Atrial natriuretic factor significantly contributes to the mineralocorticoid escape phenomenon. Evidence for a guanylate cyclase-mediated pathway.

Yokota, Naoto; Bruneau, Benoit G.; Bold, Mercedes L. Kuroski de; Bold, Adolfo J. de

doi:10.1172/jci117544

Cited by 59 publications

(29 citation statements)

References 63 publications

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“…In addition, intravascular volume expansion may also increase renal interstitial hydrostatic pressure with reductions in peritubular Starling forces at the level of the proximal tubule to reduce proximal reabsorption of sodium. 26 Other studies investigating mineralocorticoid escape have found roles for natriuretic peptides, [27][28][29][30] NO, 31 and the thiazide-sensitive sodium chloride cotransporter. 32 Titze et al 33 reported that administration of DOCA and salt to rats was associated with osmotically inactive sodium storage and osmotically neutral sodium retention balanced by potassium loss.…”

Section: Discussionmentioning

confidence: 99%

Mineralocorticoid Escape by the Kidney But Not the Heart in Experimental Asymptomatic Left Ventricular Dysfunction

et al. 2007

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Abstract-Unlike healthy subjects, overt congestive heart failure cannot "escape" the sodium-and water-retaining actions of mineralocorticoid excess. It is undefined whether escape occurs in asymptomatic left ventricular dysfunction (ALVD), which is characterized by preserved sodium homeostasis, natriuretic peptide activation, and normal circulating aldosterone. We hypothesized that, in ALVD, mineralocorticoid excess with exogenous deoxycorticosterone acetate (DOCA) would overwhelm renal compensatory mechanisms, resulting in sodium and water retention, and promote renal and cardiac collagen deposition. ALVD was induced in 2 groups (Nϭ5 each) of dogs by tachypacing at 180 bpm. Urine was collected daily and blood drawn at baseline and days 2, 5, 8, and 11. One group served as control (ALVD), and the other received DOCA (ALVDϩDOCA) starting at day 2 of pacing. Urine flow and sodium excretion were unchanged in the ALVD group. In ALVDϩDOCA, urine flow and sodium excretion decreased on the first 2 days DOCA was given but normalized starting day 4. Urine flow and urinary cGMP excretion increased in ALVDϩDOCA after DOCA escape. Plasma atrial natriuretic peptide, B-type natriuretic peptide, and cGMP increased equally in both groups. There were no differences in cardiorenal and hemodynamic parameters in an acute study on day 11. Although renal collagen area fraction was similar, left ventricular collagen area fraction in ALVDϩDOCA was significantly higher than in ALVD (3.3Ϯ0.4% versus 2.0Ϯ0.2%; Pϭ0.012). We conclude that ALVD can escape the sodium-and water-retaining effects of mineralocorticoid excess. Despite renal escape, increased left ventricular collagen deposition suggests that the heart but not the kidney failed to escape the tissue effects of DOCA. Key Words: basic science Ⅲ experimental models Ⅲ extracellular matrix Ⅲ heart failure Ⅲ kidney physiology/pathophysiology Ⅲ mineralocorticoids T he kidney plays a key role in the syndrome of congestive heart failure (CHF), especially with respect to the congestive symptoms associated with overt CHF. 1 It is increasingly appreciated that the syndrome of overt CHF is frequently preceded by a chronic stage in which Ϸ50% of subjects with decreased left ventricular (LV) ejection fraction have no heart failure (HF) symptoms, termed "asymptomatic LV dysfunction" (ALVD). 2,3 Importantly, patients with ALVD are at increased risk for progression to overt CHF and show increased mortality. 4,5 In contrast to overt CHF, ALVD is characterized by the kidney's ability to preserve urinary sodium excretion despite ventricular dysfunction. This occurs in the setting of increased plasma levels of atrial and B-type natriuretic peptide (ANP and BNP, respectively) and, in the absence of diuretic therapy, lack of activation of the renin-angiotensin-aldosterone system. 6,7 The mechanism of progression from ALVD and sodium balance to clinical symptoms of congestion and sodium retention remains unclear, although studies in experimental HF suggest that it may involve the activation of aldosterone,...

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Section: Discussionmentioning

confidence: 99%

Mineralocorticoid Escape by the Kidney But Not the Heart in Experimental Asymptomatic Left Ventricular Dysfunction

et al. 2007

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“…The 'escape' is the result of compensatory suppressed Na resorption in nephron segments proximal to the collectin ducts (2,14). There is evidence that Arial natriuretic peptide (ANP) plays an important role in mineralocorticoid escape (30,33). The mechanisms responsible for an increase in mipheral resistance and the associated hypertension are unclear (10).…”

Section: Discussionmentioning

confidence: 99%

Endocrinology: Hyperaldosteronism in a cat with metastasised adrenocortical tumour

Rijnberk

Voorhout

Kooistra³

et al. 2001

Veterinary Quarterly

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Laboratory examination revealed hypohalaemia (1.6 mmol/1; reference range 3.4-5.7 mmo1/1) and echocardiographic findings seemed to be compatible with hypertrophic cardiomyopathy. Potassium suppletion, first intravenously and then orally, and treatment with the (13-blocking agent atenolol (Tenormin®, Zeneca;6.25 mg once daily) and acetylsalicylic acid (40 mg twice daily) resulted in good recovery. On 29 June, 3 weeks after stopping potassium suppletion and atenolol, the cat was presented to the owner's veterinarian for weakness in the hind legs. The cat was not lethargic and was eating and drinking normally. The history of cardiomyopathy raised the possibility of complicating thromboembolism. A saddle thrombus at the distal aortic trifurcation was considered unlikely because the femoral pulses were easily palpated and the footpads of the hind legs were warm and pink. The previous treatment was resumed but the dose of acetylsalicylic acid was lowered to twice weekly 25 mg. The cat did well on this regimen but the plasma concentrations of potassium remained low. When potassium gluconate (Tumil Ke, Aesculaap by, Boxtel, NL) was given orally in a dose of 2 mmol four times daily, the plasma potassium concentration remained s 2.2 mmo1/1. On 1 September the cat collapsed again, even though the potassium supplementation had been increased to 2 mmol six times daily for 2 weeks. In addition to muscular weakness, there was mydriasis, restlessness, and panting. Potassium concentrations in plasma ranged from 1.9 to 2.1 mmo1/1. An angiotensin-converting enzyme inhibitor (once daily 1 mg enalapril, Enalfor®, Mycofarm) was added to the treatment. The cat recovered but the plasma potassium concentration remained at the same low level. Hyperadrenocorticism was excluded as the cause of the muscular weakness by the finding that the basal urinary corticoid/creatinine ratio (average on two consecutive days: 24 x 10-6) was below the upper limit of the reference range (37 x 10-6) (11) and the urinary corticoid/creatinine ratio was readily suppressed (to 3.0 x 10-6 ) following three oral doses of 0.5 mg dexamethasone. A possible relation to hyperthyroidism (21) was excluded by the finding of a normal plasma thyroxine concentration (29 nmi51/1).Between the episodes of muscular weakness the cat's condition and behaviour were unremarkable but in search of an explanation for the persistent hypokalaemia the cat was referred to the Utrecht University Clinic for Companion Animals in September 1998. HYPERALDOSTERONISM IN A CAT WITH METASTASISED ADRENOCORTICAL TUMOURA.Rijnberk1,6, G. Voorhout2, H.S. Kooistra1, R.J.M. van der Waarden3, F.J. van Sluijs1, J. Uzer4, P. Boer5, and W.H. Boer5 Vet Quart 2001; 23: 38-43 Accepted for publication: January 10, 2000. SUMMARYIn a 12-year-old male shorthaired cat with attacks of hypokalaemic muscular weakness in spite of oral potassium supplementation, highly elevated plasma aldosterone concentrations in combination with low plasma renin activity pointed to primary hyperaldosteronism. Ultrasonography and ...

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“…Our previous experimental work 2,30 suggests that ANF plasma levels may be a measure of extracellular volume status whereas BNP levels reflect cardiac hypertrophy and ventricular dysfunction. 31,32 These underlying events, superimposed to the specific effect(s) of the inflammatory process and together with varying degrees of the preservation of renal function in individual patients, may explain the variations in NP ratios that were found.…”

Section: Masters Et Al Natriuretic Peptides In Cardiac Transplantatiomentioning

confidence: 99%

Discoordinate Modulation of Natriuretic Peptides During Acute Cardiac Allograft Rejection in Humans

et al. 1999

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Background-Increased circulating levels of the cardiac polypeptide hormones atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) may be observed after orthotopic cardiac transplantation. Both the hypertrophic and inflammatory processes in the allograft may contribute to this increase, but no mechanistic explanation has been suggested for this observation. Methods and Results-Plasma immunoreactive ANF and BNP determinations were performed in 10 consecutive transplant patients. These were correlated with degree of rejection as reflected by histopathological findings at serial endomyocardial biopsies. Three patients had associated hemodynamic measurements and blood samples 24 hours before and after transplantation. All rejection episodes that received treatment were accompanied by a marked increase in BNP plasma levels to ϾϷ400 pg/mL. Steadily increasing BNP levels preceded overt rejection as assessed by histopathological criteria. The increase in plasma BNP was not always accompanied by an increase in ANF, which suggests the specific upregulation of BNP gene expression during acute rejection episodes. Treatment of the acute rejection episodes led to a substantial decrease of BNP plasma levels. Conclusions-The significant selective increase in plasma BNP levels found in the present study has not been previously described. This finding provides a new insight into the mechanism of allograft rejection and the modulation of natriuretic peptide synthesis and release. Furthermore, although preliminary, the data suggest that BNP plasma levels could form the basis for a new, noninvasive screening test to predict acute cardiac allograft rejection. Because treatment with the antilymphocyte monoclonal antibody OKT3 (murine monoclonal antibody to the CD3 antigen of the human T-cell) decreased BNP plasma levels, cytokine production by T-cells may mediate the selective increase in circulating BNP. (Circulation. 1999;100:287-291.)Key Words: transplantation Ⅲ natriuretic peptides Ⅲ atrial natriuretic factor Ⅲ myocarditis Ⅲ pathology U nder certain pathophysiological conditions, synthesis and release of the cardiac natriuretic peptides (NP) atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) are significantly augmented in both atrial and ventricular cardiocytes. Increased production of these hormones by the ventricle is a hallmark of cardiac hypertrophy, failure, 1,2 and inflammation. 3,4 The former increase reflects the reexpression of the cardiac fetal phenotype seen with chronic hemodynamic overload, but the basis for the increased production of NP in myocarditis has not yet been defined.We reported that after cardiac transplantation, ANF plasma concentrations remain elevated, reaching levels comparable to those found before transplantation despite the normalization of filling pressures and the renin-angiotensin-aldosterone system. 5 Elevated BNP plasma levels have also been found after cardiac transplantation. 6 -8 Because BNP is predominantly of ventricular origin, it would be expected that repla...

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Atrial natriuretic factor significantly contributes to the mineralocorticoid escape phenomenon. Evidence for a guanylate cyclase-mediated pathway.

Cited by 59 publications

References 63 publications

Mineralocorticoid Escape by the Kidney But Not the Heart in Experimental Asymptomatic Left Ventricular Dysfunction

Mineralocorticoid Escape by the Kidney But Not the Heart in Experimental Asymptomatic Left Ventricular Dysfunction

Endocrinology: Hyperaldosteronism in a cat with metastasised adrenocortical tumour

Discoordinate Modulation of Natriuretic Peptides During Acute Cardiac Allograft Rejection in Humans

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