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R A Star

Publications and source records attributed to R A Star.

58 records · Page 4Linked to original sources

Calcium and cyclic adenosine monophosphate as second messengers for vasopressin in the rat inner medullary collecting duct.

UNLABELLED: Vasopressin increases both the urea permeability and osmotic water permeability in the terminal part of the renal inner medullary collecting duct (terminal IMCD). To identify the second messengers that mediate these responses, we measured urea permeability, osmotic water permeability, intracellular calcium concentration, and cyclic AMP accumulation in isolated terminal IMCDs. After addition of vasopressin, a transient rise in intracellular calcium occurred that was coincident with increases in cyclic AMP accumulation and urea permeability. Half-maximal increases in urea permeability and osmotic water permeability occurred with 0.01 nM vasopressin. The threshold concentration for a measurable increase in cyclic AMP accumulation was approximately 0.01 nM, while measurable increases in intracellular calcium required much higher vasopressin concentrations (greater than 0.1 nM). Exogenous cyclic AMP (1 mM 8-Br-cAMP) mimicked the effect of vasopressin on urea permeability but did not produce a measurable change in intracellular calcium concentration. CONCLUSIONS: (a) Cyclic AMP is the second messenger that mediates the urea permeability response to vasopressin in the rat terminal IMCD. (b) Vasopressin increases the intracellular calcium concentration in the rat terminal IMCD, but the physiological role of this response is not yet known.

Animals↗

Luminal disequilibrium pH and ammonia transport in outer medullary collecting duct [corrected and issued with original paging in Am J Physiol 1987 Aug;253(2 Pt 2)].

We measured bicarbonate, ammonia, and luminal pH in segments of the rabbit outer medullary collecting duct (OMCD) to determine the relationship between luminal pH and ammonia transport. Both the inner-stripe and outer-stripe portions of the OMCD absorbed bicarbonate at high rates. The outer stripe OMCD generated an acidic pH disequilibrium that was reversibly dissipated by exogenous luminal carbonic anhydrase. In contrast, the inner stripe OMCD did not generate a spontaneous pH disequilibrium unless perfused with the carbonic anhydrase inhibitor acetazolamide. Ammonia secretion was three times more rapid in the outer stripe OMCD than in the inner stripe OMCD. We conclude the following. 1) Both the inner-stripe and outer-stripe portions of the rabbit OMCD secrete protons at substantial rates. 2) Functional luminal carbonic anhydrase is present in the inner stripe OMCD but absent from the outer stripe OMCD. 3) Ammonia secretion occurs predominantly by NH3 diffusion in both portions. 4) The luminal pH disequilibrium, which is normally present in the outer stripe OMCD, enhances ammonia secretion.

Acetazolamide↗

Disequilibrium pH and ammonia transport in isolated perfused cortical collecting ducts.

The present study was carried out to test directly whether isolated perfused rabbit cortical collecting ducts (CCDs) spontaneously generate a luminal disequilibrium pH. We determined disequilibrium pH as the difference between 1) the actual luminal pH measured by perfusing the lumen with a membrane-impermeant pH-sensitive dye [1,4-dihydroxyphthalonitrile (1,4-DHPN)] and 2) equilibrium pH calculated from the measured total CO2 concentration in fluid collected at the end of the tubule. When the peritubular bath and perfusate had the same composition, a statistically significant acidic disequilibrium pH was found (mean -0.14 units). To determine whether the disequilibrium pH is due to an absolute lack of luminal carbonic anhydrase, we measured the effective rate constant for carbonic acid dehydration in the lumen (k-1). To do this, a lumen-to-bath NH3 concentration gradient was imposed, and the luminal pH was measured along the tubule with 1,4-DHPN. NH3 absorption caused a luminal disequilibrium pH (due to dissociation of NH+4 to NH3 and H+), whose profile along the lumen is dependent on k-1 and NH3 permeability (PNH3). PNH3 and k-1 were estimated from the luminal pH profiles using a mathematical model of proton and buffer transport. The measured k-1 (37 s-1) is within the reported range of values for uncatalyzed H2CO3 dehydration. Calculations demonstrate that the measured PNH3 (2 X 10(-3) cm/s) is high enough and the measured k-1 is low enough to explain ammonia secretion rates seen in previous studies. We conclude that proton secretion in the CCD generates an acidic luminal disequilibrium pH, associated with an absolute lack of luminal carbonic anhydrase, which enhances the net rate of NH3 secretion.

Acid-Base Equilibrium↗

Bicarbonate secretion and chloride absorption by rabbit cortical collecting ducts. Role of chloride/bicarbonate exchange.

Cortical collecting ducts (CCD) from rabbits treated with deoxycorticosterone (DOC) actively secrete bicarbonate at high rates. To investigate the mechanism of bicarbonate secretion, we measured bicarbonate and chloride transport in CCD from rabbits treated with DOC for 9-24 d. Removal of chloride (replaced with gluconate) from both perfusate and bath inhibited bicarbonate secretion without changing transepithelial voltage. Removal of chloride only from the bath increased bicarbonate secretion, while removal of chloride only from the perfusate inhibited secretion. In contrast to the effect of removing chloride, removal of sodium from both the perfusate and bath (replacement with N-methyl-D-glucamine) did not change the rate of bicarbonate secretion. The rate of bicarbonate secretion equaled the rate of chloride absorption in tubules bathed with 0.1 mM ouabain to inhibit any cation-dependent chloride transport. Under these conditions, chloride absorption occurred against an electrochemical gradient. Removal of bicarbonate from both the perfusate and bath inhibited chloride absorption. Removal of bicarbonate only from the bath inhibited chloride absorption, while removal of bicarbonate from the lumen stimulated chloride absorption. We conclude that CCD from DOC-treated rabbits actively secrete bicarbonate and actively absorb chloride by an electroneutral mechanism involving 1:1 chloride/bicarbonate exchange. The process is independent of sodium.

Absorption↗