<i>Work of Digital Vasoconstriction Produced by Infused Norepinephrine in Cushing's Syndrome</i>

Mendlowitz, Milton; Gitlow, Stanley E.; Naftchi, Nosrat E.

doi:10.1152/jappl.1958.13.2.252

Cited by 75 publications

(25 citation statements)

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“…The failure of DEX treatment to enhance rat mesenteric vascular reactivity to NE is in disagreement with those reports indicating an enhanced response by glucocorticoids of isolated rabbit aortic strips in vitro 9 and human digital 6 and forearm 7 and rat hindlimb vessels in vivo.'" " This discrepancy between our results and those of other investigators could be due to differences in the experimental design.…”

Section: Figukii 4 Effect Ofangiotensin II (Ang Ii) On Perfusion Precontrasting

confidence: 61%

Mesenteric vascular reactivity in dexamethasone-treated hypertensive rats.

Iijima¹,

Malik²

1985

Hypertension

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SUMMARY Possible alterations in mesenteric vascular reactivity to norepinephrine, angiotensin II, and arginine vasopressin and its relationship to prostaglandins in dexamethasone-induced hypertension in rats were investigated. The animals were treated with dexamethasone or its vehicle (sesame oil) for I day (1.8 mg/kg) and for 14 days (1.8 mg/kg/wk). The superior mesenteric artery with its branches was isolated and perfused with Tyrode's solution at a constant flow rate of 5 ml/min. Administration of norepinephrine (1-10 nmol), arginine vasopressin (0.03-0.3 nmol), or angiotensin II (0.1-1 nmol) produced vasoconstriction and increased the output of 6-keto-prostaglandin F ln and prostaglandin E 2 in a dose-related manner in mesenteric vessels. Administration of 10 nmol bradykinin or 19 nmol A23187 enhanced the output of prostaglandins without altering vascular tone. The vasoconstrictor response to arginine vasopressin, but not norepinephrine or angiotensin II, was enhanced in mesenteric vessels from rats treated with dexamethasone for 14 days but not for 1 day. In contrast, the output of basal as well as norepinephrine, arginine vasopressin, angiotensin II, bradykinin, or A23187-induced prostaglandin output was significantly reduced in mesenteric vessels from rats treated with dexamethasone for 1 or 14 days. Prostaglandin output in mesenteric arteries from rats treated with dexamethasone for 1 and 14 days was not different. These data indicate that dexamethasone treatment for longer but not for shorter periods results in a selective increase in vascular reactivity of mesenteric vessels to arginine vasopressin that is independent of prostaglandin synthesis. The increase in vascular reactivity to arginine vasopressin during long-term dexamethasone treatment may contribute to the development or maintenance, or both, of glucocorticoid-induced hypertension. 198S) KKV WORDS • dexamethasone-induced hypertension • vascular responsiveness 6-keto-prostaglandin F, ( , • prostaglandin E 2 • perfused mesenteric artery G LUCOCORT1COID treatment over a pro-' longed period in some animal species or glucocorticoid excess in patients with Cushing's syndrome results in arterial hypertension.1 " 1 The demonstration by some investigators that glucocorticoid excess enhances the pressor response and vascular reactivity to norepinephrine (NE) in animals and humans suggests that this effect contributes to the pathogenesis of glucocorticoid-induced hypertension.5 "" The increase in vascular reactivity to NE caused by long-term treatment with glucocorticoids appears to be unrelated to their action to inhibit extraneuronal uptake or meta-

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Section: Figukii 4 Effect Ofangiotensin II (Ang Ii) On Perfusion Precontrasting

confidence: 61%

Mesenteric vascular reactivity in dexamethasone-treated hypertensive rats.

Iijima¹,

Malik²

1985

Hypertension

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“…26 Considerable evidence implicates the pituitary-adrenal axis and glucocorticoids as regulators of systemic BP in the preterm infant. [27][28][29][30][31][32] Glucocorticoids influence BP through several mechanisms: (1) increasing plasma and extracellular fluid by shifting fluid from the intracellular compartment, 29,30 (2) inducing the synthesis of angiotensinogen in hepatic cells, 33 (3) inhibiting the synthesis of vasodilator prostaglandins, 34,35 (4) increasing vascular responsiveness to ␣ adrenergic amines, 36,37 and (5) inhibiting nitric oxide production. 38 Preterm infants with hypotension that is resistant to vasopressors and volume expanders respond to relatively small doses of hydrocortisone.…”

Section: Discussionmentioning

confidence: 99%

Effects of Antenatal Corticosteroids on Blood Pressure in Very Low Birth Weight Infants During the First 24 Hours of Life

et al. 1999

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“…This supposition is tenable because of: (1) clinical impressions that some hypertensive patients exhibit sympathetic "hyperactivity;" (2) the enhanced vascular responsiveness of hypertensive subjects to injections of norepinephrine (1,2); and (3) the effectiveness of treatment with antiadrenergic drugs. One would expect that gross abnormality of sympathetic nerve activity would be detected by measurements of the rate of excretion of norepinephrine and its metabolites in the urine.…”

Section: Introductionmentioning

confidence: 99%

Catecholamine turnover in normotensive and hypertensive man: effects of antiadrenergic drugs

DeQuattro¹,

Sjoerdsma²

1968

J. Clin. Invest.

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A B S T R A C T Intravenous administration of tritium-labeled 3,4-dihydroxyphenylalanine (dopa) to human subjects resulted in the labeling of endogenous catecholamines and vanillylmandelic acid (VMA). Determination of the changes in specific activity of these compounds with time in fractional collections of urine and in cardiac biopsies from patients undergoing corrective cardiac surgery permitted estimation of apparent turnover rates. The average half-time of the exponential decline in specific activity of labeled urinary norepinephrine was about 8 hr and that of VMA was 11-16 hr in five normal subjects. No significant differences from normal were observed in eight patients with essential hypertension. The average half-life of norepinephrine was only 5 hr in cardiac patients undergoing surgery, and the levels and rate of decline of cardiac norepinephrine specific activity correlated well with the exponential phase of the urinary disappearance curve. There were significant effects of treatment with alpha-methyltyrosine, reserpine, and pargyline hydrochloride on the labeling and apparent turnover rates of norepinephrine and VMA; the effects noted were consistent with known actions of these three drugs. It is suggested that the technique used is a suitable means of assessing "over-all" catecholamine metabolism in man, particulary if combined with

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Work of Digital Vasoconstriction Produced by Infused Norepinephrine in Cushing's Syndrome

Cited by 75 publications

References 0 publications

Mesenteric vascular reactivity in dexamethasone-treated hypertensive rats.

Mesenteric vascular reactivity in dexamethasone-treated hypertensive rats.

Effects of Antenatal Corticosteroids on Blood Pressure in Very Low Birth Weight Infants During the First 24 Hours of Life

Catecholamine turnover in normotensive and hypertensive man: effects of antiadrenergic drugs

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