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Biomedical subjects

D D Fanestil

Publications and source records attributed to D D Fanestil.

At least 91 records · Page 5Linked to original sources

Influence of transepithelial potential difference on acidification in the toad urinary bladder.

The rate of urinary acidification by toad urinary bladders was measured in vitro by following the pH changes of the HCO3-/CO2-buffered Ringer's solutions bathing the mucosal and serosal sides of the bladder. Within the tolerated range of transepithelial potential differences (PD) (-100 to +100 mv), the rate of acidification was found to be a linear function of the PD. The rate of acidification could be increased by a favorable PD whether the PD was the spontaneous transepithelial PD due to sodium transport or a PD imposed in the absence of sodium transport, as when choline was substituted for Na or when amiloride blocked sodium transport. Acetazolamide inhibited both active and PD-driven acidification. Acidification rate was the same in 2.4 mM HCO3- and 1% CO2 as in 12 mM HCO3- and 5% CO2; again, acidification was increased equally by a favorable PD. PD-driven acidification was found to be linearly correlated with acidification occurring at short-circuit conditions. These findings suggest that the rate of acidification can be accelerated by the transepithelial PD in the absence of sodium transport and that the PD-driven component of acidification utilizes a transcellular pathway.

Acetazolamide↗

Corticoid receptors in rat brain: evidence for an aldosterone receptor.

The existence of high and low affinity mineralocorticoid-binding macromolecules (receptors) has been demonstrated in vitro in cytosols derived from the adrenalectomized rat brain by the specific binding of [3H]aldosterone (3H-A). The high-affinity aldosterone sites can be distinguished from those sites which have a higher affinity for either [3H]dexamethasone (3H-DM) or [3H]corticosterone (3H-B) on the basis of selectivity for spirolactone SC-9420 or non-radioactive A, DM, and B. The binding of 3H-A to the receptors was maximal after 2 hours of incubation of 0-4C. No significant binding of 3H-A to the receptors could be demonstrated when incubations of the radioactive ligand were performed at either 20 or 37 C, indicating that the receptor is heat-liabile. Scatchard analysis of the 3H-A binding data over a 200-fold concentration range of 3H-A indicated that there are two binding sites for aldosterone, a high affinity component (a1) with a Kd approximately equal to 1.5 X 10(-9)M and a low-affinity component (a2) with a Kd approximately equal to 6.3 X 10(-8)M. A similar study using 3H-DM as the radioactive ligand demonstrated only one site for the 3H-DM binding with a Kd = 6.2 X 10(-9)M. The presence of specific aldosterone receptors in the brain with high affinity, limited capacity, and selectivity for aldosterone suggests a possible extra-renal mechanism of action of the hormone in or mediated through the CNS.

Aldosterone↗

Etiology of postobstructive diuresis: ouabain-sensitive adenosine triphosphatase deficit and elevated solute excretion in the postobstructed dog kidney.

A selective deficit in ouabain-sensitive adenosine triphosphatase has been shown in unilaterally obstructed dog kidneys; the deficit correlates inversely with Na+ and K+ excretion following relief of obstruction. It is postulated that the enzymatic defect may play a role in the etiology of postobstructive diuresis.

Adenosine Triphosphatases↗

Inhibition of active sodium transport by radiographic contrast media.

We demonstrate that salts of diatrizoate and iothalamate, radiographic contrast agents, depress the active transport of sodium in the urinary bladder of the Columbian toad, Bufo marinus. Isolated toad bladders were incubated in isotonic Ringer's solutions with isosmolar displacement of sodium chloride by contrast media in experimental solutions. Sodium transport as measured both by short-circuit current (SCC) and by isotopic sodium flux was significantly depressed in the presence of sodium diatrizoate. Sodium transport measured by SCC was significantly depressed with sodium iothalamate and meglumine iothalamate. Equimolar methylsulfate Ringer's solution did not depress SCC. Although contrast media in isotonic Ringer's solutions depressed basal SCC, the vasopressin-stimulated increment in SCC was not depressed by contrast media. Separate experiments with hyperosmolar solutions (786 mM, as utilized in angiography) demonstrated equivalent suppression of SCC by contrast media and by other solutions made hyperosmolar with glucose or sodium methylsulfate, implying a general or nonspecific effect of hyperosomolarity. Inhibition of SCC by contrast media was reversible when the agents were removed by serial changes with standard Ringer's solution. Inhibition of sodium transport by contrast media might provide a basis for studies on some of the clinical toxicities of these agents.

Animals↗