1. This study was designed to examine the effect of dexamethasone treatment on tissue and urinary prostanoids, and to determine whether inhibition of prostaglandin biosynthesis by manipulation of dietary fatty acids accelerates the development of glucocorticoid hypertension.
2. Forty-eight rats were placed on either a 2-series prostaglandin ‘inhibitory’ diet (cod liver oil/linseed oil) or a control diet of saturated fat for an initial period of 4 weeks. The groups were then divided into two so that half of each received dexamethasone in their drinking water (2.5 mg/1) for 1 week whilst continuing their respective dietary regimens.
3. Rats on the cod liver oil diet incorporated eicosapentaenoic acid into tissue stores with a corresponding decrease in arachidonic acid, and significantly impaired ability to generate serum thromboxane B2 (33%), aortic 6-oxo-prostaglandin F1α (44%), renal homogenate prostaglandin E2 (45%) and 6-oxo-prostaglandin F1α (74%) and urinary prostaglandin E2 (84%) and 6-oxo-prostaglandin F1α (79%).
4. Despite the diminished levels of vasodilator 2-series prostaglandins, the cod liver oil diet prevented the development of glucocorticoid induced hypertension.
5. Relative to their respective dietary controls, dexamethasone treatment resulted in decreased serum thromboxane B2 (20%) but increased aortic 6-oxo-prostaglandin F1α (186%), renal homogenate prostaglandins (127–230%) and urinary excretion of prostaglandin E2 (640–860%) and 6-oxo-prostaglandin F1α(230–365%) in both dietary groups.
6. It therefore seems unlikely that glucocorticoid induced hypertension is a consequence of inhibition of vasodilator prostaglandin synthesis.