Atrial natriuretic factor (ANF) increases urinary protein excretion in patients with essential hypertension: A possible role of ANF for renal handling of protein

Suenaga, K.; Mizuno, Keiko; Niimura, Susumu; Mori, Kazuya; Sato, Masahiro; Tani, Motohiro; Yabe, R; Yatabe, Yoshihisa; Fukuchi, Soitsu

doi:10.1016/0006-291x(89)92812-x

Cited by 7 publications

(2 citation statements)

References 14 publications

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“…For example it is certain that the cardiac atrial and B-type natriuretic peptides (ANP and BNP) are involved. Plasma levels of both peptides are, unsurprisingly, elevated in patients with hypertension due to underlying unilateral renal ischemia [26][27][28] and, along with angiotensin 11, may contribute to the proteinuria [29]. They almost certainly also encourage volume depletion since the natriuretic effect of these peptides is enhanced at high levels of renal perfusion pressure [30] (as occurs in the nonischemic kidney in this syndrome) and, at least experimentally, when angiotensin 11 levels are elevated [31].…”

Section: Pathophysiologymentioning

confidence: 99%

Unilateral renal ischemia causing the hyponatremic hypertensive syndrome in children—more common than we think?

Nicholls

2006

Pediatr Nephrol

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A case report in the journal Pediatric Nephrology describes a 15-month-old girl with the syndrome of hypertension and hyponatremia (HH syndrome) due to underlying unilateral renal artery stenosis. This syndrome is typically associated with hypokalemia and severe volume depletion and sometimes proteinuria, all of which, along with hypertension and hyponatremia, are usually corrected by resolution of the underlying renal ischemia. Gross and probably sudden activation of the renin-angiotensin system in response to renal ischemia is central to the pathophysiology although the cardiac atrial and B-type natriuretic peptides probably contribute also. Initial control of the severe hypertension may, in some cases, require careful volume repletion prior to introduction of blockade of the renin-angiotensin system in order to avoid first-dose hypotension, after which correction of the underlying renal ischemia is required. Whereas the syndrome has rarely been reported in children, it is possible that, as in adults, this reflects its lack of recognition by clinicians. The HH syndrome due to unilateral renal ischemia in children may be much more common than we think.

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Section: Pathophysiologymentioning

confidence: 99%

Unilateral renal ischemia causing the hyponatremic hypertensive syndrome in children—more common than we think?

Nicholls

2006

Pediatr Nephrol

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“…Renal functional deterioration appears to be hastened when glomerular hyperfiltration or hypertension occurs concurrently with these risk factors (Brenner 1983;ODonnell et al 1989;Suenaga et al 1989). Because ANP promotes natriuresis and diuresis, in part, by increasing single nephron glomerular filtration rate (GFR) and transcapillary hydrostatic pressure (Camargo et al 1984), ANP may actually contribute to progressive protein and lipoprotein loss and declining renal function in nephrotic kidneys.…”

Section: Introductionmentioning

confidence: 99%

The Effect of Atrial Natriuretic Peptide Infusion on Renal Haemodynamics and Plasma Lipoproteins in Puromycin Aminonucleoside Nephrosis in Rats

1993

Clin Exp Pharma Physio

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1. The effect of continuous intravenous administration of 1 microgram/h atrial natriuretic peptide (ANP) for 4 days was studied in normal male Sprague-Dawley rats and rats made nephrotic with puromycin aminonucleoside (PA). 2. ANP infusion significantly increased urinary sodium and potassium excretion by 3 days of infusion in control rats but not in PA-treated rats. ANP infusion significantly increased glomerular filtration rate in PA-treated rats, while effective renal plasma flow was similarly decreased compared with non-infused nephrotic rats. 3. Plasma high density lipoproteins (HDL) were significantly decreased and low density lipoproteins (LDL) were increased in PA-treated rats that received ANP; HDL were increased in normal rats infused with ANP. 4. Competitive binding studies demonstrated a lower density of specific ANP receptors in glomerular membranes from rats injected with PA, while binding affinity was unchanged. 5. Infusion with exogenous ANP did not promote natriuresis in PA nephrosis despite an enhancement of glomerular filtration rate (GFR), thus suggesting that sodium retention in this model is due to a post-glomerular defect. Plasma lipoprotein composition in both normal and nephrotic rats may be affected by ANP.

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Atrial natriuretic factor: Its (patho)physiological significance in humans

Zeeuw¹,

Janssen²,

Jong³

1992

Kidney International

105

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The first human studies using relatively high-doses of ANF revealed similar effects as observed in the preceding animal reports, including effects on systemic vasculature (blood pressure fall, decrease in intravascular volume), renal vasculature (rise in GFR, fall in renal blood flow), renal electrolyte excretion (rises in many electrolytes), and changes in release of a number of different hormones. Whether all these changes are the result of direct ANF effects or secondary to a (single) primary event of the hormone remains to be determined. Certainly, it has been proven that more physiological doses of ANF fail to induce short-term changes in many of these parameters leaving only a rise in hematocrit, natriuresis and an inhibition of the RAAS as important detectable ANF effects in humans. This leads us to hypothesize that ANF is a "natriuretic" hormone with physiological significance. The primary function in humans is to regulate sodium homeostasis in response to changes in intravascular volume (cardiac atrial stretch). Induction of excess renal sodium excretion and extracellular volume shift appear to be the effector mechanisms. The exact mechanism of the natriuresis in humans still needs to be resolved. It appears however, that possibly a small rise in GFR, a reduction in proximal and distal tubular sodium reabsorption, as well as an ensuing medullary washout, are of importance. The pathophysiological role of ANF in human disease is unclear. One may find elevated plasma irANF levels and/or decreased responses to exogenous ANF in some disease states. Whether these findings are secondary to the disease state rather than the cause of the disease remains to be resolved. Therapeutic applications for ANF, or drugs that intervene in its production or receptor-binding, seem to be multiple. Most important could be the antihypertensive effect, although areas such as congestive heart failure, renal failure, liver cirrhosis and the nephrotic syndrome cannot be excluded. Although the data that have been gathered to date allowed us to draw some careful conclusions as to the (patho)physiological role of ANF, the exact place of ANF in sodium homeostatic control must still be better defined. To achieve this, we will need more carefully designed low-dose ANF infusion, as well as ANF-breakdown inhibitor studies. Even more promising, however, is the potential area of studies open to us when ANF-receptor (ant)agonists become available for human use.

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Atrial natriuretic factor (ANF) increases urinary protein excretion in patients with essential hypertension: A possible role of ANF for renal handling of protein

Cited by 7 publications

References 14 publications

Unilateral renal ischemia causing the hyponatremic hypertensive syndrome in children—more common than we think?

Unilateral renal ischemia causing the hyponatremic hypertensive syndrome in children—more common than we think?

The Effect of Atrial Natriuretic Peptide Infusion on Renal Haemodynamics and Plasma Lipoproteins in Puromycin Aminonucleoside Nephrosis in Rats

Atrial natriuretic factor: Its (patho)physiological significance in humans

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