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H J Binder

Publications and source records attributed to H J Binder.

At least 19 recordsLinked to original sources
PubMed1992

Gastrin and colorectal cancer. Evidence against an association.

Plasma gastrin has been reported to be elevated among patients with colorectal cancer. The objectives of the present study were to confirm this observation and, if confirmed, to shed light on the reason for the elevation. Presurgical and postsurgical fasting plasma gastrin levels were compared between 24 patients hospitalized for colorectal adenocarcinoma resection and 25 control patients hospitalized for other surgery. Elevated presurgical gastrin levels in the case group that fell after surgery would be consistent with production of gastrin by the tumor. High presurgical gastrin levels in the case group that did not change following surgery would be consistent with excess gastrin production by G cells. The mean presurgical gastrin levels were 21.9 +/- 3.7 pM (cases) and 45.1 +/- 18.0 pM (controls). The mean postsurgical gastrin levels were 20.5 +/- 3.9 pM (cases) and 43.4 +/- 14.6 pM (controls). These results do not provide support for the hypotheses that gastrin is elevated in colorectal cancer patients or that gastrin is secreted by colorectal tumors in sufficient quantities to be measurable in the plasma.

Adenocarcinoma↗
PubMed1992

Mucosal ouabain and Na+ inhibit active Rb+(K+) absorption in normal and sodium-depleted rat distal colon.

To determine the effect of mucosal sodium and mucosal ouabain on active Rb+(K+) absorption, unidirectional and net 86Rb+ fluxes were measured under voltage-clamp conditions in the distal colon of normal and sodium-depleted rats. The role of mucosal sodium (independent of serosal sodium) was evaluated in a model of Rb+(K+) absorption in which serosal ouabain markedly enhanced active Rb+(K+) absorption. In normal rats, mucosal sodium was a competitive inhibitor of Rb+(K+) absorption, and Rb+(K+) absorption consisted of a mucosal sodium-sensitive component and a mucosal sodium-insensitive component. Further, mucosal ouabain almost completely inhibited the mucosal sodium-insensitive component but did not affect the mucosal sodium-sensitive component. In sodium-depleted rats, both mucosal sodium-sensitive and mucosal sodium-insensitive fractions of Rb+(K+) absorption were also identified. Aldosterone markedly stimulated the mucosal sodium-sensitive component (1.68 +/- 0.15 vs. 0.60 +/- 0.10 muEq.h-1.cm-2) but not the sodium-insensitive component (0.88 +/- 0.09 vs. 0.64 +/- 0.06 muEq.h-1.cm-2) component of Rb+(K+) absorption; however, in contrast to normal animals, mucosal sodium in sodium-depleted animals was a noncompetitive inhibitor of Rb+(K+) absorption. The mucosal sodium-insensitive component of Rb+(K+) absorption in sodium-depleted animals was substantially inhibited by mucosal ouabain, but the mucosal sodium-sensitive component, unlike that in normal animals, was partially inhibited by mucosal ouabain. These studies indicate that the characteristics of the Rb+(K+) absorptive process in sodium-depleted animals differ significantly from those present in normal animals, suggesting that aldosterone induces an Rb+(K+) absorptive mechanism not present in normal animals.

Animals↗
PubMed1991

Mechanism of short-chain fatty acid uptake by apical membrane vesicles of rat distal colon.

In this study, the presence of a bicarbonate gradient-dependent, carrier-mediated anion exchange process for butyrate (a representative short-chain fatty acid) uptake in apical membrane vesicles isolated from rat distal colon is described. An outward gradient of both butyrate- and bicarbonate-stimulated [14C]butyrate uptake and resulted in transient accumulation (an "overshoot" phenomenon). Butyrate gradient-stimulated [14C]butyrate uptake was not altered either by an imposed pH gradient or at different pH values. In contrast, bicarbonate gradient-stimulated [14C]butyrate uptake was stimulated severalfold by an additional imposition of an outward pH gradient (pHi = 7.5; pH0 = 6.0). This bicarbonate- and pH gradient-stimulated butyrate uptake was not inhibited by either voltage clamping, with equimolar intravesicular and extravesicular K+ and valinomycin, or 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS), an anion-exchange inhibitor. Increasing butyrate concentrations saturated the bicarbonate- and pH gradient-stimulated butyrate uptake with a half-maximal concentration (Km) of 26.9 +/- 1.6 mmol/L. Butyrate uptake was substantially inhibited by 20 mmol/L propionate (45%) and acetate (60%) but was not inhibited by oxalate, inorganic anions (SO4(2-) and NO3-), and transport inhibitors (amiloride, acetazolamide, furosemide, and ouabain). It is concluded from these results that bicarbonate gradient-stimulated butyrate uptake in apical membrane vesicles of rat distal colon occurs via a carrier-mediated anion-exchange process that differs from other DIDS-sensitive anion exchanges [e.g., the Cl- -OH- (HCO3-) process].

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1991

Apical membrane localization of ouabain-sensitive K(+)-activated ATPase activities in rat distal colon.

This study sought to establish the presence of K(+)-activated adenosinetriphosphatase (ATPase) activity in the colonic mucosa of the rat distal colon. K(+)-activated ATPase activity was present in apical membranes but not in basolateral membranes. K(+)-activated ATPase activity in apical membranes represented an approximate 10-fold enrichment compared with that in the homogenate. Na(+)-K(+)-activated ATPase activity was also present in homogenate but was enriched less than fourfold in apical membranes. K(+)-activated ATPase activity in apical membranes had both ouabain-sensitive and ouabain-insensitive components. In contrast, Na(+)-K(+)-activated ATPase activity was completely inhibited by ouabain. Similar half-maximal concentrations for K+ and pH activation curves were found for both ouabain-sensitive and ouabain-insensitive fractions. In addition to K+, the ouabain-sensitive fraction of K(+)-activated ATPase activity was stimulated by Rb+, NH+4, and Cs+, whereas the ouabain-insensitive fraction was activated only by Rb+. K(+)-activated ATPase activity was significantly inhibited by vanadate but not by N-ethylmaleimide or omeprazole. In the proximal colon, in contrast to the distal colon, active K+ absorption is not present, and K(+)-activated ATPase is approximately 20% of that in the distal colon. These studies demonstrate that K(+)-activated ATPase is present in apical membranes of rat distal colon and permit the speculation that this enzyme represents a unique and distinct ATPase (compared with either Na(+)-K(+)-ATPase or gastric parietal cell K(+)-ATPase) and is likely linked closely to the active K+ absorptive process present in this epithelium.

Adenosine Triphosphatases↗
PubMed1991

Sodium uptake across basolateral membrane of rat distal colon. Evidence for Na-H exchange and Na-anion cotransport.

This study sought to characterize the mechanism of Na transport across basolateral membrane vesicles of rat distal colon. Both an outward proton gradient and an inward bicarbonate gradient stimulated 22Na uptake. Proton gradient-stimulated 22Na uptake was activated severalfold by the additional presence of an inward bicarbonate gradient, and bicarbonate gradient-stimulated 22Na uptake was significantly enhanced by an imposed intravesicular membrane positive potential. 0.1 mM amiloride inhibited both proton gradient- and bicarbonate gradient-stimulated 22Na uptake by 80 and 95%, respectively, while 1 mM 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS) inhibited both proton gradient- and bicarbonate gradient-stimulated 22Na uptake by 40 and 80%, respectively. Both proton gradient- and bicarbonate gradient-stimulated 22Na uptake saturated as a function of increasing Na concentration: the apparent kinetic constants (Km) for Na for the DIDS-insensitive component of proton gradient-stimulated 22Na uptake was 46.4 mM, while the DIDS-sensitive component of proton gradient- and bicarbonate gradient-stimulated 22Na uptake had Km for Na of 8.1 and 6.4 mM, respectively. Amiloride inhibited both DIDS-insensitive proton gradient- and bicarbonate gradient-stimulated 22Na uptake with an inhibitory constant (Ki) of approximately 35 and 1 microM, respectively. We conclude from these results that proton gradient-stimulated 22Na uptake represents both DIDS-insensitive Na-H exchange and DIDS-sensitive electrogenic Na-OH cotransport, and that the DIDS-sensitive component of proton gradient-stimulated 22Na uptake and bicarbonate gradient-stimulated 22Na uptake may represent the same electrogenic Na-anion cotransport process.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1990

Pathophysiology of acute diarrhea.

Diarrhea, a major health problem worldwide, is both a sign and a symptom. As a symptom, diarrhea has been described as an increase in stool frequency, an increase in stool volume, and/or a decrease in stool consistency. As a sign, diarrhea is characterized by an increase in stool water excretion to greater than 150 to 200 ml every 24 hours. Four mechanisms that may be responsible for the alterations in fluid and electrolyte movement associated with diarrhea are increased luminal osmolality, decreased fluid absorption, increased intestinal secretion, and altered intestinal motility. Specific pathogenic mechanisms for acute infectious diarrhea include tissue invasion, enterotoxin production, and adhesion of infectious agents to epithelial cells. Antidiarrheal agents remove secretagogues from the intestinal tract, stimulate fluid absorption, and inhibit electrolyte movement.

Acute Disease↗
PubMed1990

Characterization of Na-H exchange in apical membrane vesicles of rat colon.

This study establishes the characteristics of electroneutral Na-H exchange present in apical membrane vesicles isolated from colonocytes of rat large intestine. An outward directed proton gradient stimulated 22Na uptake and demonstrated transient accumulation that was not altered by voltage clamping with K and its ionophore, valinomycin. Amiloride inhibited proton gradient-stimulated 22Na (0.1 mM) uptake by 97% by a noncompetitive mechanism with a Ki of 27 microM. 5-(N-ethyl-N-isopropyl)amiloride, an amiloride analogue which is a specific potent inhibitor of electroneutral Na-H exchange, inhibited proton gradient-stimulated 22Na uptake with a Ki of 400 nM. Increasing Na concentration saturated the proton gradient-stimulated 22Na uptake with an apparent Km of 11.7 +/- 2.2 mM. Increasing intravesicular proton concentration also resulted in saturation of 22Na uptake with a Km of 2.8 microM. Proton gradient-stimulated 22Na uptake was inhibited significantly by 10 mM Na+, Li+, and NH4+, while outward directed gradients of these ions in the absence of proton gradient accelerated 22Na uptake. The mechanism of Li+ inhibition of proton gradient-stimulated 22Na uptake was competitive with a Ki of 2 mM. 22Na uptake either stimulated by an outward directed Na gradient (i.e. Na-Na exchange) at pH 5.5, 6.5, and 7.5 or stimulated by 10-fold outward directed proton gradient at different pH values was similar; observations that do not suggest proton activation of Na-H exchange. We conclude from these results that proton gradient-stimulated 22Na uptake in colonic apical membrane vesicles represents tightly coupled electro-neutral Na-H exchange with several kinetic properties unlike those described in other epithelia.

Amiloride↗
PubMed1990

Characterization of butyrate-dependent electroneutral Na-Cl absorption in the rat distal colon.

Recent studies have established that mucosal butyrate stimulates electroneutral sodium-chloride (Na-Cl) absorption in the distal colon of the rat and a model in which Na-hydrogen (H) and Cl-butyrate exchanges are coupled has been proposed as the mechanism of butyrate-dependent electroneutral Na-Cl absorption. These studies were designed to examine butyrate-dependent electroneutral Na-Cl absorption in experimental conditions in which HCO3-dependent electroneutral Na-Cl absorption is inhibited: in Na-depleted (aldosterone-treated) animals and in the presence of increased mucosal cyclic adenosine monophosphate (AMP). Butyrate-dependent electroneutral Na-Cl absorption was markedly reduced in Na-depleted rats. In contrast, the inhibition of both net Na and net Cl absorption by 5 mM serosal theophylline was significantly less in butyrate-containing, HCO3-free Ringer solution than in butyrate-free- HCO3-containing Ringer solution. These studies indicate that cyclic AMP does not inhibit butyrate-dependent electroneutral Na-Cl absorption and we propose that the mechanism of cyclic AMP inhibition of HCO3-dependent electroneutral Na-Cl absorption may be a result of its inhibition of Cl-HCO3, not Na-H exchange.

Aldosterone↗
PubMed1990

Active potassium absorption in rat distal colon.

1. Active potassium (K+) absorption in rat distal colon was investigated by measuring mucosal-to-serosal (JK, ms) and serosal-to-mucosal (JK, sm) 42K+ fluxes (mu equiv h-1 cm-2) across isolated stripped mucosa under short-circuit conditions in normal and dietary Na-depleted animals. As previously demonstrated, removal of Na+ from both mucosal and serosal solutions bathing the normal colon slightly increased net K+ absorption as a result of inhibition of JK, sm without affecting JK, ms, while in the Na-depleted group net K+ secretion (-0.54 +/- 0.11) was converted to a marked net K+ absorption (1.68 +/- 0.30, P less than 0.001). 2. In both groups of animals in Na(+)-free Ringer solution, JK, ms exhibited saturable and linear components, while JK, sm was a linear function of [K+]. Estimated affinity constants (mM) for saturable net K+ absorption were similar in normal (0.52 +/- 0.12) and Na-depleted (0.67 +/- 0.11) animals; however, there was a greater than 3-fold increase in the saturable flux (Jmax) from 0.54 +/- 0.04 in the normal colon to 1.78 +/- 0.08 mu equiv h-1 cm-2 in Na-depleted animals. 3. Mucosal orthovanadate (100 microM) inhibited JK, ms in both normal (control, 0.66 +/- 0.05 vs. orthovanadate, 0.36 +/- 0.03 mu equiv h-1 cm-2, P less than 0.001) and Na-depleted animals (control 1.20 +/- 0.13 vs. orthovanadate 0.77 +/- 0.07 mu equiv h-1 cm-2, P less than 0.01) without affecting JK, sm or the short-circuit current. In the Na-depleted group mucosal omeprazole or SCH28080 (100 microM), inhibitors of gastric K(+)-H(+)-ATPase, insignificantly or slightly reduced (by 10%) JK, ms respectively; in contrast, mucosal ouabain (1 mM) markedly inhibited JK, ms (control, 1.61 +/- 0.16 vs. ouabain, 0.83 +/- 0.98 mu equiv h-1 cm-2, P less than 0.001). 4. Mucosal Na+ appeared to be a competitor of K+ uptake across the apical membrane. 5. These results indicate that dietary Na-depletion increases electroneutral K+ absorption by increasing its transport capacity and suggest that the mechanism of this active K+ absorption process may involve an apical K(+)-ATPase with properties that are unlike the gastric K(+)-H(+)-ATPase but similar, in part, to Na(+)-K(+)-ATPase.

Adenosine Triphosphatases↗
PubMed1990

Aldosterone and glucocorticoid receptor-specific agonists regulate ion transport in rat proximal colon.

Dietary sodium depletion increases electroneutral Na-Cl absorption and potassium secretion in the proximal colon of the rat. Although sodium depletion results in secondary hyperaldosteronism, the stimulation of electroneutral Na-Cl absorption is not a typical mineralocorticoid-mediated event. These studies were performed to determine whether the aldosterone or glucocorticoid receptor mediates these changes in electrolyte transport. Continuous infusion of aldosterone at 70 micrograms.100 g body wt-1.day-1 for 7 days resulted in a significant increase in net Na+ and Cl- absorption (5.5 +/- 0.8 and 5.9 +/- 1.0 mueq.h-1.cm-2, respectively). A 7-day infusion of RU 28362, a glucocorticoid receptor-specific agonist, at 70 micrograms.100 g body wt-1.day-1 similarly increased net Na+ and Cl- absorption (5.4 +/- 1.3 and 4.1 +/- 0.5 mueq.h-1.cm-2, respectively). Both aldosterone and RU 28362 produced a minimal increase in Isc (0.4 +/- 0.2 and 0.8 +/- 0.2, respectively). Administration of spironolactone prevented the stimulation of Na+ absorption induced by aldosterone but not that by RU 28362, and aldosterone but not RU 28362 stimulated active potassium secretion. These studies indicate that aldosterone mediates the stimulation of both electroneutral Na-Cl absorption and K+ secretion produced by dietary sodium depletion and that both aldosterone and glucocorticoid agonists each stimulate electroneutral Na-Cl absorption as a result of interacting with the mineralocorticoid and glucocorticoid receptors, respectively.

Aldosterone↗
PubMed1989

Aldosterone induction of electrogenic sodium transport in the apical membrane vesicles of rat distal colon.

Na-H exchange is present in apical membrane vesicles (AMV) isolated from distal colon of normal rats. Because in intact tissue aldosterone both induces amiloride-sensitive electrogenic sodium transport and inhibits electroneutral sodium absorption, these studies with AMV were designed to establish the effect of aldosterone on sodium transport. An outward-directed proton gradient stimulated 22Na uptake in AMV isolated from distal colon of normal and dietary sodium depleted (with elevated aldosterone levels) experimental rats. Unlike normal AMV, proton gradient-dependent 22Na uptake in experimental AMV was inhibited when uptake was measured under voltage-clamped conditions. 10 microM amiloride inhibited the initial rate of proton gradient-dependent 22Na uptake in AMV of normal and experimental rats by 30 and 75%, respectively. In contrast, 1 mM amiloride produced comparable inhibition (90 and 80%) of 22Na uptake in normal and experimental AMV. Intravesicular-negative potential stimulated 22Na uptake in experimental but not in normal AMV. This increase was inhibited by 90% by 10 microM amiloride. An analogue of amiloride, 5-(N-ethylisopropyl) amiloride (1 microM), a potent inhibitor of electroneutral Na-H exchange in AMV of normal rat distal colon, did not alter potassium diffusion potential-dependent 22Na uptake. Increasing sodium concentration saturated proton gradient-dependent 22Na uptake in normal AMV. However, in experimental AMV, 22Na uptake stimulated by both proton gradient and potassium diffusion potential did not saturate as a function of increasing sodium concentration. We conclude from these results that an electrically sensitive conductive channel, not electroneutral Na-H exchange, mediates 22Na uptake in AMV isolated from the distal colon of aldosterone rats.

Aldosterone↗
PubMed1989

Short-chain fatty acids stimulate active sodium and chloride absorption in vitro in the rat distal colon.

Studies were performed to determine the mechanism by which short-chain fatty acids increase colonic Na and Cl absorption by determining unidirectional 22Na and 36Cl fluxes across isolated stripped mucosa from the rat distal colon under voltage clamp conditions. Mucosal butyrate (25 mM, in the absence of bicarbonate) significantly enhanced both net Na and net Cl absorption by 7.0 +/- 1.3 and 6.9 +/- 1.0 microEq/h.cm2, respectively, without increasing the short-circuit current. Net Na and Cl absorption in butyrate-Ringer's solution and HCO3-Ringer's solution were identical. Butyrate stimulation of Na (and Cl) absorption was Cl-dependent and prevented by 1 mM mucosal amiloride, an inhibitor of Na-H exchange, but was HCO3-independent and not inhibited by acetazolamide, a carbonic anhydrase inhibitor. In contrast, bicarbonate-stimulated Na (and Cl) absorption was also Cl-dependent and amiloride-sensitive, but was significantly inhibited by acetazolamide. The effect of mucosal butyrate on net Na and Cl absorption was substantially greater than serosal butyrate, which in the presence of bicarbonate did not alter ion transport. The stimulation of Na and Cl absorption by mucosal butyrate was significantly greater than by propionate and acetate, whereas mucosal formate did not alter Na transport. The results of this study permit the following model: short-chain fatty acid stimulation of active Na and Cl absorption involves uptake of the nonionized form of butyrate and the coupling of Na-H and Cl-butyrate exchanges.

Acetazolamide↗
PubMed1989

Effects of corticosteroid hormones on the electrophysiology of rat distal colon: implications for Na+ and K+ transport.

1. Conventional microelectrodes, the Na+ channel blocker amiloride (0.1 mM), and the K+ channel blocker tetraethylammonium chloride (TEA, 30 mM) were used to examine the effects of corticosteroid hormones administered in vivo on the Na+ and K+ transport properties of isolated rat distal colon. The cell membrane changes induced by aldosterone (a specific mineralocorticoid), RU 28362 (a synthetic glucocorticoid with negligible affinity for mineralocorticoid receptors), and dexamethasone (an activator of both mineralocorticoid and glucocorticoid receptors) were compared. 2. In control animals, there was no amiloride-sensitive apical Na+ conductance, and only a relatively small TEA-sensitive apical K+ conductance. 3. Hyperaldosteronism secondary to dietary Na+ depletion for 10-14 days, dexamethasone (600 micrograms 100 g-1 day-1 for 3 days), and RU 28362 (600 micrograms 100 g-1 day-1 for 3 days) induced amiloride-sensitive electrogenic Na+ transport, with the potency of aldosterone greater than dexamethasone greater than RU 28362. 4. With each corticosteroid, increased electrogenic Na+ transport reflected enhanced apical Na+ conductance, and in the case of aldosterone and dexamethasone, 3.3-fold and 2-fold increases respectively in the maximum activity of the basolateral Na+-K+ pump. In contrast, RU 28362 suppressed the maximum activity of the basolateral Na+-K+ pump by 45%. 5. All three corticosteroids enhanced the K+ conductance of the apical membrane, with the potency of aldosterone greater than dexamethasone greater than RU 28362. 6. Co-administration of spironolactone (5 mg 100 g-1 day-1) inhibited the effects of aldosterone on Na+ and K+ transport, but in dexamethasone-treated animals spironolactone resulted in a pattern of response similar to that found in RU 28362-treated animals. 7. The results support the view that mineralocorticoid receptors mediate changes in colonic Na+ and K+ transport which differ quantitatively and qualitatively from those mediated by glucocorticoid receptors. Dexamethasone and similar 'glucocorticoids' activate both types of receptor, with an overall epithelial response which mimics that induced by aldosterone.

Aldosterone↗
PubMed1989

Characterization of aldosterone-induced potassium secretion in rat distal colon.

The role of apical and basolateral membranes in aldosterone-induced active potassium (K) secretion in rat distal colon was investigated by measuring mucosal-to-serosal (Jms) and serosal-to-mucosal (Jsm) 42K fluxes (mueq.h-1.cm-2) across isolated stripped mucosa under short-circuit conditions in normal and secondary-hyperaldosterone animals. In normal colons mucosal tetraethylammonium (TEA; 30 mM) or barium (Ba; 5 mM), but not cesium (Cs; 15 mM), reduced Jsm without affecting Jms. In aldosterone animals (a) net K secretion (-0.54 +/- 0.11) was converted to net K absorption (0.63 +/- 0.15) by mucosal TEA, which produced a marked reduction in Jsm (0.82 +/- 0.07) and an increase in Jms (0.35 +/- 0.07). In contrast mucosal Ba resulted in a relatively smaller reduction in JK(sm) without altering JK(ms), whereas mucosal Cs was ineffective; (b) serosal bumetanide or the removal of serosal Na or Cl markedly inhibited JK(sm and abolished net K secretion; and (c) serosal ouabain (1 mM) produced qualitatively similar effects to those of serosal bumetanide. These results demonstrate that (a) normal rat distal colon contains apical TEA- and Ba-sensitive K channels; (b) aldosterone induces TEA-sensitive and Ba-sensitive apical K channels; (c) aldosterone-induced K secretion requires both the Na,K-pump and Na-K-2Cl cotransport for K uptake across the basolateral membrane; and (d) alteration of any of these processes results in inhibition of aldosterone-induced active K secretion simultaneously with stimulation of K absorption.

Aldosterone↗
PubMed1989

Regulation of active sodium and potassium transport in the distal colon of the rat. Role of the aldosterone and glucocorticoid receptors.

To determine whether mineralocorticosteroids and glucocorticosteroids have specific effects on colonic electrolyte transport, we compared the effect of aldosterone and RU 28362, a glucocorticoid receptor-specific agonist that does not bind to the aldosterone receptor, on unidirectional Na, Cl, and K fluxes across isolated mucosa of the rat distal colon. Continuous infusion of aldosterone for 7 d produced changes in four specific transport processes: induction of both active electrogenic, amiloride-sensitive sodium absorption and active electrogenic potassium secretion, enhancement of active electroneutral potassium absorption, and inhibition of electroneutral Na-Cl absorption, the predominant transport process in this epithelium. In contrast, continuous infusion of RU 28362 for 1-11 d produced a sustained increase in electroneutral Na-Cl absorption. This glucocorticoid receptor-specific agonist did not induce electrogenic sodium absorption nor affect either potassium absorption or secretion. These studies demonstrate that aldosterone (i.e., mineralocorticoid) and glucocorticoid receptors modulate separate and specific changes in active sodium and potassium transport. These results suggest that other glucocorticoids (e.g., dexamethasone, methylprednisolone) are not glucocorticoid receptor-specific and that their effects on electrogenic sodium absorption and potassium transport most likely represent the binding of these agonists to the aldosterone receptor.

Aldosterone↗