Effect of rat cardionatrin I (rat ANF 99–126) on the response of toad skin to angiotensin II

1989 ◽  
Vol 67 (4) ◽  
pp. 362-365 ◽  
Author(s):  
Alfredo Coviello ◽  
Marcelo O. Soria ◽  
Maria C. Proto ◽  
Dora M. Berman ◽  
Silvia S. Gamundi ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Factor ◽  
Epithelial Transport ◽  
Short Circuit ◽  
Extracellular Fluid ◽  
Short Circuit Current ◽  
Osmotic Water Permeability ◽  
Toad Skin ◽  
Osmotic Water ◽  
Atrial Natriuretic

The atrial natriuretic peptide cardionatrin I (cardionatrin I is ANF 99–126) was used in studies directed to assess its effects on osmotic water permeability (Posm) and short-circuit current (SCC) in isolated toad skin. Results showed that ANF 99–126 (10−7 M) added to the dermal side of the skin had no effect on basal Posm or SCC. However, ANF 99–126 (3.3 × 10−8 M) was able to produce a 50% reversible inhibition of the maximal Posm response to angiotensin II (AH) (3.2 × 10−8 M). These effects were seen when the skins were preincubated with ANF 99–126 for 10 min or less before the addition of AII Longer preincubation appeared to inactivate ANF 99–126 through proteolysis. ANF 99–126 (10−7 M) failed to inhibit the SCC response to AII (10−5 M) in toad skin. These results are compatible with a modulatory function for ANF on several systems including those involved in the regulation of extracellular fluid volume.Key words: atrial natriuretic factor, natriuretic peptides, epithelial transport.

Effects of high potassium concentration on theophylline responses of toad bladder

1977 ◽  
Vol 232 (2) ◽  
pp. F173-F177
Author(s):  
S. A. Mendoza ◽  
K. K. Nakamoto
Keyword(s):  
Cyclic Amp ◽  
Water Permeability ◽  
Potassium Concentration ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Toad Bladder ◽  
Osmotic Water Permeability ◽  
High Potassium ◽  
Bathing Medium ◽  
Osmotic Water

It has been demonstrated previously that a high concentration of potassium in the serosal bathing medium (5–21.5 mM) potentiates the increase in short-circuit current caused by vasopressin or exogenous cyclic AMP. The same concentration of potassium in the bathing medium inhibited the increase in short-circuit current caused by theophylline. The increases in osmotic water permeability caused by vasopressin or cyclic AMP were unaffected by a serosal potassium concentration of 21.5 mM. The increase in osmotic water permeability caused by theophylline was inhibited by 21.5 mM potassium. The concentration of cyclic AMP in either intact total bladder or isolated toad bladder cells was increased two- or three-fold by theophylline. Increasing the concentration of potassium to 21.5 mM did not alter cyclic AMP concentration in either the absence of presence of theophylline. One interpretation of these results is that theophylline increases osmotic water flow and short-circuit current by a mechanism other than by inhibition of cyclic nucleotide phosphodiesterase.

Atrial natriuretic factor inhibits Na-K-Cl cotransport in teleost intestine

1985 ◽  
Vol 249 (5) ◽  
pp. C531-C534 ◽  
Author(s):  
S. M. O'Grady ◽  
M. Field ◽  
N. T. Nash ◽  
M. C. Rao
Keyword(s):  
Atrial Natriuretic Factor ◽  
Brush Border Membrane ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Marine Teleost ◽  
Pseudopleuronectes Americanus ◽  
Lower Salinity ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Addition of atrial natriuretic factor (ANF) to the contraluminal side of the intestinal mucosa of a marine teleost, the winter flounder Pseudopleuronectes americanus, inhibits short-circuit current, net transepithelial fluxes of Na and Cl, and the unidirectional influx of Rb across the brush border membrane. This action of ANF is closely mimicked by addition of 8-bromo-guanosine 3',5'-cyclic monophosphate (8-BrcGMP). In contrast to the intestine, the opercular epithelium of the flounder did not respond to the in vitro addition of either ANF or 8-BrcGMP. Because intestinal salt and water absorption diminishes when marine fish enter water of lower salinity, ANF may be an important hormonal regulator through which euryhaline fish adapt to varying salinities.

Control of atrial natriuretic factor release in conscious dogs

1986 ◽  
Vol 251 (5) ◽  
pp. R947-R956 ◽  
Author(s):  
K. M. Verburg ◽  
R. H. Freeman ◽  
J. O. Davis ◽  
D. Villarreal ◽  
R. C. Vari
Keyword(s):  
Sodium Excretion ◽  
Atrial Natriuretic Factor ◽  
Isotonic Saline ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Conscious Dogs ◽  
Base Line ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The aim of this study was to examine the changes in the concentration of plasma immunoreactive atrial natriuretic factor (iANF) that occur in response to expansion or depletion of the extracellular fluid volume in conscious dogs. The plasma iANF concentration was also measured postprandially after the ingestion of a meal containing 125 meq of sodium. Postprandial plasma iANF increased 45% (P less than 0.05) above the base-line concentration, and this increase was accompanied by a brisk natriuresis. After a low-sodium meal, however, plasma iANF and sodium excretion failed to increase. The plasma iANF concentration increased from 57 +/- 5 to 139 +/- 36 pg/ml (P less than 0.05) immediately after volume expansion with intravenous isotonic saline infusion (2.5% body wt) administered over a 30-min period; plasma iANF remained elevated at 90 +/- 14 pg/ml (P less than 0.05) for an additional 30 min before returning toward preinfusion levels. Plasma iANF decreased 45% from 78 +/- 17 to 43 +/- 7 pg/ml (P less than 0.05) in response to the administration of ethacrynic acid (2.0 mg/kg, iv bolus) that produced an estimated 15% depletion of intravascular volume. In additional experiments the infusion of synthetic alpha-human ANF at 100 and 300 ng X kg-1 X min-1 increased (P less than 0.05) both the plasma iANF concentration and the urinary excretion of iANF. This study demonstrates that the secretion of ANF is consistently influenced by changes in the extracellular fluid volume. Furthermore, the results support the concept that ANF functions to increase postprandial sodium excretion following the ingestion of a high-sodium meal.

Atrial Natriuretic Factor and Angiotensin Ii Stimulate Nitric Oxide Release from Human Proximal Tubular Cells

1995 ◽  
Vol 89 (5) ◽  
pp. 527-531 ◽  
Author(s):  
J. S. McLay ◽  
P. K. Chatterjee ◽  
S. K. Mistry ◽  
R. P. Weerakody ◽  
A. G. Jardine ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Atrial Natriuretic Factor ◽  
Nitric Oxide Production ◽  
Proximal Tubular Cells ◽  
Tubular Cells ◽  
Oxide Production ◽  
Natriuretic Factor ◽  
Proximal Tubular ◽  
Atrial Natriuretic

1. It has been recently reported that angiotensin II can enhance atrial natriuretic factor-stimulated cyclic GMP release from brain capillary endothelial cells and stimulate directly the release of cyclic GMP by Neuro 2a cells. A possible mechanism mediating such cyclic GMP release could be via the production of nitric oxide and the resultant stimulation of soluble guanylate cyclase. 2. The ability of angiotensin II, atrial natriuretic factor and c(4–23) atrial natriuretic factor to stimulate nitric oxide production was investigated in primary cultures of human proximal tubular cells. 3. Freshly prepared human proximal tubular cells were seeded onto 6-well plates and allowed to reach confluence. Cells were then incubated with incremental concentrations of either angiotensin II, atrial natriuretic factor or c(4–23) atrial natriuretic factor alone for 1, 4, 12 or 24 h or in the presence of the nitric oxide synthase inhibitor NG-monomethyl-l-arginine. Angiotensin II was also incubated with human proximal tubular cells in the presence of the AT, and AT2 receptor antagonists DuP 753 and PD 123319. 4. Incubation of human proximal tubular cells with angiotensin II, atrial natriuretic factor or c(4–23) atrial natriuretic factor produced a dose- and time-dependent increase in nitric oxide production, which was inhibited in the presence of NG-monomethyl-l-arginine. A similar increase in nitric oxide production was observed after incubation with atrial natriuretic factor or c(4–23) atrial natriuretic factor. 5. The angiotensin-induced increase in nitric oxide production was not inhibited in the presence of either the angiotensin AT1 or AT2 receptor antagonists DuP 753 or PD 123319. 6. This study demonstrates that primary cultures of human proximal tubular cells can be stimulated to produce nitric oxide by both atrial natriuretic factor and angiotensin II. Furthermore, the atrial natriuretic factor-induced response appears to be mediated via the atrial natriuretic factor-C receptor, while the angiotensin II-induced response appears to be mediated by a novel, as yet unidentified, angiotensin II receptor.

scholarly journals Site-1 Protease-Derived Soluble (Pro)Renin Receptor Contributes to Angiotensin II–Induced Hypertension in Mice

Hypertension ◽  
2020 ◽  
Author(s):  
Ye Feng ◽  
Kexin Peng ◽  
Renfei Luo ◽  
Fei Wang ◽  
Tianxin Yang
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Collecting Duct ◽  
Short Circuit ◽  
Ussing Chamber ◽  
Short Circuit Current ◽  
Duct Cell ◽  
Ang Ii ◽  
Cortical Collecting Duct ◽  
Induced Hypertension

Activation of PRR ([pro]renin receptor) contributes to enhancement of intrarenal RAS and renal medullary α-ENaC and thus elevated blood pressure during Ang II (angiotensin II) infusion. The goal of the present study was to test whether such action of PRR was mediated by sPRR (soluble PRR), generated by S1P (site-1 protease), a newly identified PRR cleavage protease. F1 B6129SF1/J mice were infused for 6 days with control or Ang II at 300 ng/kg per day alone or in combination with S1P inhibitor PF-429242 (PF), and blood pressure was monitored by radiotelemetry. S1P inhibition significantly attenuated Ang II–induced hypertension accompanied with suppressed urinary and renal medullary renin levels and expression of renal medullary but not renal cortical α-ENaC expression. The effects of S1P inhibition were all reversed by supplement with histidine-tagged sPRR termed as sPRR-His. Ussing chamber technique was performed to determine amiloride-sensitive short-circuit current, an index of ENaC activity in confluent mouse cortical collecting duct cell line cells exposed for 24 hours to Ang II, Ang II + PF, or Ang II + PF + sPRR-His. Ang II–induced ENaC activity was blocked by PF, which was reversed by sPRR-His. Together, these results support that S1P-derived sPRR mediates Ang II–induced hypertension through enhancement of intrarenal renin level and activation of ENaC.

Apical nonspecific cation conductances in rabbit cecum

1994 ◽  
Vol 266 (3) ◽  
pp. G475-G484 ◽  
Author(s):  
J. H. Sellin ◽  
W. P. Dubinsky
Keyword(s):  
Epithelial Transport ◽  
Apical Membrane ◽  
Divalent Cations ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Na Channel ◽  
Similar Response ◽  
Electrogenic Transport

Rabbit cecum exhibits electrogenic Na absorption in vitro. However, because this transport process is not inhibited by amiloride nor does it demonstrate saturation kinetics typical of the amiloride-inhibitable Na channel, we considered whether the cecal transporter represented one of a recently described family of nonselective cation conductances or channels (NSCC). Both transepithelial and vesicle studies demonstrated that K, Cs, and Rb were transported via an apical conductance. Electrogenic transport was inhibited by divalent cations including Ca, Mg, and Ba but was unaffected by either lanthanum or gadolinium. Parallel studies in distal colon did not exhibit a similar response to either K substitution or Ba inhibition. Phenamil, verapamil, and nicardipine significantly inhibited the short-circuit current (Isc). stimulated by nominal Ca- and Mg-free conditions. Flux studies demonstrated a correlation between changes in Isc and Na transport. Microelectrode impalement studies suggested that there may be both NSCC and K conductance in the apical membrane. Planar bilayer studies identified a 190-pS cation channel that may correlate with the macroscopic transport properties of this epithelium. These studies are consistent with a model of cecal Na absorption mediated by a NSCC in the apical membrane; this may be the mechanism underlying the distinct epithelial transport characteristics of this intestinal segment.

Transport properties of toad kidney epithelia in culture

1981 ◽  
Vol 241 (3) ◽  
pp. C154-C159 ◽  
Author(s):  
F. M. Perkins ◽  
J. S. Handler
Keyword(s):  
Electrical Resistance ◽  
Hormonal Regulation ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Transepithelial Electrical Resistance ◽  
Apical Surface ◽  
Osmotic Water ◽  
Sodium Flux ◽  
Regulation Of Transport ◽  
Osmotic Water Flow

The characteristics of a continuous line of toad kidney epithelial cells (A6) are described. These cells form a monolayer epithelium of high transepithelial electrical resistance (about 5,000 omega . cm2). The cells generate a transepithelial potential difference (apical surface negative) of about 9 mV. The short-circuit current is equivalent to net sodium flux. Net sodium flux is stimulated by aldosterone and by analogues of cAMP. The stimulation is readily reversible. Neither urea permeability nor osmotic water flow is altered by analogues of cAMP. Amiloride eliminates 90% of the short-circuit current. Thus A6 cells form an epithelium with several differentiated properties including hormonal regulation of transport.

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