Key result
In Dahl salt-sensitive rats, high sodium intake induced hypertension and acetylcholine caused release of an endothelium-derived contracting factor (likely PGH2/TXA2) that depressed relaxation.
In hypertensive Dahl salt-sensitive rats, acetylcholine elicits the release of an endothelium-derived contracting factor (likely PGH2 and TXA2) that contributes to impaired vasorelaxation.
No immediate clinical implications for hypertension; leaves open whether endothelium-derived contracting factors mediate salt sensitivity in humans.
The present study is designed to investigate whether acetylcholine (ACh) elicits an endothelium-derived contracting factor (EDCF) and whether it contributes to decreased relaxant response induced by ACh in Dahl rats. Dahl salt-sensitive (DS) and -resistant (DR) rats were fed a 0.4% NaCl or an 8% NaCl diet for 4 weeks. High sodium intake significantly increased blood pressure in DS rats but not in DR rats. The carotid rings were suspended for isometric tension recording. ACh caused an endothelium-dependent contraction in carotid rings from hypertensive DS rats but not from normotensive Dahl rats. Atropine, indomethacin, SQ29548, or ONO-3708 (prostaglandin H(2) [PGH(2)]/thromboxane A(2) [TXA(2)] receptor antagonist) abolished ACh-induced contraction, and OKY-046 (inhibitor of TXA(2) synthetase) partially attenuated the contraction. High sodium intake significantly enhanced contraction evoked by U46619, a PGH(2)/TXA(2) receptor agonist, in both DS and DR rats. In contrast, ACh-induced relaxation was significantly depressed in the rings from hypertensive DS rats, and ONO-3708 partially improved the depressed relaxation. Administration of ONO-8809 (an orally active PGH(2)/TXA(2) receptor antagonist; 30 micrograms per body per day) for 4 weeks neither reduced blood pressure nor improved the depressed ACh-induced relaxation in hypertensive DS rats. These results suggest that ACh causes release of EDCF in carotid rings of hypertensive DS rats, which is likely to be PGH(2) and TXA(2). The EDCF contributed in part to the depressed ACh-induced relaxation.
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Zhou et al. (1999) studied Hypertension. High sodium diet (8% NaCl) vs. 0.4% NaCl diet was evaluated on Blood pressure and acetylcholine-induced contraction/relaxation in carotid rings. In Dahl salt-sensitive rats, high sodium intake induced hypertension and acetylcholine caused release of an endothelium-derived contracting factor (likely PGH2/TXA2) that depressed relaxation.
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