PMID- 7631800
OWN - NLM
STAT- MEDLINE
DCOM- 19950901
LR  - 20171213
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 269
IP  - 1 Pt 1
DP  - 1995 Jul
TI  - Enzyme- and mineralocorticoid receptor-controlled electrogenic Na+ absorption in 
      human rectum in vitro.
PG  - G42-8
AB  - In vivo electrogenic Na+ absorption (JeNa) in the human rectum is controlled by 
      acute variation of aldosterone in nanomolar concentration range. In this study we 
      report both the induction of JeNa in human rectum epithelium by nanomolar 
      aldosterone added in vitro and the enzymatic control of glucocorticoid action on 
      JeNa. JeNa was measured as amiloride-sensitive short-circuit current 8 h after 
      addition of the respective steroid. Aldosterone (10 nM) caused JeNa of 5.7 +/- 
      1.4 mumol.h-1.cm-2. Cortisol in the same concentration did not induce significant 
      JeNa. Because cortisol is readily inactivated by 11 beta-hydroxysteroid 
      dehydrogenase (11 beta-HSD), the true mineralocorticoid activity of cortisol was 
      evaluated after inhibition of 11 beta-HSD by carbenoxolone. Carbenoxolone alone 
      did not exhibit mineralocorticoid activity. If cortisol (10 nM) was given 
      together with carbenoxolone (1 microM), the resulting JeNa (4.5 +/- 0.4 
      mumol.h-1.cm-2) was not significantly different from that after 10 nM 
      aldosterone, indicating equal intrinsic mineralocorticoid activity of cortisol 
      and aldosterone. The same mechanisms were found in rat late distal colon. Kinetic 
      data of carbenoxolone at 10 nM cortisol resulted in a Michaelis constant of 0.3 
      microMs, maximal absorption of 8.4 mumol.h-1.cm-2, and a Hill coefficient of 1.8. 
      The effects of carbenoxolone and glycyrrhetinic acid did not differ. We conclude 
      that JeNa is under complete control of mineralocorticoid action. "Spontaneous" 
      JeNa in the beginning of the in vitro period can be explained by elevated steroid 
      levels before tissue removal.(ABSTRACT TRUNCATED AT 250 WORDS)
FAU - Epple, H J
AU  - Epple HJ
AD  - Institut fur Klinische Physiologie, Universitatsklinikum Benjamin Franklin, Freie 
      Universitat Berlin, Germany.
FAU - Schulzke, J D
AU  - Schulzke JD
FAU - Schmitz, H
AU  - Schmitz H
FAU - Fromm, M
AU  - Fromm M
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Am J Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 0 (Receptors, Mineralocorticoid)
RN  - 4964P6T9RB (Aldosterone)
RN  - 9NEZ333N27 (Sodium)
RN  - EC 1.1.- (Hydroxysteroid Dehydrogenases)
RN  - EC 1.1.1.146 (11-beta-Hydroxysteroid Dehydrogenases)
RN  - MM6384NG73 (Carbenoxolone)
RN  - WI4X0X7BPJ (Hydrocortisone)
SB  - IM
MH  - 11-beta-Hydroxysteroid Dehydrogenases
MH  - Absorption
MH  - Aged
MH  - Aldosterone/pharmacology
MH  - Carbenoxolone/pharmacology
MH  - Colon/metabolism
MH  - Dose-Response Relationship, Drug
MH  - Electrophysiology
MH  - Female
MH  - Humans
MH  - Hydrocortisone/pharmacology
MH  - Hydroxysteroid Dehydrogenases/antagonists & inhibitors/*physiology
MH  - In Vitro Techniques
MH  - Male
MH  - Middle Aged
MH  - Receptors, Mineralocorticoid/*physiology
MH  - Rectum/*metabolism
MH  - Sodium/*metabolism
EDAT- 1995/07/01 00:00
MHDA- 1995/07/01 00:01
CRDT- 1995/07/01 00:00
PHST- 1995/07/01 00:00 [pubmed]
PHST- 1995/07/01 00:01 [medline]
PHST- 1995/07/01 00:00 [entrez]
AID - 10.1152/ajpgi.1995.269.1.G42 [doi]
PST - ppublish
SO  - Am J Physiol. 1995 Jul;269(1 Pt 1):G42-8. doi: 10.1152/ajpgi.1995.269.1.G42.