Atrial natriuretic factor inhibits sodium transport in medullary collecting duct

1986 ◽  
Vol 250 (6) ◽  
pp. F963-F966 ◽  
Author(s):  
H. Sonnenberg ◽  
U. Honrath ◽  
C. K. Chong ◽  
D. R. Wilson
Keyword(s):  
Sodium Transport ◽  
Intravenous Infusion ◽  
Atrial Natriuretic Factor ◽  
Collecting Duct ◽  
Inhibitory Effect ◽  
Sodium Permeability ◽  
Natriuretic Factor ◽  
Tubular Lumen ◽  
Medullary Collecting Duct ◽  
Atrial Natriuretic

Characteristics of sodium transport in the inner medullary collecting duct were determined in anesthetized rats before and during intravenous infusion of synthetic atrial natriuretic factor (atriopeptin II). Infusion of the factor was associated with increased sodium delivery and reduced fractional reabsorption in the duct. Increasing delivery to the same extent by KCl infusion had no effect on fractional reabsorption. The results demonstrate that atrial natriuretic factor has a specific inhibitory effect on net sodium transport in this part of the nephron. The mechanism of this inhibition may involve induction of sodium permeability and consequent backflux into the tubular lumen.

Interaction of amiloride and hydrochlorothiazide with atrial natriuretic factor in the medullary collecting duct

1988 ◽  
Vol 66 (5) ◽  
pp. 648-654 ◽  
Author(s):  
Douglas R. Wilson ◽  
U. Honrath ◽  
H. Sonnenberg
Keyword(s):  
Atrial Natriuretic Factor ◽  
Collecting Duct ◽  
Sodium Reabsorption ◽  
Second Phase ◽  
Potassium Excretion ◽  
Additive Effects ◽  
Natriuretic Factor ◽  
Medullary Collecting Duct ◽  
Atrial Natriuretic

Medullary collecting duct function was studied using the in vivo microcatheterization technique in three groups of rats receiving amiloride, hydrochlorothiazide, or both diuretics. In each group of animals, atrial natriuretic factor (ANF 99–126) was given in the second phase of the experiment. The combination of amiloride and hydrochlorothiazide resulted in a more marked natriuresis than either diuretic given as a single agent. Sodium reabsorption in the medullary collecting duct, as a fraction of the delivered load, was reduced from 64% (amiloride) and 69% (hydrochlorothiazide) to 29% (amiloride and hydrochlorothiazide). Atrial natriuretic factor reduced collecting duct sodium reabsorption when added to amiloride or hydrochlorothiazide to 23% and to 41%, respectively, but had no additional effect when given with amiloride and hydrochlorothiazide. Potassium excretion with amiloride and hydrochlorothiazide was intermediate between amiloride or hydrochlorothiazide given as single agents. With the diuretic combination, potassium transport showed no significant reabsorption or secretion along the medullary collecting duct, amiloride was associated with potassium reabsorption, and hydrochlorothiazide was associated with potassium secretion in the duct. The results confirm the importance of the medullary collecting duct as a site of diuretic action. The known additive effects of amiloride and hydrochlorothiazide on sodium excretion and the opposing effects of these agents on potassium excretion occur, to a major degree, in the medullary collecting duct. Furthermore, the additive effects of amiloride and ANF indicate that blocking of amiloride-sensitive sodium channels is not the only mechanism of action of ANF on duct salt transport in vivo.

Inhibitory effect of atrial natriuretic factor on sympathetic ganglionic neurotransmission in humans

1995 ◽  
Vol 269 (2) ◽  
pp. R406-R412 ◽  
Author(s):  
J. S. Floras
Keyword(s):  
Atrial Natriuretic Factor ◽  
Muscle Sympathetic Nerve Activity ◽  
Acetylcholinesterase Inhibitor ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Inhibitory Effect ◽  
Double Blind Study ◽  
Double Blind ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

I have previously documented an inhibitory effect of atrial natriuretic factor (ANF) on postganglionic muscle sympathetic nerve activity (MSNA) in normal subjects that was consistent with either a central or ganglionic sympathoinhibitory action. To test the latter hypothesis, I examined, in seven young normotensive men, the effect of saline (as vehicle) and ANF (50 micrograms, then 50 ng.kg-1.min-1), given on 2 separate days according to a random double-blind study design, on blood pressure, heart rate, and MSNA before and after ganglionic neurotransmission was stimulated with edrophonium (ED; 12 mg iv), a rapidly reversible acetylcholinesterase inhibitor without central nervous system effects, and during subsequent augmentation of central sympathetic outflow by a cold pressor test (CPT). In five of these subjects, the protocol was replicated during nitroprusside infusion (0.4 micrograms.kg-1.min-1). ED increased MSNA during vehicle (P < 0.005) and nitroprusside (P < 0.003) but not during ANF infusion. The sympathoneural response to the combined stimuli of ED and CPT was also attenuated by ANF compared with either saline or nitroprusside infusions. Conclusions were that 1) postganglionic MSNA is increased by ED, 2) this facilitative effect of ED is attenuated by ANF, and 3) modulation of ganglionic neurotransmission is one mechanism for the relative sympatho-inhibition observed when ANF is infused at this dose.

Mechanisms of hypoxia-induced atrial natriuretic factor release from rat hearts

1989 ◽  
Vol 257 (1) ◽  
pp. H147-H156 ◽  
Author(s):  
R. A. Lew ◽  
A. J. Baertschi
Keyword(s):  
Atrial Natriuretic Factor ◽  
Isolated Heart ◽  
Inhibitory Effect ◽  
Atropine Sulfate ◽  
Base Line ◽  
Adrenergic Stimulation ◽  
Natriuretic Factor ◽  
Rat Hearts ◽  
6 Hydroxydopamine ◽  
Atrial Natriuretic

Potential mechanisms of hypoxia-induced atrial natriuretic factor (ANF) release [A.J. Baertschi, J.M. Adams, and M.P. Sullivan. Am. J. Physiol. 255 (Heart Circ. Physiol. 24): H295-H300, 1988] were investigated in Langendorff-perfused rat hearts. The ANF release was graded with stimulus intensity; 10 min of perfusion with Krebs-Henseleit solution equilibrated with 95, 20, 10, 5, and 0% oxygen led to peak ANF levels of 140 +/- 31 (SE), 202 +/- 20, 407 +/- 76, 659 +/- 119, and 516 +/- 83% of base-line ANF (159 +/- 14 pg/ml), respectively. Hypoxia-induced release of lactate dehydrogenase and creatine kinase did not correlate with ANF release; this finding, along with other experiments, rules out tissue damage as a significant factor. Phentolamine (1.3 microM) and propranolol (0.1 microM) each reduced peak hypoxia-induced (0% O2) ANF release to 333 and 310%, respectively, whereas atropine sulfate (15 microM) had no inhibitory effect. The three antagonists combined reduced the peak hypoxia-induced ANF release to the same extent (307%) as either phentolamine or propranolol alone. Earlier (24 h) catecholamine depletion of rats with 100 mg/kg 6-hydroxydopamine also significantly reduced peak hypoxia-induced ANF release to 330%. Neither the reduction of the ANF secretory responses by these interventions nor the remaining ANF response could be attributed to changes in atrial mechanics. Therefore, these studies demonstrate that alpha- and beta-adrenergic stimulation is responsible for approximately half the hypoxia-induced ANF release from the isolated heart, whereas an as yet undefined mechanism accounts for the remainder of the response.

Attenuation of renal effects of atrial natriuretic factor during rat pregnancy

1995 ◽  
Vol 268 (3) ◽  
pp. F416-F422 ◽  
Author(s):  
S. Omer ◽  
S. Mulay ◽  
P. Cernacek ◽  
D. R. Varma
Keyword(s):  
Atrial Natriuretic Factor ◽  
Collecting Duct ◽  
Sprague Dawley ◽  
Pregnant Rats ◽  
Renal Effects ◽  
Natriuretic Factor ◽  
Sprague Dawley Rats ◽  
Collecting Duct Cells ◽  
Renal Responses ◽  
Atrial Natriuretic

The influence of pregnancy on renal responses to atrial natriuretic factor (ANF) was determined in urethane-anesthetized Sprague-Dawley rats. Infusions of ANF caused a significantly greater increase in urinary excretion of fluid, sodium, and potassium in virgin than in pregnant (13-15 days and 21 days) rats. Guanosine 3',5'-cyclic monophosphate (cGMP) excretion, mean arterial pressure, plasma immunoreactive ANF, and glomerular filtration rate (GFR) following ANF infusions were not different in virgin and gravid rats, although increments in GFR over basal were greater in virgin than in gravid animals. Renal responses to ANF normalized during postpartum and were attenuated by progesterone treatment of virgin rats. Natriuretic effects of infusions of ANF plus ANF-(4-23) (a ligand for clearance receptors) or of ANF plus thiorphan (an endopeptidase inhibitor) in virgin and pregnant rats did not differ; ANF-(4--23) and thiorphan alone caused greater natriuresis in pregnant than in virgin rats. Effects of ANF on cGMP production by collecting duct cells isolated from virgin and pregnant rats did not differ. We concluded that the attenuation in the renal effects of ANF during pregnancy might be mediated by progesterone by an increase in the intrarenal metabolism of ANF and might reflect physiological adjustment to facilitate fluid/electrolyte expansion.

Dietary Salt Extremes and Renal Function in Rats: Effect of Atrial Natriuretic Factor

1994 ◽  
Vol 87 (5) ◽  
pp. 525-531 ◽  
Author(s):  
U. Honrath ◽  
C. K. Chong ◽  
D. R. Wilson ◽  
H. Sonnenberg
Keyword(s):  
Atrial Natriuretic Factor ◽  
Collecting Duct ◽  
Tubular Reabsorption ◽  
Kidney Weight ◽  
Salt Diet ◽  
Group Iii ◽  
Natriuretic Factor ◽  
Group Ii ◽  
Group 1 ◽  
Atrial Natriuretic

1. Chronic reduction of salt intake can reduce the natriuretic effect of exogenously administered atrial natriuretic factor. The purpose of this study was to elucidate the intrarenal site(s) of such atrial natriuretic factor resistance. Renal clearance and collecting duct microcatheterization experiments were made before and during infusion of atrial natriuretic factor in three groups of rats: group 1 consisted of rats fed a high salt diet (8% NaCl) for 1 week before the experiment; group II were fed a low salt diet (< 0.008%); group III received the same low salt diet, but were acutely replenished with salt at the time of experiment. 2. Baseline sodium chloride excretion was 6480 ± 810 nmol min−1g−1 kidney weight in group 1 compared to 99 ± 16 in group 1. Fractional re-absorptions in the medullary collecting duct were 37 ± 6% and 95 ± 2% of delivered load, respectively (P < 0.05). The fractions of filtered sodium remaining at the beginning of the medullary duct were 6.6 ± 1.0% of filtered load in group 1 and 2.7 ± 0.7% in group II (P < 0.05), indicating increased tubular reabsorption in group II, not only in the medullary duct, but also in upstream nephron segments. 3. During infusion of atrial natriuretic factor, marked saluresis (13240 ± 750 nmol min−1 g−1 kidney weight), together with decreased fractional reabsorption at both sites (duct, −13 ± 9%; upstream remainder, 7.9 ± 0.7%; P < 0.05 each, compared to corresponding control values) was found in group 1, whereas the excretory (150 ± 28 nmol min−1 g−1 kidney weight), and the tubular transport (duct = 84 ± 3%; upstream remainder =2.2 ± 0.4%) changes were quantitatively insignificant in group II. Glomerular filtration rate was increased in group 1 from 1.07 ± 0.03 to 1.26 ± 0.04 ml min−1g−1 kidney weight (P < 0.05), but not in group II (0.93 ± 0.07 to 0.96 ± 0.09, not significant). 4. In group III, acute salt replenishment was associated with increased excretion (1940 ± 440 nmol mm−1 g−1 kidney weight, P < 0.05 compared to group II) and with reduction of tubular reabsorption in the collecting duct only (69 ± 8%, P < 0.05). Infusion of atrial natriuretic factor in this group further increased natriuresis (7810 ± 780 nmol min−1 g−1 kidney weight) and decreased tubular reabsorption in the duct (−32 ± 22%, P < 0.05 compared to the corresponding control value). 5. We conclude that chronic salt deprivation can effectively prevent, via a rapidly reversible counter-regulatory mechanism, the expected actions of atrial natriuretic factor on sodium reabsorption in the medullary collecting duct. Operation of such a mechanism may explain salt retention despite elevated endogenous levels of atrial natriuretic factor in pathological states such as congestive heart failure and liver cirrhosis.

Centrally administered atrial natriuretic factor increases renal water excretion

1987 ◽  
Vol 252 (6) ◽  
pp. F1011-F1015 ◽  
Author(s):  
J. Lee ◽  
J. Q. Feng ◽  
R. L. Malvin ◽  
B. S. Huang ◽  
R. J. Grekin
Keyword(s):  
Intravenous Infusion ◽  
Atrial Natriuretic Factor ◽  
Renal Plasma Flow ◽  
Plasma Concentrations ◽  
Urine Volume ◽  
Free Water ◽  
Water Excretion ◽  
Arterial Blood ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The effects of intracerebroventricular (ICV) infusion of atrial natriuretic factor (ANF; atriopeptin III) on renal function, plasma concentrations of antidiurectic hormone, aldosterone, and plasma renin activity (PRA) were examined in anesthetized rats and sodium-depleted conscious sheep. The results were compared with those obtained by intravenous infusion of the same dose of ANF. In both rats and sheep, urine volume was increased four- to sixfold over basal values by ICV infusion of ANF. The response was not associated with increased excretion of sodium or potassium. However, urine osmolality was decreased, and free water clearance increased. Intravenous infusion of the same dose of ANF was without effect. Neither mean arterial blood pressure nor heart rate was changed by the ICV infusion of ANF. In the sheep, renal plasma flow showed no significant changes and glomerular filtration rate was unaltered with the exception of a single experimental period out of four periods of ICV ANF infusion. Plasma concentration of ADH was decreased and PRA increased, whereas aldosterone levels remained unchanged as a function of ICV ANF. In the rat, the diuretic response to ANF was prevented by continuous intravenous infusion of a subpressor dose of ADH. These results suggest that ANF within the central nervous system inhibits secretion of ADH.

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