6. SODIUM AND POTASSIUM SECRETION BY IGUANA SALT GLANDS:

Iguanas ◽  
2019 ◽  
pp. 84-94
1987 ◽  
Vol 253 (1) ◽  
pp. R83-R90 ◽  
Author(s):  
T. J. Shuttleworth ◽  
J. L. Thompson ◽  
W. H. Dantzler

Potassium secretion by the nasal salt glands of the herbivorous desert lizard Sauromalus obesus was determined in vivo by a new technique. Intraperitoneal injection of KCl rapidly increased the potassium secretion rate from 0.28 to 15.35 mumol X 100 g-1 X h-1. A second identical intraperitoneal injection, given 15 h after the first, further increased potassium secretion to 50.09 mumol X 100 g-1 X h-1. This was associated with a doubling of plasma K+ concentration and salt gland Na+-K+-adenosinetriphosphatase (ATPase) activity. Neither salt gland weight or residual (Mg2+) ATPase activity were affected. In an isolated perfused head preparation, potassium secretion from the nasal salt glands was stimulated from 0.99 to 10.76 mumol X 100 g-1 X h-1 by methacholine and to 14.68 mumol X 100 g-1 X h-1 by forskolin. In this perfused preparation, simultaneous determination of salt gland perfusion flow (using radiolabeled microspheres) and the rate of potassium secretion revealed that the secreting glands removed 68% of the perfusing potassium ions. Calculations indicated that secretion at the maximal rate observed in vivo would necessitate a fourfold increase in the rate of blood flow to the gland.


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.


1990 ◽  
Vol 124 (1) ◽  
pp. 47-52 ◽  
Author(s):  
C. J. Edmonds ◽  
C. L. Willis

ABSTRACT The effect of hypothyroidism on potassium adaptation (shown by increased potassium secretion in response to potassium loading) and on the action of aldosterone on potassium secretion and sodium fluxes was examined in the rat distal colon. Potassium adaptation, particularly the response to an acute potassium load, was impaired by hypothyroidism which also considerably reduced the rise of transepithelial electrical potential difference (p.d.) of total and transcellular (active) lumen-to-plasma sodium fluxes and of potassium secretion normally produced by aldosterone. These changes were, in part, corrected by a short period (3 days) of tri-iodothyronine replacement. Moreover in aldosterone-treated hypothyroid rats, amiloride in the lumen was considerably less effective in reducing the p.d. and sodium fluxes than in aldosterone-treated normal rats. The intracellular sodium transport pool was greater in the hypothyroid than in the normal rats (5·0± 1·1 (s.e.m.) nmol/mg dry weight compared with 2·9 ± 0·2 nmol/mg dry weight; P<0·02). Aldosterone increased the pool in the normal but not in the hypothyroid rats while amiloride had little effect on the pool in the aldosterone-treated hypothyroid rats but almost abolished it in aldosterone-treated normal rats. Aldosterone plays a major part in the adaptation of colonic sodium and potassium transport to sodium depletion or potassium excess; these adaptations were much impaired in hypothyroid animals. The present results are consistent with a deficiency in aldosterone induction of potassium- and amiloride-sensitive sodium pathways in the apical membrane of colonic epithelial cells in hypothyroid rats, a deficiency which limits the stimulant effect of aldosterone on sodium and potassium transport. Journal of Endocrinology (1990) 124, 47–52


1977 ◽  
Vol 233 (2) ◽  
pp. F138-F144 ◽  
Author(s):  
N. B. Clark ◽  
R. F. Wideman

Renal excretion patterns of calcium, phosphate, sodium, and potassium were studied in parathyroidectomized (PTX) and parathyroid extract (PTE)-injected PTX starlings. Sturnus vulgaris. Anesthetized birds (Equi-Thesin or Dial) were infused intravenously with 2.5% mannitol containing [14C]inulin. PTX caused significant hypocalcemia, hyperphosphatemia, increased relative calcium clearance (CCa/CIn), and decreased relative clearances of phosphate and potassium, but did not change the clearance of sodium. Glomerular filtration rate (GFR=CIn) and urine flow remained unchanged up to 2 h after PTX. PTE administration 3 h after PTX returned serum calcium and phosphate values to control levels and caused a transient (10-min) increase in GFR. Following PTE, the relative clearances of phosphate, sodium- and potassium increased, while that of calcium decreased significantly relative to the PTX levels. PTE caused net tubular secretion of phosphate, decreased tubular reabsorption of sodium and potassium (sometimes potassium secretion), and a return of excretion of calcium to control levels. These studies indicate that the parathyroid role in calcium and phosphate homeostasis in starlings is predominantly on the kidney.


1985 ◽  
Vol 248 (4) ◽  
pp. F507-F512 ◽  
Author(s):  
D. Hirsch ◽  
P. Pace ◽  
H. J. Binder ◽  
J. P. Hayslett

The present study was performed to answer the question: Is the action of aldosterone on electrolyte transport and electrical properties similar in all target tissues? Studies were performed in vivo in control animals and rats with secondary hyperaldosteronism, caused by a sodium-free diet, to compare the effects of hyperaldosteronism on distal colon with hormone-induced changes in proximal colon. In distal colon aldosterone increased net sodium absorption and potassium secretion approximately threefold. Transmural potential difference increased from -15 +/- 2 to -83 +/- 3 mV (lumen negative) and ISC rose from 167 +/- 26 to 1,023 +/- 17 microA X cm-2. These aldosterone-induced responses were completely inhibited by 0.1 mM amiloride. In contrast, in proximal colon potential difference was unchanged or increased slightly in experimental animals and ISC increased only 28% above control, although increases in net sodium and potassium transport were similar to changes observed in distal colon. Amiloride did not reduce sodium absorption in proximal colon of animals with hyperaldosteronism; ISC was decreased by 43%. These studies demonstrate that rat proximal colon is an aldosterone-sensitive tissue, but that the mechanism by which aldosterone influences sodium transport is not identical in distal and proximal portions of colon.


The processes involved at the apical and basal cell membranes in the formation of the hypertonic sodium chloride secretion in marine birds are discussed. Recent work indicates that the concentration gradient is established across the apical, i.e. luminal membrane probably by a sodium pump. There is also some evidence to suggest that during secretion, the uptake of sodium and chloride by the cell across the basal membrane may not be passive but may involve the exchange of sodium for hydrogen ions and chloride for bicarbonate. There is also the possibility that potassium secretion at high concentrations in some marine and desert species may involve an active extrusion across the apical membrane. Stimulation of secretion by acetylcholine and the possible effects of hormones on the secretory mechanism are considered.


1959 ◽  
Vol 197 (2) ◽  
pp. 337-341 ◽  
Author(s):  
P. Jay Howard ◽  
Walter S. Wilde ◽  
Richard L. Malvin

We have performed a first series of experiments using our stop flow technique to localize renal transport of calcium in dogs. Calcium is found to be actively reabsorbed in a far distal area but does not appear to be actively lowered in concentration in proximally derived samples. In a second series of dogs, elevation of plasma calcium by infusion of the salt CaCl2 caused a 43% reduction in the additional volume of water reabsorbed by the proximal tubule during stop flow. Calcium does not interfere with the active reabsorption of sodium in the distal area and does not cause significant increases in sodium excretion. In contrast calcium causes a considerable increase in potassium secretion at a far distal site. When calcium gluconate was employed, severe impairment of distal sodium and calcium reabsorption occurred in addition to the increased potassium secretion. We suggest that the gluconate anion restricts the movement of sodium, calcium and potassium electrostatically thus obligating cations to remain in the tubular urine depending upon their reabsorption potential.


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