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Query: UNIPROT:P41181 (collecting duct)
 5,183 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In vivo microcatheterization of the medullary collecting duct of rat kidney was used to compare the functional effects of intravenous infusion of rat atrial natriuretic factor, human urodilatin (a peptide produced in the kidney), or porcine brain natriuretic peptide. All three peptides resulted in striking and quantitatively similar inhibition of NaCl and water reabsorption in the duct. In addition, all three induced significant K+ secretion in this part of the nephron. These results could not be explained by functional alterations in upstream tubular segments. We conclude that the three peptides are equivalent in their transport effects on the inner medullary collecting duct system, when administered at the same (presumably supramaximal) dose.
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PMID:Endogenous natriuretic peptides: effect on collecting duct function in rat kidney. 214 99

In addition to the well-documented stretch-induced secretion of atrial natriuretic factor (ANF), we have shown that addition of agonists such as vasopressin or angiotensin, added to incubation medium with freshly excised rat atria, caused marked release of the hormone in vitro. Others have had difficulty in reproducing these results. In experiments designed to address this problem we found that removal of the atrial endothelium was necessary to demonstrate agonist-induced release of ANF. The results suggest that the endothelial lining of atrial tissue may limit access of the agonists to the myocytes, and thereby play a modulating role in receptor-stimulated secretion of the hormone. The renal mechanism of action of ANF includes inhibition of Na transport in the medullary collecting duct (MCD). Recent in vitro studies have suggested that this inhibition occurs via blockade of amiloride-sensitive Na channels. However, ANF-induced reduction of MCD transport in vivo is much greater than that obtainable with amiloride. Although, by luminal administration of ANF in vivo, we were able to confirm an amiloride-like action of the hormone at this site, we could not thereby mimic the effects of systemic ANF on MCD Na reabsorption. The results thus indicate that a peritubular effect is an important determinant of ANF natriuresis.
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PMID:Mechanisms of release and renal action of atrial natriuretic factor. 214 25

The inner medullary collecting duct (IMCD) is thought to be a major target site for atrial natriuretic factor (ANF) action. The IMCD is divided into two subsegments (IMCD1, outer third; and IMCD2,3, inner two-thirds) based on differences in urea and water permeability. IMCD1 has similar characteristics to the outer medullary collecting duct (OMCD). To elucidate whether there are any differences among these segments in ANF actions, we investigated the effects of ANF on guanosine 3',5'-cyclic monophosphate (cGMP) synthesis in IMCD subsegments and the OMCD. We also examined the effects of arginine vasopressin (AVP) on adenosine 3',5'-cyclic monophosphate (cAMP) synthesis. IMCD subsegments (IMCD1,2,3) and OMCD were microdissected; and ANF-stimulated cGMP synthesis and AVP-stimulated cAMP synthesis were measured. cGMP synthesis stimulated by 10(-6) M ANF in IMCD1,2,3 (0.78 +/- 0.15, 0.81 +/- 0.19, 0.62 +/- 0.10 fmol.mm-1 x 3 min-1, mean +/- SE respectively, n = 10-11) was significantly (greater than 20-fold) higher than that in OMCD (0.03 +/- 0.02 fmol.mm-1 x 3 min-1, n = 7), and there was no difference among IMCD subsegments. On the other hand, cAMP synthesis stimulated by 10(-7) M AVP in IMCD subsegments was similar to that in OMCD. We conclude that IMCD is homogenous as a target site of ANF and is clearly distinguished from OMCD. In addition, more than half of ANF-stimulated cGMP synthesis in IMCD are considered to occur in IMCD1, simply because IMCD1 is dominant in population among IMCD subsegments. As target sites of AVP, IMCD subsegments are similar to OMCD.
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PMID:Effects of ANF on cGMP synthesis in inner medullary collecting duct subsegments of rats. 216 80

The greater than 40-fold range of voluntary salt intake in humans requires corresponding adjustments in renal excretion to maintain balance. Although many mechanisms have been implicated in the regulation of salt output by the kidney, surprisingly little consideration has been given to their quantitative significance and possible interaction. This survey summarizes the effects of changes in glomerular filtration rate, proximal peritubular physical factors, and plasma concentrations of aldosterone and atrial natriuretic factor (ANF), singly and in combination, on the level of salt excretion. Contrary to expectation, even large increases in filtration or decreases in proximal reabsorption have only minor natriuretic effects, due to constancy of fractional reabsorption in downstream nephron segments. Lack of aldosterone release increases salt excretion as much or more than the upstream mechanisms, whereas ANF-induced inhibition of reabsorption in the medullary collecting duct has the largest effect. It may be concluded, therefore, that the potency of these natriuretic factors increases with distance along the nephron, even though each is operating on a progressively small tubular load. However, none of the mechanisms, in isolation, is sufficient to explain salt balance over the range of voluntary intake. Combination of factors demonstrates synergism rather than simple additivity, resulting in more than enough reserve capacity for salt excretion.
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PMID:Renal regulation of salt balance: a primer for non-purists. 220 3

Atrial natriuretic factor (ANF) is a peptide hormone that causes a large increase in urinary sodium chloride and water excretion when its plasma concentration rises above basal levels. As yet, there is no consensus regarding the chief site of action of ANF in the kidney. We microdissected and perfused rat cortical collecting ducts in vitro to determine whether ANF-(1-28) can directly inhibit net sodium and fluid absorption. ANF decreased both net sodium absorption and vasopressin-stimulated net fluid absorption by 50-90% when added to the peritubular bath solution. Approximately 50% inhibition of net fluid absorption occurred at 0.1 nM ANF, a level equivalent to plasma concentrations in volume-expanded rats. The action of ANF was mimicked by the addition of exogenous guanosine 3',5'-cyclic monophosphate. If ANF has a similar action on the cortical collecting duct in vivo, it could account for a substantial part of the ANF-mediated increase in urinary sodium and water excretion.
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PMID:ANF inhibits NaCl and fluid absorption in cortical collecting duct of rat kidney. 252 30

Atrial natriuretic factor (ANF) is a peptide hormone that increases renal NaCl and water excretion. Several renal sites of ANF action have been identified, but general agreement has not been reached concerning the quantitative contribution of each action to the natriuresis and diuresis. Using a five-nephron central core model of NaCl, urea, KCl, and water transport in the rat kidney, we have quantitatively evaluated the hypothetical effects on whole kidney function of three experimentally observed ANF actions: 1) inhibition of active NaCl absorption in the collecting duct, 2) inhibition of osmotic water permeability in the collecting duct, and 3) increased NaCl and water delivery out of the proximal convoluted tubule simulating an increase in glomerular filtration rate. The simulations show that inhibition of collecting duct active NaCl absorption by greater than or equal to 50% can increase NaCl and water excretion to levels that match experimental values. In addition, the model predicted that the urinary sodium concentration will increase to greater than plasma levels as observed experimentally. Simulated decreases in collecting duct water permeability predicted an increase in water excretion with little change in NaCl excretion. Simulated 2.5-5% increases in glomerular filtration rate also increased simulated NaCl and water excretion rates to experimentally observed levels in response to ANF. However, this action was less effective than inhibition of collecting duct active NaCl absorption in increasing the urinary NaCl concentration. We conclude that a combination of several actions are likely to account for the overall renal effect of ANF.
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PMID:Renal actions of atrial natriuretic factor: a mathematical modeling study. 253 76

The hypotensive, natriuretic, and diuretic actions of human atrial natriuretic factor-(99-126) (hANF) are accompanied by an elevation of cyclic guanosine monophosphate (cGMP) in plasma and urine. However, the oxidized hANF analogue, human [Met-O110]ANF-(99-126) (Met-O-ANF), has been reported to be unable to increase cGMP (Biochem. Biophys. Res. Commun. 128: 538-546). We employed this oxidized peptide to evaluate the relationship between its biological effects and cGMP generation, with cGMP serving as a marker of the recognized property of ANF to stimulate particulate guanylate cyclase. Met-O-ANF appeared to be a partial agonist, exhibiting a decreasing order of relative potency of hypotensive, vasorelaxant, diuretic, and natriuretic functions compared to hANF. A lower degree of cGMP increases was achieved by this analogue in cultured smooth muscle and endothelial cells. Met-O-ANF doses, which led to a significant increase in diuresis, were neither natriuretic nor accompanied by an increase of urinary cGMP. We were thus able to dissociate the diuretic and natriuretic effects of ANF. High doses of the oxidized analogue were required to elevate cGMP levels in plasma and urine. In isolated kidney fractions, Met-O-ANF's action on cGMP was significantly lower in glomeruli (fivefold less), virtually absent in the collecting duct, yet only slightly different (20% less) in thick ascending limb. Our results indicate that the diuretic and natriuretic effects are exerted at distinct sites, with only the natriuresis being related to an increase of extracellular cGMP. The variability of differential potency of biological and biochemical effects from tissue to tissue of these two forms of human ANF support the notion of the heterogeneity of the ANF effector system.
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PMID:Dissociation of natriuresis and diuresis and heterogeneity of the effector system of atrial natriuretic factor in rats. 253 99

The inner medullary collecting duct (IMCD) has been proposed to be a site of atrial natriuretic factor (ANF) action. We carried out experiments in isolated perfused terminal IMCDs to determine whether ANF (rat ANF 1-28) affects either osmotic water permeability (Pf) or urea permeability. In the presence of a submaximally stimulating concentration of vasopressin (10(-11) M), ANF (100 nM) significantly reduced Pf by an average of 46%. Lower concentrations of ANF also significantly inhibited vasopressin-stimulated Pf by the following percentages: 0.01 nM ANF, 18%; 0.1 nM, 46%; 1 nM, 48%. Addition of exogenous cyclic GMP (0.1 mM) mimicked the effect of ANF, decreasing Pf by an average of 48%. ANF also inhibited cyclic AMP-stimulated Pf by an average of 31%. ANF did not affect urea permeability, nor did it alter vasopressin-stimulated cyclic AMP accumulation. We conclude that ANF at physiological concentrations causes a large inhibition of vasopressin-stimulated Pf in the rat terminal IMCD, and that cyclic GMP is the second messenger mediating the effect. ANF appears to act at a site distal to cyclic AMP generation in the chain of events linking vasopressin receptor binding to an increase in osmotic water permeability.
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PMID:Atrial natriuretic factor inhibits vasopressin-stimulated osmotic water permeability in rat inner medullary collecting duct. 284 55

We have demonstrated previously that atrial natriuretic factor (ANF) augments urinary, plasma and kidney cGMP levels but has no significant effect upon cAMP. Using cGMP as a marker, we searched for specific target sites involved in the action of ANF in the dog kidney, and observed no change of cGMP in the proximal tubules, a 2-fold increase over basal levels in the thick loop of Henle and a 3-fold elevation in the collecting duct. The most striking action on cGMP occurred in the glomeruli with a rise of up to 50-fold being evident at 1-2 min. after the addition of ANF. The results obtained in the absence or presence of a phosphodiesterase inhibitor support the notion that the effects of ANF were exerted at the level of guanylate cyclase stimulation rather than cGMP phosphodiesterase inhibition. The action of sodium nitroprusside (SNP), a direct stimulator of soluble guanylate cyclase, differed from that of ANF. The ability of the factor to enhance cGMP levels was correlated with the distribution of particulate guanylate cyclase. This study identifies the glomeruli and the distal part of the nephron as specific targets of ANF and implicates particulate guanylate cyclase as the enzyme targetted for the expression of its action.
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PMID:The increase of cGMP by atrial natriuretic factor correlates with the distribution of particulate guanylate cyclase. 285 57

A family of biologically active peptides (atrial natriuretic factor - ANF) has recently been identified in mammalian heart atria. The peptides derive from a common 152 amino acid precursor and at least 1% of total messenger RNA activity is specific for the factor. When injected intravenously ANF is hypotensive and natriuretic. Data indicate that atrial natriuretic factor represents a newly discovered hormone involved in the regulation of blood pressure and volume. Cellular release of ANF does not require the activation of the adenylate cyclase system, but is associated with receptor-mediated activation of the cellular polyphosphoinositide mechanism. The natriuretic effect includes increased glomerular filtration rate and specific inhibition of normal sodium reabsorption from the medullary collecting duct. The mechanism of this transport inhibition is not yet known.
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PMID:Atrial natriuretic factor--a new hormone affecting kidney function. 293


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