Control of arterial pressure and renal function during glucocorticoid excess in dogs.

Hall, John E.; Morse, Cheryl L.; Smith, M. J.; Young, David B.; Guyton, Arthur C.

doi:10.1161/01.hyp.2.2.139

Cited by 43 publications

(26 citation statements)

References 19 publications

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“…Indeed, in our present study there was a striking loss of salt and water, and a decrease in MAP during cortisol infusion. Accordingly, we have observed in our laboratory 30 (and unpublished data) that chronic infusion of high levels of either cortisol or methylprednisolone (a glucocorticoid with virtually no mineralocorticoid activity) is associated with a decrease in extracellular fluid volume as well as a reduction in arterial pressure. In contrast to cortisol infusion, however, we have observed that chronic ACTH infusion in dogs is associated with an increase in extracellular fluid volume in spite of negative salt and water balance (unpublished data).…”

Section: Discussionmentioning

confidence: 83%

Chronic effects of ACTH and cortisol excess on arterial pressure in normotensive and hypertensive dogs.

Lohmeier¹,

Kastner²

1982

Hypertension

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The chronic effects of ACTH and cortisol on mean arterial pressure (MAP) and related variables were studied in normotensive dogs and, subsequently, in the same dogs after they had been made hypertensive by chronic infusion of angiotensin II (All). MAP was recorded continuously, 24 hours/day, and sodium intake was 71 mEq/day. In both normotensive and hypertensive dogs, 8 to 10 days of ACTH infusions caused natriuresis, kaliuresis, diuresis, hypernatremia, and hypokalemia; additionally, plasma renin activity (PRA) was suppressed to undetectable levels. During ACTH infusion there was a sustained 12-fold increase in plasma cortisol concentration, but only a transient elevation in plasma aldosterone concentration; this steroidogenic response occurred even in dogs with All hypertension where plasma AH concentration was maintained at elevated levels by infusion. In normotensive dogs, increases in MAP were not consistently observed during ACTH infusion, whereas, in dogs with AH hypertension, ACTH invariably exacerbated the hypertension (AMAP = + 16 mm Hg). Cortisol infusion, like ACTH infusion, caused a 12-fold increase in plasma cortisol concentration , and negative sodium and water balance; however, cortisol did not produce kaliuresis, hypokale-mia, suppression of PRA, or hypertension. In fact, cortisol induced chronic hypotension (AMAP =-7 mm Hg) when infused in normotensive dogs, and in dogs with AH hypertension there were no detectable changes in MAP during cortisol treatment. Thus, the changes in plasma cortisol concentration and PRA that accompany ACTH infusion do not mediate, but seem actually to oppose, the hypertensive effects of ACTH. Indeed, when ACTH was infused in hypertensive dogs with fixed plasma levels of All, the hypertensive effects of ACTH were manifested. Finally, failure of chronic ACTH administration to maintain an elevated secretion rate of aldosterone cannot be attributed to suppression of PRA. (Hypertension 4: 652-661, 1982) KEY WORDS • ACTH • cortisol • aldosterone • arterial pressure • angiotensin sodium balance • potassium balance • water balance • S INCE Harvey Cushing first drew attention to the clinical syndrome that bears his name,' the high incidence of hypertension in patients with Cush-ing's syndrome has become widely recognized. Although it has been almost 50 years since Cushing's original findings, the precise mechanisms whereby ACTH and adrenocortical hormones produce hyper-tension have not been elucidated. One mechanism usually suggested to contribute to the hypertension of

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Section: Discussionmentioning

confidence: 83%

Chronic effects of ACTH and cortisol excess on arterial pressure in normotensive and hypertensive dogs.

Lohmeier¹,

Kastner²

1982

Hypertension

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“…The increased ^-adrenergic receptor number and response due to glucocorticoid treatment may result in increased potential for vasodilation and, ultimately, lower blood pressure. Indeed, using pure glucocorticoid excess, Hall et al 17 found lower mean arterial pressure in methylprednisolone-treated dogs compared with values in controls.…”

Section: American Heart Associationmentioning

confidence: 98%

Glucocorticoid modulation of beta-adrenergic receptors of cultured rat arterial smooth muscle cells.

Jazayeri

Meyer

1988

Hypertension

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SUMMARY Since both ghicocortkoids and catecholamines are involved in the regulation of normal blood pressure, we Investigated the modulation of /3-adrenergic receptors of cultured rat arterial smooth muscle cells by glucocorticoids. The synthetic glucocorticoids dexamethasone and RU 28362, at 10~8 M concentration, increased maximum 0-adrenergic binding but had no effect on the dissociation constant (£d). Each steroid caused an Increase hi maTimnm [^dihydroalprenolol binding over the concentration range of 10~8 to 10"* M, but not at 10~9 M. The glucocorticoid effect on /3-adrenergk receptors of arterial smooth muscle cells required a minlmnm of 20 hours of incubation in the presence of the steroid and was significantly inhibited by cycloheximlde (10 Mg/ml), indicating that the glucocorticoid effect required protein synthesis. The effect of dexamethasone on [ and rat lung. 4 Glucocorticoids are also involved in the regulation of agonist-mediated )3-adrenergic response in human neutrophils.56 Both glucocorticoids and catecholamines are involved in the regulation and maintenance of normal blood pressure. 78 Synthetic glucocorticoids have been shown to augment pressor response to angiotensin II and norepinephrine, and this effect is blocked by glucocorticoid antagonists.9 In addition, in Cushing's syndrome, the pressor response to angiotensin II and norepinephrine is elevated. 10Our laboratory has previously shown that cultured rat arterial smooth muscle cells (ASMCs) contain

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“…4 For example, glucocorticoids have been shown either to increase or to decrease blood pressure, 4 -5 to increase renal blood flow, 6 and to reduce vascular smooth muscle contractile responses to prostaglandin (PG) F^ and U46619, a synthetic agonist for the thromboxane A 2 and PG endoperoxide receptor.…”

Section: Onsistent With a Role For Glucocorticoids Inmentioning

confidence: 99%

Reciprocal effects of dexamethasone on vasodilatory responses to arachidonic acid and prostanoids in the isolated perfused rabbit kidney.

1990

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We reported that dexamethasone treatment of rabbits causes a reduction in renal vasoconstrictor responses to prostaglandin F^ and U46619, an agonist at the thromboxane-endoperoxide receptor, but not to phenylephrine. The purpose of this study was to examine if dexamethasone treatment can affect the renal vasodilatory responses to prostacydin (PGIi) and prostaglandin Ej (PGE2) in isolated Krebs-perfused kidneys constricted with phenylephrine. In kidneys from dexamethasone-treated rabbits, the vasodilatory response to PGI 2 was reduced by 57%, whereas that to PGE^ was converted to a vasoconstrictor response. This effect of dexamethasone appears to be specific in that the renal vasodilatory responses to forskolin and to sodium

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Control of arterial pressure and renal function during glucocorticoid excess in dogs.

Cited by 43 publications

References 19 publications

Chronic effects of ACTH and cortisol excess on arterial pressure in normotensive and hypertensive dogs.

Chronic effects of ACTH and cortisol excess on arterial pressure in normotensive and hypertensive dogs.

Glucocorticoid modulation of beta-adrenergic receptors of cultured rat arterial smooth muscle cells.

Reciprocal effects of dexamethasone on vasodilatory responses to arachidonic acid and prostanoids in the isolated perfused rabbit kidney.

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