Influence of corticosteroids on mechanical performance of isolated rat papillary muscles

Am, Lefer

doi:10.1152/ajplegacy.1968.214.3.518

Cited by 44 publications

(21 citation statements)

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“…The systemic hemodynamic alterations that accompanied this defect in maximal urine concentration included a decrease in cardiac output and MAP. A decrease in myocardial contractility has been reported in the presence of glucocorticoid deficiency (21)(22)(23). The response of the peripheral vasculature to catecholamines has also been demonstrated to be dependent on glucocorticoid hormones (24).…”

Section: Discussionmentioning

confidence: 99%

Molecular Mechanisms of Impaired Urinary Concentrating Ability in Glucocorticoid-Deficient Rats

Chen¹,

Cadnapaphornchai²,

Summer³

et al. 2005

Journal of the American Society of Nephrology

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The purpose of this study was to examine urinary concentrating ability and protein expression of renal aquaporins and ion transporters in glucocorticoid-deficient (GD) rats in response to water deprivation as compared with control rats. Rats underwent bilateral adrenalectomies, followed only by aldosterone replacement (GD) or both aldosterone and dexamethasone replacement (control). As compared with control rats, the GD rats demonstrated a decrease in cardiac output and mean arterial pressure. In response to 36-h water deprivation, GD rats demonstrated significantly greater urine flow rate and decreased urine osmolality as compared with control rats at comparable serum osmolality and plasma vasopressin concentrations. The initiator of the countercurrent concentrating mechanism, the sodium-potassium-2 chloride co-transporter, was significantly decreased, as was the medullary osmolality in the GD rats versus control rats. There was also a decrease in inner medulla aquaporin-2 (AQP2) and urea transporter A1 (UT-A1) in GD rats as compared with control rats. There was a decrease in outer medulla Gs␣ protein, an important factor in vasopressin-mediated regulation of AQP2. Immunohistochemistry studies confirmed the decreased expression of AQP2 and UT-A1 in kidneys of GD rats as compared with control. In summary, impairment in the urinary concentrating mechanism was documented in GD rats in association with impaired countercurrent multiplication, diminished osmotic equilibration via AQP2, and diminished urea equilibration via UT-A1. These events occurred primarily in the relatively oxygen-deficient medulla and may have been initiated, at least in part, by the decrease in mean arterial pressure and thus renal perfusion pressure in this area of the kidney.

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Section: Discussionmentioning

confidence: 99%

Molecular Mechanisms of Impaired Urinary Concentrating Ability in Glucocorticoid-Deficient Rats

Chen¹,

Cadnapaphornchai²,

Summer³

et al. 2005

Journal of the American Society of Nephrology

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“…Interestingly, isolated. papillary muscles taken from adrenalectomized rats are known to show a more rapid decline in contractile tension ex vivo than those from control animals and this can be prevented by treatment with dexamethasone in vivo or in vitro (Lefer, 1968). Whether the protection afforded by dexamethasone is due to its prevention of NO-stimulated increases in cyclic GMP levels or to inhibition of NO-mediated cytotoxicity (O'Connor & Moncada, 1991) is not yet known.…”

Section: No Synthase Infreshly Isolated Cardiac Myocytesmentioning

confidence: 99%

Induction and potential biological relevance of a Ca²⁺‐independent nitric oxide synthase in the myocardium

Schulz

Nava

Moncada

1992

British J Pharmacology

592

217

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We have investigated whether the myocardium and isolated cardiac myocytes can express a Ca2+‐independent NO synthase after treatment with endotoxin or cytokines. Nitric oxide synthesis was measured in cytosols from the left ventricular wall from rats treated with endotoxin, or from freshly isolated myocytes from adult rats treated in vitro with cytokines. Cytosols from the ventricle of saline‐treated control animals showed only Ca2+‐dependent NO synthesis. After treatment with endotoxin, the expression of an inducible, Ca2+‐independent NO synthase was observed. The activity of this enzyme was maximal at 6 h and returned towards control levels by 18 h; no alterations occurred in the Ca2+‐dependent NO synthase activity. Parallel to this enzyme induction there was an increase in myocardial guanosine 3′:5′‐cyclic monophosphate (cyclic GMP) and plasma nitrite and nitrate (NO−x). All these changes were prevented by pretreatment of the rats with dexamethasone. Myocytes possessed Ca2+‐dependent NO synthase activity and expressed, after treatment with tumour necrosis factor‐α (TNF‐α) and interleukin‐1β (IL‐1β), a Ca2+‐independent NO synthase, the induction of which was prevented by dexamethasone and cycloheximide. Since increases in cyclic GMP levels in the heart are associated with reduced myocardial contractility, it is possible that the enhanced production of NO by a Ca2+‐independent enzyme accounts, at least in part, for the depression of myocardial contractility seen in septic shock, cardiomyopathies, allograft rejection, burn trauma, as well as during anti‐tumour therapy with cytokines.

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“…In the absence of evidence for extracellular fluid volume depletion, the effect of glucocorticoid deficiency to impair cardiac function (26)(27)(28)(29) seems the likely initiating event for increased sympathetic tone in the glucocorticoid deficiency state. In this regard, it is interesting to note that not only were the plasma vasopressin levels higher and stroke volume lower in the glucocorticoid-deficient state, but these parameters actually increased and decreased, respectively, during acute water loading.…”

Section: Plasma Vasopressin In Glucocorticoid Deficiencymentioning

confidence: 99%

Role of Plasma Vasopressin in Impaired Water Excretion of Glucocorticoid Deficiency

Boykin¹,

deTORRENTE²,

Erickson³

et al. 1978

J. Clin. Invest.

113

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A B S T R A C T In the present study, the effect of selective glucocorticoid deficiency on renal water excretion was investigated in conscious, trained, adrenalectomized dogs. The animals were studied before and after a water load while on replacement therapy of desoxycorticosterone acetate, 5 mg/day, and dexamethasone, 0.8 mg/day (group I), and while off dexamethasone for 5-9 days (group II). Before the water load the weight, inulin space, cardiac output, blood pressure, glomerular filtration rate, renal blood flow, plasma osmolality, and plasma antidiuretic hormone measured by radioimmunoassay were similar in both groups I and II. However, after a 40 ml/kg water load a marked impairment in renal water excretion in the glucocorticoid deficient dogs became apparent. Maximal free water clearance was -0.046±0.16 vs. 6.51±0.72 ml/min (P < 0.001) and minimal urinary osmolality was 425±56 vs. 82±3.5 mosmol/kg H20 (P < 0.001) in group II as compared to group I. Plasma antidiuretic hormone was maximally suppressed during the water load in group I to 0.34±0.08 pg/ml but remained elevated at 9.18±1.79 pg/ml (P <0.005) in group II. This nonsuppressibility of plasma antidiuretic hormone during water loading in group II was associated with a significant tachycardia of 145±6 vs. 87±6 beats/min (P < 0.001) in group I and a significantly lower stroke volume of 27±0 vs. 59±0.5 ml/beat (P < 0.001). In conclusion, our results implicate a persistent secretion of antidiuretic hormone as an important factor in the impaired water excretion of glucocorticoid deficiency. A deleterious effect of glucocorticoid deficiency on cardiac function was observed and this hemodynamic alteration could be involved in initiating a nonosmolar, baroreceptormediated release of vasopressin.

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Influence of corticosteroids on mechanical performance of isolated rat papillary muscles

Cited by 44 publications

References 0 publications

Molecular Mechanisms of Impaired Urinary Concentrating Ability in Glucocorticoid-Deficient Rats

Molecular Mechanisms of Impaired Urinary Concentrating Ability in Glucocorticoid-Deficient Rats

Induction and potential biological relevance of a Ca²⁺‐independent nitric oxide synthase in the myocardium

Role of Plasma Vasopressin in Impaired Water Excretion of Glucocorticoid Deficiency

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Influence of corticosteroids on mechanical performance of isolated rat papillary muscles

Cited by 44 publications

References 0 publications

Molecular Mechanisms of Impaired Urinary Concentrating Ability in Glucocorticoid-Deficient Rats

Molecular Mechanisms of Impaired Urinary Concentrating Ability in Glucocorticoid-Deficient Rats

Induction and potential biological relevance of a Ca2+‐independent nitric oxide synthase in the myocardium

Role of Plasma Vasopressin in Impaired Water Excretion of Glucocorticoid Deficiency

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Induction and potential biological relevance of a Ca²⁺‐independent nitric oxide synthase in the myocardium