Role of plasma ANG II in the excretion of acute sodium load in a bird with salt glands (Anas platyrhynchos)

2001 ◽  
Vol 281 (1) ◽  
pp. R346-R351 ◽  
Author(s):  
Myriam K. Heinz ◽  
David A. Gray
Keyword(s):  
Intravenous Infusion ◽  
Sodium Excretion ◽  
Isotonic Saline ◽  
Salt Gland ◽  
Pekin Duck ◽  
Ang Ii ◽  
Salt Glands ◽  
Sodium Load ◽  
Total Sodium

This study was designed to further examine the role of plasma ANG II in the excretion of sodium in the Pekin duck, a bird with salt glands. Renal and extrarenal (salt gland) excretion of an intravenously administered isotonic saline load was monitored over a 4-h period in a group of eight birds under two conditions: the control condition, in which isotonic saline infusion decreased endogenous plasma ANG II from 102.6 to 16.5 pg/ml, and the experimental condition, in which ANG II suppression was prevented by intravenous infusion of a 3.5 ng · kg−1 · min−1 dose of synthetic ANG II. ANG II infusion significantly decreased the total sodium excretion (by 15%), primarily via an inhibition of salt gland output. The results suggest that ANG II suppression facilitates the excretion of an administered sodium load in birds with salt glands.

Mechanisms of angiotensin II natriuresis and antinatriuresis

1985 ◽  
Vol 249 (2) ◽  
pp. F299-F307 ◽  
Author(s):  
M. E. Olsen ◽  
J. E. Hall ◽  
J. P. Montani ◽  
A. C. Guyton ◽  
H. G. Langford ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Sodium Excretion ◽  
Distal Tubule ◽  
Urinary Sodium Excretion ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Sodium Load ◽  
Proximal Tubular ◽  
Anesthetized Dogs

The aim of this study was to determine the role of changes in renal arterial pressure (RAP), renal hemodynamics, and tubular reabsorption in mediating the natriuretic and antinatriuretic actions of angiotensin II (ANG II). In seven anesthetized dogs, endogenous ANG II formation was blocked with captopril, and ANG II was infused intravenously at rates of 5-1,215 ng X kg-1 X min-1 while RAP was either servo-controlled at the preinfusion level or permitted to increase. When RAP was servo-controlled, ANG II infusion at all rates from 5-1,215 ng X kg-1 X min-1 decreased urinary sodium excretion (UNaV) and fractional sodium excretion (FENa) while increasing fractional reabsorption of lithium (FRLi) (an index of proximal tubular fractional sodium reabsorption) and causing no change in calculated distal tubule fractional sodium reabsorption (FRDNa). When RAP was permitted to increase, ANG II infusion rates up to 45 ng X kg-1. min-1 also decreased UNaV and FENa while increasing FRLi and causing no change in FRDNa. However, at 135 ng X kg-1 X min-1 and above, UNaV and FENa increased while FRLi and FRDNa decreased when RAP was allowed to rise, even though renal blood flow and filtration fraction were not substantially different from the values observed when RAP was servo-controlled. Filtered sodium load was slightly higher when RAP was permitted to increase during ANG II infusion compared with when RAP was servo-controlled, although the differences were not statistically significant. Thus, even very large doses of ANG II cause antinatriuresis when RAP is prevented from increasing.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of 20-hydroxyeicosatetraenoic acid in the renal and vasoconstrictor actions of angiotensin II

2002 ◽  
Vol 283 (1) ◽  
pp. R60-R68 ◽  
Author(s):  
Magdalena Alonso-Galicia ◽  
Kristopher G. Maier ◽  
Andrew S. Greene ◽  
Allen W. Cowley ◽  
Richard J. Roman
Keyword(s):  
Urinary Excretion ◽  
Intravenous Infusion ◽  
Pressor Response ◽  
Maximal Response ◽  
Epoxyeicosatrienoic Acids ◽  
Ang Ii ◽  
Hydroxyeicosatetraenoic Acid ◽  
Peripheral Vasculature ◽  
Oxide Synthase

The present study examined the effects of ANG II on the renal synthesis of 20-hydroxyeicosatetraenoic acid (20-HETE) and its contribution to the renal vasoconstrictor and the acute and chronic pressor effects of ANG II in rats. ANG II (10−11 to 10−7mol/l) reduced the diameter of renal interlobular arteries treated with inhibitors of nitric oxide synthase and cyclooxygenase, lipoxygenase, and epoxygenase by 81 ± 8%. Subsequent blockade of the synthesis of 20-HETE with 17-octadecynoic acid (1 μmol/l) increased the ED50 for ANG II-induced constriction by a factor of 15 and diminished the maximal response by 61%. Graded intravenous infusion of ANG II (5–200 ng/min) dose dependently increased mean arterial pressure (MAP) in thiobutylbarbitol-anesthetized rats by 35 mmHg. Acute blockade of the formation of 20-HETE with dibromododecenyl methylsulfimide (DDMS; 10 mg/kg) attenuated the pressor response to ANG II by 40%. An intravenous infusion of ANG II (50 ng · kg−1 · min−1) in rats for 5 days increased the formation of 20-HETE and epoxyeicosatrienoic acids (EETs) in renal cortical microsomes by 60 and 400%, respectively, and increased MAP by 78 mmHg. Chronic blockade of the synthesis of 20-HETE with intravenous infusion of DDMS (1 mg · kg−1 · h−1) or EETs and 20-HETE with 1-aminobenzotriazole (ABT; 2.2 mg · kg−1 · h−1) attenuated the ANG II-induced rise in MAP by 40%. Control urinary excretion of 20-HETE averaged 350 ± 23 ng/day and increased to 1,020 ± 105 ng/day in rats infused with ANG II (50 ng · kg−1 · min−1) for 5 days. In contrast, urinary excretion of 20-HETE only rose to 400 ± 40 and 600 ± 25 ng/day in rats chronically treated with ANG II and ABT or DDMS respectively. These results suggest that acute and chronic elevations in circulating ANG II levels increase the formation of 20-HETE in the kidney and peripheral vasculature and that 20-HETE contributes to the acute and chronic pressor effects of ANG II.

scholarly journals Role of ANG II in mediating somatosensory-induced renal nerve-dependent antinatriuresis in the rat

1998 ◽  
Vol 275 (1) ◽  
pp. R194-R202 ◽  
Author(s):  
Chunlong Huang ◽  
Edward J. Johns
Keyword(s):  
Sodium Excretion ◽  
Renal Perfusion ◽  
Urine Flow ◽  
Renal Nerves ◽  
Ang Ii ◽  
Renal Nerve ◽  
Somatosensory Stimulation ◽  
Two Stages ◽  
The Brain

This study examined the renal nerve-dependent renal hemodynamic and tubular responses to somatosensory stimulation in the anesthetized rat by use of subcutaneously applied capsaicin when the action of ANG II was blocked peripherally or selectively within the brain. Activation of skin somatosensory receptors caused a transient reversible 10–15% increase in blood pressure, and while renal perfusion pressure was regulated at control levels, there was a transient fall in urine flow and sodium excretion even though both renal blood flow and glomerular filtration rate were unchanged. These reflexly induced excretory responses were abolished when the renal nerves were sectioned. Administration of the ANG II AT1-receptor antagonist, losartan, either intravenously at 3 or 10 mg/kg or locally into the lateral cerebroventricles at 15 μg plus 7.5 μg/h, had no effect on capsaicin-induced vasopressor responses but blocked the reductions in urine flow and sodium excretion. These findings are consistent with ANG II being involved in at least two stages in the reflex, one centrally and one at the periphery.

Angiotensin II suppression is a major factor permitting excretion of an acute sodium load in humans

1994 ◽  
Vol 266 (1) ◽  
pp. F89-F93 ◽  
Author(s):  
D. R. Singer ◽  
N. D. Markandu ◽  
J. J. Morton ◽  
M. A. Miller ◽  
G. A. Sagnella ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Crossover Study ◽  
Healthy Subjects ◽  
Saline Infusion ◽  
Ang Ii ◽  
Sodium Load ◽  
Acute Increase ◽  
Major Factors

We examined the role of circulating angiotensin II (ANG II) in the excretion of an acute Na+ load in eight healthy subjects given 2 liters 0.9% saline in a placebo-controlled crossover study. On the control day, plasma ANG II decreased to 40-60% of basal values and 35 +/- 9 (SE) mmol of Na+ was excreted in the 5 h after the start of saline infusion. When ANG II was infused to maintain plasma ANG II levels at around basal values (6.6 +/- 1.6 pmol/l), only 7 +/- 8 mmol of Na+ was excreted in the same period (P < 0.05). In a previous similar study in which the fall in aldosterone was prevented by infusion of aldosterone, 16 +/- 16 mmol of Na+ was excreted vs. 36 +/- 16 mmol on the control day in comparable 5-h periods. Suppression of ANG II is one of the major factors permitting the acute increase in Na+ excretion after an intravenous Na+ load. ANG II has direct actions on Na+ excretion in addition to its effects on aldosterone.

scholarly journals Current Understanding of Role of Vesicular Transport in Salt Secretion by Salt Glands in Recretohalophytes

2021 ◽  
Vol 22 (4) ◽  
pp. 2203 ◽  
Author(s):  
Chaoxia Lu ◽  
Fang Yuan ◽  
Jianrong Guo ◽  
Guoliang Han ◽  
Chengfeng Wang ◽  
...  
Keyword(s):  
Vesicular Transport ◽  
Salt Gland ◽  
Soil Salinization ◽  
The Body ◽  
Molecular Evidence ◽  
Salt Glands ◽  
Functional Roles ◽  
Secretion Process ◽  
Salt Secretion

Soil salinization is a serious and growing problem around the world. Some plants, recognized as the recretohalophytes, can normally grow on saline–alkali soil without adverse effects by secreting excessive salt out of the body. The elucidation of the salt secretion process is of great significance for understanding the salt tolerance mechanism adopted by the recretohalophytes. Between the 1950s and the 1970s, three hypotheses, including the osmotic potential hypothesis, the transfer system similar to liquid flow in animals, and vesicle-mediated exocytosis, were proposed to explain the salt secretion process of plant salt glands. More recently, increasing evidence has indicated that vesicular transport plays vital roles in salt secretion of recretohalophytes. Here, we summarize recent findings, especially regarding the molecular evidence on the functional roles of vesicular trafficking in the salt secretion process of plant salt glands. A model of salt secretion in salt gland is also proposed.

Circulating angiotensin II mediates sodium appetite in adrenalectomized rats

2001 ◽  
Vol 281 (3) ◽  
pp. R723-R729 ◽  
Author(s):  
G. H. M. Schoorlemmer ◽  
A. K. Johnson ◽  
R. L. Thunhorst
Keyword(s):  
Intravenous Infusion ◽  
Sodium Intake ◽  
Peripheral Circulation ◽  
Ang Ii ◽  
Sodium Depletion ◽  
Sodium Appetite ◽  
Brain Ventricle ◽  
The Brain ◽  
Adrenalectomized Rats

We investigated the role of circulating ANG II in sodium appetite after adrenalectomy. Adrenalectomized rats deprived of their main access to sodium (0.3 M NaCl) for 9 h drank 14.1 ± 1.5 ml of the concentrated saline solution in 2 h of access. Intravenous infusion of captopril (2.5 mg/h) during the last 5 h of sodium restriction reduced sodium intake by 77 ± 12% ( n = 5) without affecting the degree of sodium depletion and hypovolemia incurred during deprivation. Functional evidence indicates that this dose of captopril blocked production of ANG II in the peripheral circulation, but not in the brain; that is, injection of ANG I into the lateral brain ventricle stimulated intake of both water and 0.3 M NaCl. Intravenous infusion of ANG II (starting 10–15 min before 0.3 M NaCl became available) in adrenalectomized, captopril-treated rats restored both sodium intake and blood pressure to values seen in rats not treated with captopril. Longer (20 h) infusions of captopril in 22-h sodium-restricted rats also blocked sodium appetite, but reduced or prevented sodium depletion. Intravenous infusion of ANG II after these long captopril infusions stimulated sodium intake, but intake was less than in controls not treated with captopril. These results indicate that most or all of the sodium appetite of adrenalectomized rats is mediated by circulating ANG II.

Endogenous plasma atrial natriuretic peptide and the control of salt gland function in the Pekin duck

1997 ◽  
Vol 273 (3) ◽  
pp. R1080-R1085 ◽  
Author(s):  
D. A. Gray ◽  
C. Downing ◽  
N. Sayed
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Salt Gland ◽  
Gland Secretion ◽  
Pekin Duck ◽  
Salt Glands ◽  
Experimental Conditions ◽  
Salt Gland Secretion ◽  
Gland Function ◽  
Atrial Natriuretic

Polyclonal antibodies raised in a rabbit against avian atrial natriuretic peptide (ANP) were used to investigate the role of endogenous plasma ANP in the control of salt gland function of conscious, saltwater-adapted Pekin ducks. Salt gland secretion was initiated and maintained either by a hypervolemic (290 mosmol/kg NaCl i.v. at 2 ml/min) or hyperosmotic (1,000 mosmol/kg NaCl i.v. at 0.4 ml/min) stimulus. Both experimental conditions caused significant elevations in endogenous plasma ANP concentrations. At steady states of secretion driven by hypervolemia, the administration of ANP antiserum (anti-ANP), which reduced plasma ANP concentrations by 90%, caused an immediate 30% reduction in fluid secretion rate and sodium excretion that lasted for 20-30 min. The activity of salt glands driven by hyperosmolality was not changed by anti-ANP. The results show that the high circulating concentrations of endogenous ANP associated with conditions of sustained volume expansion promote salt gland secretion.

Effects of saline intake, sex, and season on Pekin duck osmoregulatory organ masses and comparison with wild Mallards

2004 ◽  
Vol 82 (1) ◽  
pp. 30-40 ◽  
Author(s):  
Maryanne R Hughes ◽  
Darin C Bennett
Keyword(s):  
Adrenal Glands ◽  
Relative Size ◽  
Salt Gland ◽  
Harderian Gland ◽  
Pekin Duck ◽  
Salt Glands ◽  
Male And Female ◽  
Pekin Ducks ◽  
Harderian Glands ◽  
Induced Changes

Osmoregulatory organ masses of freshwater Mallards (Anas platyrhynchos) do not differ between the sexes, but drinking saline induces changes that are sexually disparate in some organs. We examined relative size of organ masses of male and female Pekin ducks (that were domesticated from Mallards) and compared their responses to saline intake with those of Mallards. Organ masses of male and female Mallards do not differ in size. The liver and kidneys are heavier in female Pekin ducks and their digestive tract (except for the proventriculus and duodenum) is longer and heavier; male Pekin ducks have heavier salt glands. Mallards acclimated to saline drinking water have enlarged salt glands but not kidneys, adrenal glands, or Harderian glands, their proventriculus tends to be shorter and lighter, the jejunum longer in males, and the ileum longer and heavier in both sexes. In Pekin ducks that drink saline, the salt and Harderian glands are larger and their kidneys (but not adrenal glands) tend to be larger; the proventriculus is unaffected, but the small intestine is lighter, but not shorter, in females. Body, salt gland, Harderian gland, ventriculus, and duodenum masses vary seasonally in Pekin ducks. Discussion considers the effects of season and sex on relative organ masses and how saline-induced changes in them reflect domestication and may influence salt tolerance.

Role of intrarenal angiotensin II in mediating renal response to volume expansion

1991 ◽  
Vol 261 (3) ◽  
pp. R619-R625 ◽  
Author(s):  
J. M. Pinilla ◽  
M. C. Perez ◽  
I. Hernandez ◽  
T. Quesada ◽  
J. Garcia-Estan ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Volume Expansion ◽  
Left Kidney ◽  
Extracellular Volume ◽  
Isotonic Saline ◽  
Relative Role ◽  
Ang Ii ◽  
Renal Response ◽  
The Right

Natriuresis induced by extracellular volume expansion (ECVE) is accompanied by a decrease in renin release and by an increase of renal interstitial hydrostatic pressure (RIHP). This study was undertaken to examine, in anesthetized dogs, the relative role of intrarenal angiotensin II (ANG II) changes in mediating natriuresis, diuresis, and increases in RIHP induced by two different levels of volume expansion (1.5 and 5% body wt in 45 min) with isotonic saline. Intrarenal ANG II levels were maintained in the right kidney throughout the experiment by simultaneously infusing captopril (0.8 micrograms.kg-1.min-1) and ANG II (1 ng.kg-1.min-1) into the right renal artery. In response to 5% ECVE, increases in RIHP, natriuresis, and diuresis were inhibited in the right kidney by 55, 40, and 47% respectively, when compared with the left kidney. Significant increases occurred in plasma atrial natriuretic peptide (ANP) levels during 5% ECVE. Maintenance of constant intrarenal ANG II levels during 1.5% ECVE completely abolished the increment of RIHP and diuresis and inhibited the natriuretic response by 80% in the right kidney when compared with the left kidney. Plasma ANP levels did not change during the 1.5% ECVE. No differences between kidneys were found when the intrarenal effects of ANG II were blocked with saralasin before saline loading. These results suggest that increases in RIHP, natriuresis, and diuresis during ECVE are partially mediated by decreases in intrarenal ANG II levels. Furthermore, these results indicate that the role of intrarenal ANG II levels in mediating the renal response to ECVE is more important when plasma ANP levels do not change than when they are increased.

Effect of Hypertonic and Hypotonic Infusions on Aldosterone in Conscious Sodium-Depleted Dogs

1981 ◽  
Vol 61 (2) ◽  
pp. 191-199 ◽  
Author(s):  
Jennifer W. Childers ◽  
E. G. Schneider
Keyword(s):  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Sodium Concentration ◽  
Plasma Aldosterone ◽  
Plasma Sodium ◽  
Aldosterone Secretion ◽  
Plasma Aldosterone Concentration ◽  
Plasma Sodium Concentration ◽  
Sodium Load

1. The role of the plasma sodium concentration in the regulation of aldosterone secretion and sodium excretion was investigated by comparing in 13 conscious sodium-depleted dogs the effects of the same sodium load (2.5 mmol/kg) given as either a hypertonic or hypotonic infusion. 2. The plasma sodium concentration was significantly higher and the plasma aldosterone concentration and urinary aldosterone excretion were significantly lower after the hypertonic infusion as compared with the hypotonic infusion. 3. The cumulative urinary sodium excretion during the 22 h after beginning the infusion was significantly greater after the hypertonic infusion, but this difference was not observed in five sodium-depleted dogs who were treated with deoxycorticosterone acetate before the infusions were given. 4. These data suggest that elevations in plasma sodium concentration are effective in decreasing aldosterone secretion and, hence, in increasing sodium excretion in conscious sodium-depleted dogs.

Sign in / Sign up

Export Citation Format

Share Document