Decreased renal prostaglandins, specifically PGE2, contribute to the blunted pressure natriuresis observed in Dahl salt-sensitive rats.
Implicates reduced PGE2 in salt-sensitive hypertension mechanisms; hypothesis-generating and should not yet change clinical practice.
To examine the role of prostaglandins on pressure natriuresis in Dahl salt-sensitive (DS) rat, the pressure-natriuresis relationships in DS and Dahl salt-resistant (DR) rats were characterized with or without indomethacin (2 mg/kg/h) by utilizing an in vivo renal perfusion study. When untreated, in the DS rat the pressure-natriuresis curve was blunted (P less than .05) and excretion of prostaglandin E2 (38 +/- 11 to 109 +/- 43 pg/min) was decreased in comparison to the DR rat. With indomethacin, the pressure-natriuresis curve in the DR rat was blunted, while no significant changes were observed in the DS rat. Plasma renin activity and concentration of atrial natriuretic peptide were not changed by the treatment of indomethacin in both strains. These results suggest that the decrease in renal prostaglandins, at least in prostaglandin E2, plays some role in blunting pressure natriuresis in DS rat.
No takes yet. Share an insight, caveat, or question.
Takenaka et al. (1991) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: