The effect of selective glucocorticoid or mineralocorticoid replacement on pressor responses to angiotensin I and II and norepinephrine was studied in adrenaiectomized rats given high salt intake. Four groups were prepared by 1) adrenalectomy only (n = 5); 2) adrenalectomy plus aldosterone, 6 /ig/24 hr i.p. (n = 5); or 3) adrenalectomy plus dexamethasone, 10 /ig/24 hr i.p. (n = 5), using miniosmotk pumps; and 4) sham adrenalectomy (controls; n = 5). Plasma corticosterone was undetectable in all

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... three adrenaiectomized groups. Plasma aldosterone concentration was similar in aldosterone-replaced and sham-operated controls. Pressor responses to various doses of angiotensin I, angiotensin H, and norepinephrine were determined in unanesthetized, undisturbed rats. Compared with both control and dexamethasone-replaced rats, pressor responses to all three agonists were significantly reduced in both nonreplaced adrenaiectomized and aldosterone-replaced groups. Comparing the ratios of the pressor responses to angiotensin I and angiotensin II in the four groups over the entire dose range suggests that a greater fraction of injected angiotensin I was converted to angiotensin II in nonreplaced adrenaiectomized rats than in the other three groups. We conclude that glucocorticoid action markedly contributes to the systemic pressor effect of angiotensin and norepinephrine. However, glucocorticoid deficiency does not impair in vivo conversion of angiotensin I to angiotensin H. (Hypertension 11: 174-178 , 1988) KEY WORDS • norepinephrine adrenal insufficiency • mineralocorticoid cardiovascular reactivity • angiotensin glucocorticoid