no effect of
salt on TxA2/
PGH2 receptor
mRNA expression in the aorta. Maximal TGF responses were assessed from the increase in proximal stop flow pressure (an index of glomerular capillary pressure) during increases in loop of Henle perfusion with artificial tubular fluid from 0 to 40 nl/min. Compared with vehicle, the enhancement of maximal TGF with U-46,619 (10(-6) M) added to the perfusate was greater in rats adapted to high-
salt than normal
salt (HS: +9.6 +/- 1.1 vs. NS: +5.1 +/- 0.4 mmHg; P < 0.001) or low-
salt (LS: +3.8 +/- 1.3 mmHg; P < 0.001) intakes. Responses to U-46,619 at each level of
salt intake were blocked by > 70% by the TxA2/
PGH2 receptor antagonist
ifetroban. In contrast, enhancement of TGF by peritubular capillary perfusion of
arginine vasopressin (AVP; 10(-7) M) was similar in high-
salt and low-
salt rats (HS: +1.5 +/- 0.6 vs. LS: +1.6 +/- 0.5 mmHg; not significant). We conclude that
salt loading increases selectively the abundance of TxA2/
PGH2 receptor transcripts in the kidney cortex and glomerulus, relative to the aorta, and enhances selectively TGF responses to TxA2/
PGH2 receptor activation but not to AVP.