Effects of antiglucocorticoids on glucocorticoid hypertension in the rat.

Grünfeld, Jean‐Pierre; Eloy, Laure; Moura, A M; Ganeval, D; Ramos-Frendo, B; Worcel, Manuel

doi:10.1161/01.hyp.7.2.292

Cited by 56 publications

(24 citation statements)

References 28 publications

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“…Glucocorticoids are known to activate transcription in a number of systems (39- The role of glucocorticoid regulation of ANP genetic expression in the intact animal is not well understood. We have reported previously that large doses of Dex increase ANP mRNA levels in both atrial and extraatrial tissues in vivo (22), an effect that may be related to the prominent natriuretic properties of similar doses of the steroid (20). Others have reported increased circulating levels of ANP following administration of more physiological doses ofglucocorticoids in vivo (21).…”

Section: Resultsmentioning

confidence: 94%

Gene for the rat atrial natriuretic peptide is regulated by glucocorticoids in vitro.

Gardner¹,

Gertz²,

Deschepper³

et al. 1988

J. Clin. Invest.

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Section: Resultsmentioning

confidence: 94%

Gene for the rat atrial natriuretic peptide is regulated by glucocorticoids in vitro.

Gardner¹,

Gertz²,

Deschepper³

et al. 1988

J. Clin. Invest.

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“…This compound prevents or reverses the early phase of glucocorticoidinduced hypertension in the rat. 3 In the present study the pressor responses to norepinephrine (NE), Ang II, and AVP as well as cardiac output and renal blood flow were measured in unanesthetized and anesthetized rats pretreated with either RU 486 or vehicle. The systemic and renal hemodynamic effects of RU 486 were also studied in rats on chronic low sodium intake, a condition in which the pressor systems are activated.…”

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confidence: 99%

Glucocorticoids modulate vascular reactivity in the rat.

1987

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SUMMARY To clarify the role of endogenous glucocorticoids in the regulation of blood pressure, the cardiovascular effects of RU 486, a steroid derivative with antiglucocorticoid properties, were investigated in Wistar rats. Pressor responses to angiotensin II (Ang II), norepinephrine, and vasopressin were studied in normal conscious rats before and after administration of RU 486. At 20 mg/kg/day, RU 486 significantly blunted pressor responses to Ang II and norepinephrine, whereas those to vasopressin were not greatly affected. At a lower dose, RU 486 did not alter pressor responses; at a higher dose, it augmented them, probably through its agonistic glucocorticoid effect. At 20 mg/kg/day, RU 486 antagonized the enhancing effect of a glucocorticoid agonist on pressor responses to Ang II, norepinephrine, and vasopressin. Cardiac output and renal blood flow were measured in anesthetized rats by the microsphere method. RU 486 at 20 mg/kg/day did not alter basal cardiac output and renal blood flow. RU 486 pretreatment attenuated pressor responses to Ang II and norepinephrine but did not alter cardiac output. It significantly blunted the decrease in renal blood flow and the increase in renal vascular resistance induced by Ang II. In rats fed a low sodium diet (where the pressor systems are stimulated), administration of RU 486 (20 mg/kg/day for 5 days) decreased total peripheral vascular resistance by 29% and mean blood pressure by 20 mm Hg. This effect was unrelated to any antimineralocorticoid activity of the compound, as shown by unchanged urinary sodium excretion, sodium balance, and plasma renin concentration. In contrast, it was due to the antiglucocorticoid activity, as shown by restoration of mean blood pressure by corticosterone, the major glucocorticoid in rats. Renal vascular resistance decreased during RU 486 administration in anesthetized ( -25%) and unanesthetized ( -19%) rats. Glomerular filtration rate, estimated from inulin clearance in conscious rats, did not change significantly. In conclusion, the present results suggest that endogenous glucocorticoids increase vascular reactivity and therefore contribute to blood pressure regulation. They also participate in the control of renal hemodynamics. This effect is most apparent in salt-restricted rats. The vascular action of glucocorticoids was unmasked by the administration of the antiglucocorticoid compound RU 486. (Hypertension 10: 608-618, 1987) KEY WORDS • antiglucocorticoid • norepinephrine • angiotensin II • vasopressin low sodium intake • renal hemodynamics • cardiac output • microspheres T HE regulation of blood pressure depends on the interplay of multiple control systems. Analysis of these interactions has been facilitated by the synthesis and development of inhibitors of the hormones or mediators involved. In this regard, the use of inhibitors or antagonists of the adrenergic or renin-angiotensin system, prostaglandin and arginine From the

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“…Corticosteroid-induced hypertension responds better to diuretic therapy as compared to other anti-hypertensives 13 . All these evidences have been found to be related with the chronic administration of steroids whereas, our patient developed hypertension acutely after a single dose of hydrocortisone.…”

Section: Discussionmentioning

confidence: 95%

“…All these evidences have been found to be related with the chronic administration of steroids whereas, our patient developed hypertension acutely after a single dose of hydrocortisone. Spironolactone being an aldosterone antagonist, acts to decrease the mineral ocorticoid activity and reduces the hypertension 13 .…”

Section: Discussionmentioning

confidence: 99%