Extracellular fluid volume and the initiation of salt gland secretion in ducks and gulls

1989 ◽  
Vol 67 (1) ◽  
pp. 194-197 ◽  
Author(s):  
Maryanne R. Hughes

The effect of intraperitoneal NaCl loading on extracellular fluid volume, plasma concentration, and initiation of salt gland secretion was measured in freshwater- and sea water-acclimated Glaucous-winged Gulls, Larus glaucescens, and Mallards, Anas platyrhynchos. In both species salt loading was associated with a significant increase in plasma [Na] and [Cl]. In freshwater- and sea water-acclimated gulls the extracellular fluid volume increased and salt gland secretion occurred; in freshwater- and seawater-acclimated ducks the extracellular fluid volume decreased and salt gland secretion did not occur.

1980 ◽  
Vol 239 (5) ◽  
pp. R489-R496
Author(s):  
H. T. Hammel ◽  
C. Simon-Oppermann ◽  
E. Simon

Pekin ducks were reared and maintained on 620 mosmol NaCl/kg H2O to enhance the secretory capability of their salt glands. When a control solution of 1,000 mosmol NaCl/kg H2O was infused intravenously at 0.2, 0.4, or 0.6 ml/min for 60-90 min, the infused loads were secreted in approximately equal quantities, indicating that the amount of NaCl in the extracellular fluid (ECF) before and after each infusion did not change. Salt and water secreted in response to experimental infusions of hyposmotic saline or blood were less than the solute and water infused. Thus, ECF volume increased and the Na+ concentration decreased. Infusions of control solution followed these experimental infusions. The salt and water secreted again equaled the amounts infused, indicating that the threshold concentration of Na+ ([Na+]th) for salt gland secretion was decreased by the increase in ECF volume. When the colloid dextran was added to the control solution, its infusion increased the colloid osmotic pressure of the blood and decreased nasal secretion. Because dextran increased the intravascular volume while the interstitial fluid volume (ISFV) decreased, we conclude that the [Na+]th was inversely correlated with ISFV.


1969 ◽  
Vol 47 (6) ◽  
pp. 1133-1138 ◽  
Author(s):  
Maryanne Robinson Hughes ◽  
Frank E. Ruch Jr.

The spontaneously produced salt gland secretion (SGS) and tears of the domestic duck, Anas platyrhynchos, were analyzed for sodium (Na), potassium (K), and chloride (Cl) (Cl in SGS only). Acclimation to seawater did not enhance the concentrating ability of the salt glands. The NaCl concentration exceeded that of seawater by only a small margin. The tears of saline-acclimated birds contained less Na and more K than birds drinking water with low NaCl content. Salt stress significantly increased the weight of the salt glands and of the Harderian glands; the lacrymal glands were not affected. An estimation of the relative possible contribution of the cloacal fluid, SGS, and tears to cation excretion was made.


1979 ◽  
Vol 56 (6) ◽  
pp. 547-553 ◽  
Author(s):  
H. J. Kramer ◽  
T. Moch ◽  
L. Von Sicherer ◽  
R. Düsing

1. Aprotinin, a potent kallikrein inhibitor, was given to conscious rats with and without expansion of the extracellular fluid volume with isotonic saline. 2. In noa-expanded rats aprotinin had no effect on arterial pressure, glomerular filtration rate (GFR), hippuran clearance, urinary flow rate, absolute sodium and potassium excretion or free-water clearance. 3. In volume-expanded rats aprotinin significantly reduced GFR, hippuran clearance, urine volume (V) UNaV, UKV and Cwater/GFR without effect on systemic arterial pressure. 4. Urinary immunoreactive prostaglandin E2 excretion significantly increased during the expansion phase but returned to below the control range during stable extracellular fluid volume expansion. 5. Aprotinin significantly suppressed urinary immunoreactive prostaglandin E2 excretion in non-expanded rats and in volume-expanded rats during the expansion phase, but not during stable expansion. 6. The results suggest that the kallikrein-kinin system may contribute to changes in renal function during extracellular volume expansion. This action may not necessarily be associated with changes in renal prostaglandin E2 activity.


1988 ◽  
Vol 255 (4) ◽  
pp. R575-R582 ◽  
Author(s):  
R. Gerstberger ◽  
H. Sann ◽  
E. Simon

The neuromodulatory role of vasoactive intestinal peptide (VIP) in avian salt gland secretion and blood flow was investigated in conscious saltwater-acclimated Pekin ducks. Glandular blood flow was measured by laser-Doppler flowmetry or the radioactive microspheres technique. Osmolal excretion was closely related to salt gland blood flow during salt loading. At threshold conditions of salt gland secretion, VIP infused intracarotidally induced both osmolal excretion and arteriolar vasodilation dose dependently (30-240 pmol.min-1.kg body wt-1). The VIPergic effect on the secretory process for NaCl was enhanced by simultaneous intracarotid application of acetylcholine (5 nmol.min-1.kg body wt-1), whereas the intrinsic vasodilatory potency of acetylcholine appeared to be nonadditive in coinfusion experiments. Ongoing secretion induced by systemic infusion of hypertonic saline could be suppressed by muscarinic antagonists, with salt gland blood flow being sustained at the reduced level of atropine-resistant vasodilation. Subsequent intracarotid infusion of VIP stimulated glandular blood perfusion and also, to a minor extent, osmolal excretion, suggesting an independent, functional VIP system in efferent salt gland control.


1979 ◽  
Vol 237 (5) ◽  
pp. R355-R359
Author(s):  
R. Kaul ◽  
H. T. Hammel

Acute salt and water balance measurements were made in two conscious salt water-acclimated Pekin ducks at and above their osmotic threshold for salt gland secretion. Intravneous infusion of 1,000 mosmol/kg H2O NaCl at 0.350 ml/min increased plasma tonicity less than 0.5% and increased secretion from nearly zero to a rate matching the infusion. Continuous secretion at a similar submaximal rate was driven by 5,600 mosmol/kg H2O NaCl infused at 0.070 ml/min. Osmolality of secreted fluid was constant for any secretion rate, so that net water loss occurred when the concentration of infusate exceeded that of secreted fluid. Threshold plasma osmolality increased by 9 mosmol/kg H2O after the loss of 77 g water (3% body wt). Solutes were always secreted at the infusion rate, even when body fluid osmolality increased while body water decreased. We conclude that the salt gland controller is sensitive to more than just extracellular fluid (ECF) tonicity, and we suggest that elevation of the osmotic threshold may occur in response to decreased ECF volume.


1975 ◽  
Vol 229 (4) ◽  
pp. 1068-1072 ◽  
Author(s):  
Norman RA ◽  
TG Coleman ◽  
Wiley TL ◽  
Manning RD ◽  
AC Guyton

The goal of these studies was to determine whether the hypertension caused by excessive salt loading results from sodium-induced expansion of the extracellular fluid volume or whether the salt increases the pressure in some other way, such as by causing vascular constriction. In one group of sheep, a combination of total nephrectomy and hemodialysis was used to produce and maintain step increases in extracellular fluid volume for 1 wk without a significant change in sodium ion concentration. In a 2nd group, unilateral nephrectomy, dialysis, and DOCA administration were used to cause step increases in sodium ion concentration while the extracellular fluid volume was held as close to normal as possible. The results showed a 41% increase in arterial pressure in the high-volume sheep and only a 4% increase in pressure in the high-sodium sheep. In both instances the total exchangeable sodium increased almost equally--a 21% increase in the high-sodium sheep. The data support the concept that sodium retention causes hypertension almost entirely because of sodium-induced expansion of the extracellular fluid volume.


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