Hormonal determinants of sodium excretion in rats with experimental high-output heart failure

Winaver, Joseph; Hoffman, Aaron; Burnett, John C.; Haramati, Aviad

doi:10.1152/ajpregu.1988.254.5.r776

Cited by 46 publications

(98 citation statements)

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“…In addition, this experimental model is characterized by a marked activation of the systemic and intracardiac renin-angiotensin system in proportion to the severity of the disease. 14,15 Indeed, an association between Ang II and induction of MCP-1 gene expression has been documented in rat vascular smooth muscle cells, in aortic tissues of hypertensive rats, and in rat mesangial cells in experimental nephritis. 12,13,27 In vascular smooth muscle cells, the Ang II-induced MCP-1 mRNA accumulation was mediated by the AT 1 receptor.…”

Section: Discussionmentioning

confidence: 99%

“…Similar findings have been reported previously. 15 Echocardiography demonstrated that decompensated CHF was associated with a marked degree of cardiac dilatation (Table 2). Figure 1 presents the data on the expression of MCP-1 and rpL32 mRNA, by Northern hybridization, in control and ACF animals at 24 hours, 3 days, and 7 days, respectively.…”

Section: Mcp-1 Binding Studiesmentioning

confidence: 99%

“…14 -17 Furthermore, rats with ACF can be subdivided, on the basis of their daily urinary sodium excretion, into compensated and decompensated subgroups, which differ in the degree of severity of CHF. 15 Thus, in addition to renal retention of sodium and water, rats with decompensated CHF display a marked degree of neurohormonal activation compared with the compensated subgroup. 14,15 Therefore, in the present study, we characterized the changes in the expression of MCP-1 mRNA and protein in rats with compensated and decompensated heart failure, using a novel real-time polymerase chain reaction (PCR) technique 18 combined with standard Northern blotting and immunohistochemistry.…”

mentioning

confidence: 99%

“…15 Thus, in addition to renal retention of sodium and water, rats with decompensated CHF display a marked degree of neurohormonal activation compared with the compensated subgroup. 14,15 Therefore, in the present study, we characterized the changes in the expression of MCP-1 mRNA and protein in rats with compensated and decompensated heart failure, using a novel real-time polymerase chain reaction (PCR) technique 18 combined with standard Northern blotting and immunohistochemistry. In addition, because no data are available on MCP-1 receptors in the myocardium in CHF, binding assays were performed to confirm the presence of and characterize the alterations in MCP-1 receptor in this experimental model of heart failure.…”

mentioning

confidence: 99%

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Monocyte Chemoattractant Protein-1 is Upregulated in Rats With Volume-Overload Congestive Heart Failure

Behr¹,

Wang²,

Aiyar³

et al. 2000

Circulation

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Background-Chemokines are potent proinflammatory and immune modulators. Increased expression of chemokines, eg, monocyte chemoattractant protein-1 (MCP-1), has recently been described in clinical and experimental heart failure. The present report is aimed at exploring the expression, localization, and binding site regulation of MCP-1, a member of the C-C chemokine family, in a rat model of volume-overload congestive heart failure (CHF). Methods and Results-An aortocaval fistula was surgically created between the abdominal aorta and inferior vena cava.Rats with CHF were further subdivided into compensated and decompensated subgroups. Northern blot analysis and real-time quantitative polymerase chain reaction demonstrated upregulation of MCP-1 mRNA expression correlating with the severity of CHF (288Ϯ22, 502Ϯ62, and 826Ϯ138 copies/ng total RNA for sham, compensated, and decompensated animals, respectively; nϭ5, PϽ0.05). MCP-1 protein was localized by immunohistochemistry in cardiomyocytes, vascular endothelium and smooth muscle cells, infiltrating leukocytes, and interstitial fibroblasts, and its intensity increased with severity of CHF. In addition, rats with CHF displayed a significant decrease of 125 I-labeled MCP-1 binding sites to myocardium-derived membranes (384.3Ϯ57.0, 181.3Ϯ8.8, and 123.3Ϯ14.1 fmol/mg protein for sham, compensated, and decompensated animals, respectively). Conclusions-Volume-overload CHF in rats is associated with alterations in the expression, immunohistochemical localization, and receptor binding of the MCP-1 chemokine in the myocardium. These changes were more pronounced in rats with decompensated CHF. The data suggest that activation of the MCP-1 system may contribute to the progressive cardiac decompensation and development of CHF in rats with aortocaval fistula. (Circulation.

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Section: Discussionmentioning

confidence: 99%

Section: Mcp-1 Binding Studiesmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Monocyte Chemoattractant Protein-1 is Upregulated in Rats With Volume-Overload Congestive Heart Failure

Behr¹,

Wang²,

Aiyar³

et al. 2000

Circulation

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“…The rats used had 'compensated' for the A-V shunt; those animals that fail to 'compensate' die within the first 7 days after surgery (Winaver et al, 1988). Mean plasma renin activity was 10.3 ± 2.2 ng angiotensin I ml-' h-' in A-V fistula rats (n = 7) and 7.4+ 1.5 ng angiotensin I ml-' h-' in sham-operated controls (n = 9; NS).…”

Section: A -V Fistula Ratsmentioning

confidence: 99%

Renal effects of concurrent E‐24.11 and ACE inhibition in the aorto‐venocaval fistula rat

Kirk¹,

Wilkins²

1996

British J Pharmacology

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1 The present studies compare the early renal response to (a) an endopeptidase-24.11 (E-24.11) inhibitor (candoxatrilat) (b) an angiotensin-converting enzyme (ACE) inhibitor (lisinopril) and (c) the combination of endopeptidase-24.11 and ACE inhibition in the rat A-V fistula model of chronic volume overload. 2 Candoxatrilat (3 and 10 mg kg-') i.v. produced a prompt 3 fold increase in urinary sodium and cyclic GMP excretion without affecting significantly blood pressure or glomerular filtration rate (GFR).3 Lisinopril (0.03 mg kg-') alone inhibited the pressor response to angiotensin I but had no significant effect on urinary sodium excretion or blood pressure.4 Lisinopril (0.03 mg kg-') attenuated significantly the early natriuretic response to candoxatrilat (3 mg kg-1) and the associated rise in urinary cyclic GMP, but sodium excretion eventually reached levels associated with acute E-24.11 inhibition. 5 Doses of the dual E-24. 11/ACE inhibitor, sampatrilat, that inhibited the pressor response to angiotensin I reduced mean arterial blood pressure and produced a delayed natriuresis and rise in urinary cyclic GMP excretion when compared to candoxatrilat alone. 6 Concurrent administration of an ACE inhibitor reduces the early renal response to E-24.11 inhibition in the A-V fistula rat, an effect attributable to the hypotensive action of this combination.

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Blunted natriuretic response and low blood pressure after atrial natriuretic factor in early cirrhosis

Beutler¹,

Koomans²,

Rabelink³

et al. 1989

Hepatology

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We compared the natriuretic response to a standard dose of atrial natriuretic factor in nine patients with early cirrhosis (no ascites or edema) with the response in normal subjects displaying a range of baseline sodium excretions due to different sodium intakes (20 mmoles per day, n = 9; 100 mmoles per day, n = 9, and 200 mmoles per day, n = 9). In these normal subjects, sodium output rose, in the same order, from 49 +/- 12 to 177 +/- 26, from 116 +/- 21 to 365 +/- 106 and from 228 +/- 29 to 901 +/- 85 mumoles per min in the first 20 min after 100 micrograms atrial natriuretic factor (human atrial natriuretic factor 99-126). Thus, irrespective of basal excretion, natriuresis rose by at least 2-fold. In the cirrhotic patients, natriuresis rose from 173 +/- 42 to 305 +/- 77 mumoles per min, that is by hardly 1-fold, significantly less than in the normal subjects (p less than 0.01). Renal function studies indicated that atrial natriuretic factor caused less rise in glomerular filtration rate and in fractional sodium excretion. Atrial natriuretic factor induced a fall in blood pressure only in the cirrhotic group, from 130 +/- 4/81 +/- 2 to 108 +/- 4/68 +/- 3 mmHg (p less than 0.001). Plasma atrial natriuretic factor was not low in the cirrhotic patients. Although these data are compatible with a primary disturbance of sodium excretion in early cirrhosis without ascites, such an explanation is complicated by the concomitant drop in blood pressure after atrial natriuretic factor.(ABSTRACT TRUNCATED AT 250 WORDS)

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Hormonal determinants of sodium excretion in rats with experimental high-output heart failure

Cited by 46 publications

References 0 publications

Monocyte Chemoattractant Protein-1 is Upregulated in Rats With Volume-Overload Congestive Heart Failure

Monocyte Chemoattractant Protein-1 is Upregulated in Rats With Volume-Overload Congestive Heart Failure

Renal effects of concurrent E‐24.11 and ACE inhibition in the aorto‐venocaval fistula rat

Blunted natriuretic response and low blood pressure after atrial natriuretic factor in early cirrhosis

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