Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P41181 (collecting duct)
 5,183 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The collecting ducts are thought to represent a low-capacity high-gradient acidification system. However, the inaccessibility of the various regions of the collecting duct system has prevented direct segmental analysis of its contribution to distal acidification. The present in vitro microperfusion studies compare bicarbonate transport (in pmol . mm-1 . min-1) in rabbit cortical (CCT) and outer medullary collecting tubules (MCT) perfused and bathed with symmetrical Ringer bicarbonate solution at pH 7.4. Cortical segments from normal animals exhibited no net bicarbonate transport (-2.15 +/- 1.93) whereas MCT from normal animals reabsorbed bicarbonate at a rate of 11.3 +/- 1.4. Both bicarbonate reabsorption and the lumen-positive voltage (+9.4 +/- 1.1 mV) in MCT were totally inhibited by 10(-4) M acetazolamide. CCT from NH4Cl-treated rabbits demonstrated significant bicarbonate reabsorption (1.8 +/- 0.7) when perfused at slow rates. CCT harvested from animals given a NaHCO3 load for 48 h prior to death secreted bicarbonate (-6.2 +/- 2.5). These studies confirm earlier observations of the ability of the CCT to reabsorb or secrete bicarbonate. In addition, they demonstrate significant axial heterogeneity in acidification in the collecting duct system and identify the outer medullary collecting tubule from inner stripe of outer medulla as a segment of major capacity.
 ...
PMID:Bicarbonate transport in cortical and outer medullary collecting tubules. 682 61

We examined the effects of trimethoprim (TMP) on metabolic parameters and renal ATPases in rats after a 90 minute infusion (9.6 mg/hr/kg body wt, i.v.) and after 14 days (20 mg/kg body wt/day, i.p.). After one dose of TMP, plasma electrolytes, arterial pH and aldosterone levels were normal, but a natriuresis, bicarbonaturia, and decreased urinary potassium excretion occurred. Na-K-ATPase activity in microdissected segments from these animals was decreased by 36 +/- 0.9% in proximal convoluted tubule (PCT) (P < 0.005); decreases of 50 +/- 2.1% and 40 +/- 1.1% were seen in cortical and medullary collecting tubules (CCT and MCT), respectively (P < 0.005). Na-K-ATPase activity was unaffected in medullary thick ascending limb (MTAL). H-ATPase (in PCT and collecting duct) and H-K-ATPase (in CCT and MCT)-activities were not changed. Following chronic TMP administration, plasma potassium increased as compared to control (5.16 +/- 0.05 mEq/liter vs. 3.97 +/- 0.05 mEq/liter, P < 0.05), however, acid-base status and plasma aldosterone levels were normal. Na-K-ATPase activity was decreased by 45 +/- 2.6% in PCT (P < 0.005), 73 +/- 2.0% in CCT (P < 0.001), and 53 +/- 2.5% in MCT (P < 0.005). Na-K-ATPase, activity in MTAL and H-K-ATPase activity in CCT and MCT were unchanged. H-ATPase activity in PCT and MTAL was normal, but in the collecting tubule (CCT and MCT) it was decreased by approximately 25% (P < 0.05). TMP inhibited Na-K-ATPase activity in a dose-dependent fashion in PCT, CCT, and MCT when tubules from normal animals were incubated in vitro with the drug; TMP in vitro did not affect H-ATPase or H-K-ATPase activity. These results suggest that TMP-induced hyperkalemia may result from decreased urinary potassium excretion caused by inhibition of distal Na-K-ATPase, in the face of intact H-K-ATPase activity.
 ...
PMID:Studies on the mechanism of trimethoprim-induced hyperkalemia. 873 Nov 2