Failure of Atrial Myocardial Extract to Inhibit Renal Na&lt;sup&gt;+&lt;/sup&gt;, K&lt;sup&gt;+&lt;/sup&gt;-ATPase

Pollock, David M.; Mullins, Margaret M.; Banks, Robert O.

doi:10.1159/000172915

Cited by 23 publications

(13 citation statements)

References 7 publications

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“…The natriuresis cannot be fully accounted for by changes in renal hemodynamics and/or physical factors governing in part tubular reabsorption of Na+ (4), suggesting that ANF may inhibit directly the tubular transport of Na+. Unlike another recently described natriuretic factor (4), ANF has no effect on the activity of (Na+-K+)-ATPase (4)(5)(6) or Na+ transport in amphibian epithelia (5,6).…”

Section: Introductionmentioning

confidence: 74%

“…Besides luminal entry across BBM, another major component operative in transepithelial Na' reabsorption and in Na'-linked transport systems in proximal tubules is the activity of (Na+-K+)-ATPase at basolateral membranes, an active Na+ pump that continuously maintains low intracellular Na' and lumen-to-cell Na' gradient (11)(12)(13)(14)(15). Studies reported by other investigators show that ANF does not influence (Na'-K+)-ATPase activity (4)(5)(6).…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Administration of atrial natriuretic factor inhibits sodium-coupled transport in proximal tubules.

Hammond

Yusufi²,

Knox³

et al. 1985

J. Clin. Invest.

117

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The newly discovered peptides extracted from cardiac atria, atrial natriuretic factors (ANFs), when administered parenterally cause renal hemodynamic changes and natriuresis. The nephron sites and cellular mechanism accounting for profound increase in Na' excretion in response to ANFs are not yet clarified. In the present study we investigated whether synthetic ANF peptide alters the reabsorption of Na' and reabsorption of solutes cotransported with Na' in the proximal tubules of rats.Synthetic ANF peptide consisting of 26 amino acids, 4 ag/kg body wt/h, or vehicle in controls, was infused to surgically thyroparathyroidectomized anesthetized rats. After determination of the fractional excretion (FE) of electrolytes (Na', K+, P,, Ca2+, Mg2+, HCO3), the kidneys were removed and luminal brush border membrane vesicles (BBMVs) were prepared from renal cortex. Solute transport was measured in BBMVs by rapid filtration techniques. Infusion of ANF peptide increased FENa, FEp,, and FEHCO,; but FEc., FEK, and FEMg were not changed. The increase in FENa was significantly correlated, on the one hand, with increase of FEp, (r = 0.9, n = 7; P < 0.01) and with increase of FEHCO3 (r = 0.89, n = 7; P < 0.01). On the other hand, FEN. did not correlate with FEK, FEca, or with FEM.. The Na+ gradient-dependent uptake of Pi by BBMVs prepared from renal cortex of rats receiving ANF infusion was significantly (P < 0.05) decreased (-25%), whereas the Na+ gradient-dependent uptake of L-13H]proline and of D-I3Higlucose or the diffusional uptake of 22Na+ were not changed. ANF-elicited change in FEn showed a close inverse correlation with decrease of Na+-dependent Pi uptake by BBMVs isolated from infused rats (r = 0.99, n = 7; P < 0.001). Direct addition of ANF to BBMVs in vitro did not change the Na+ gradient-dependent Pi uptake. In rats infused with ANF, the rate of amiloride-sensitive Na+-H+ exchange across the brush border membrane (BBM) was significantly (P < 0.05) decreased (-40%), whereas the diffusional 22Na+ uptake (0.5 min) and the equilibrium (120 min) uptake of 22Na+ were not changed. The inhibition of Na+-H+ exchange after ANF was likely due to alteration of the BBM antiporter itself, in that the H+ conductance of BBMVs was not increased. We conclude that synthetic ANF (a) decreases tubular Na+ reabsorption linked to reabsorption of HCO3 in proximal tubules, and (b) inhibits proximal tubular reabsorption of Pi coupled to Na+ reabsorption, independent of secretion and/or

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Section: Introductionmentioning

confidence: 74%

Section: Resultsmentioning

confidence: 99%

Administration of atrial natriuretic factor inhibits sodium-coupled transport in proximal tubules.

Hammond

Yusufi²,

Knox³

et al. 1985

J. Clin. Invest.

117

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“…Micropuncture studies indicate that ANF exerts its effects in the distal tubules (32,33). ANF does not alter the active sodium ion transport by inhibition of the Na+,K+-ATPase (34)(35)(36) or sodium ion flux in the proximal tubule as measured by Na NMR and tubular oxygen consumption (M. J. Avison, S. Gullans, and R. Shulman, personal communication) or oxygen consumption in kidney slices (34). The LLC-PK1 cells exhibit properties that are consistent with both distal (37)(38)(39), including the medullary portion of the thick ascending limb of the loop of Henle (39), and proximal tubules (26,40,41).…”

Section: Discussionmentioning

confidence: 99%

Specific membrane receptors for atrial natriuretic factor in renal and vascular tissues.

Napier¹,

Vandlen²,

Albers-Schönberg³

et al. 1984

Proc. Natl. Acad. Sci. U.S.A.

230

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Membranes from rabbit aorta and from rabbit and rat kidney cortex possess high-affinity (Kd = 10-10 M) specific binding sites for atrial natriuretic factor (ANF). Similar high-affinity sites are present in an established cell line from pig kidney, LLC-PK,. Results of fractionation studies indicate that the receptors are localized in the plasma membrane of these tissues. The binding is time-dependent and saturable. An excellent quantitative correlation was found between the affinity of synthetic ANF and analogs of intermediate activity to aorta membranes and the half-maximal concentration needed for relaxation of rabbit aorta rings contracted by addition of serotonin. Furthermore, the binding affinity of the receptor in kidney membranes is consistent with the concentration required for in vivo natriuresis in the rat. Biologically inactive synthetic ANF fragments and other peptide hormones such as angiotensin II and vasopressin do not significantly inhibit binding. These data suggest that the receptors for ANF in vascular and renal tissues are responsible for mediating the physiological actions of this peptide in these target tissues.A possible role for the cardiac atria in the regulation of extracellular fluid volume and electrolyte concentration has been shown by the induction of sodium and water excretion in response to changes in intraatrial pressure and stretch of the atrial wall (1). The cardiac atria possess granules that have the appearance of secretory granules (2-4) and whose number can be altered by manipulation of the water-electrolyte balance in experimental animals (5). Crude extracts of atria from several species have been shown to possess potent diuretic and natriuretic activity when given intravenously to rats (6). Subcellular fractionation (7) and immunocytochemistry (8) indicated that these granules are storage sites for an atrial natriuretic factor (ANF). Furthermore, in vitro, atrial extracts were shown to be potent vasorelaxants (9-14). As little as 0.0006 atrial equivalent per milliliter gave 50% relaxation of precontracted aorta tissues (12). In vivo, ANF caused lowering of mean arterial blood pressure in normal and hypertensive animals (6,15,16). Recently, a family of peptides has been isolated from acidic extracts of rat (10,11,(19)(20)(21)(22) and human (23) atria and sequenced independently by several laboratories. From rat atria, the longest peptide that has been reported contains 33 amino acids, 1, and was isolated as the free COOH-terminal tyrosine acid (20,21). Shorter rat ANF peptides are truncated at either the NH2 or COOH terminus.5 10 H-Leu -Ala-Gly-Pro -Arg-Ser -Leu-Arg-Arg-Ser-Ser-15 20Cys-Phe-Gly-Gly-Arg-Ile -Asp-Arg-Ile -Gly-Ala--30Gln -Ser-Gly-Leu-Gly-Cys -Asn-Ser-Phe-Arg-Tyr-OH 1 A peptide consisting of residues 8-33, designated sANF, has been synthesized (21, 24) and shown to possess full biological activity (12,16,21,24). The IC50 of sANF for relaxation of precontracted rabbit aorta rings is 550 pM (12). The amount of sANF required for half-maximal natriuresis wh...

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“…1 " 6 This peptide has a potent natriuretic, diuretic, and direct vasorelaxant action, but the molecular mechanisms of its action have not been well elucidated. The action of ANF seem to be independent of prostaglandins (PGs) 4 ' 5 and Na, + K + -ATPase> 7 Recent studies have focused on the vascular effects of ANF in terms of cyclic nucleotides, especially cyclic guanosine 3',5'-monophosphate (cGMP). 8 " 12 Cyclic nucleotides have been shown to act as mediators for vasorelaxant actions of various compounds and hormones, 13 ' M and the vascular action of ANF has been found to be qualitatively similar to that of sodium nitroprusside (SNP), 15 ' l6 which is thought to relax vascular smooth muscle through cGMP accumulation.…”

mentioning

confidence: 99%

Atrial natriuretic factor and cyclic guanosine 3',5'-monophosphate in vascular smooth muscle.

et al. 1986

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SUMMARY To elucidate the molecular mechanism of the vascular action of atrial natriuretic factor (ANF), we investigated the effects of synthetic ANF and sodium nitroprusside on the levels of intracellular cyclic nucleotides and prostacyclin (measured as its stable metabolite 6-keto-prostaglandin F,a) in cultured vascular smooth muscle cells from rat mesenteric artery and, in some experiments, from rat renal artery. Both ANF and sodium nitroprusside increased intracellular cyclic guanosine 3',5'-monophosphate (cGMP) levels in a dose-dependent manner but did not affect cyclic adenosine 3',5'-monophosphate levels or 6-keto-prostaglandin F, tt synthesis. The stimulatory effects of ANF and sodium nitroprusside on cGMP levels were additive. Neither the deprivation of extracellular Ca

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Failure of Atrial Myocardial Extract to Inhibit Renal Na<sup>+</sup>, K<sup>+</sup>-ATPase

Cited by 23 publications

References 7 publications

Administration of atrial natriuretic factor inhibits sodium-coupled transport in proximal tubules.

Administration of atrial natriuretic factor inhibits sodium-coupled transport in proximal tubules.

Specific membrane receptors for atrial natriuretic factor in renal and vascular tissues.

Atrial natriuretic factor and cyclic guanosine 3',5'-monophosphate in vascular smooth muscle.

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