Omeprazole and SCH 28080 inhibit acid secretion by the turtle urinary bladder

Area of Science:

• Physiology
• Renal Physiology
• Ion Transport

Background:

• The distal nephron utilizes vacuolar-type H(+)-ATPase and gastric-type H(+)/K(+)-ATPase for acidification.
• The presence and role of H(+)/K(+)-ATPase in turtle bladder acidification remain unclear.

Purpose of the Study:

• To investigate the potential presence of gastric-type H(+)/K(+)-ATPase in turtle bladders.
• To determine the mechanism of acid secretion in turtle bladders using specific inhibitors.

Main Methods:

• Examined acid secretion dependence on mucosal potassium (K+).
• Assessed effects of omeprazole and SCH 28080 on electrogenic H+ secretion (RSCC).
• Investigated drug effects under conditions of inhibited acid secretion and altered K+ levels.

Main Results:

• Omeprazole and SCH 28080 dose-dependently inhibited CO2-stimulated H+ secretion.
• Inhibition was independent of mucosal K+ and unaffected by prior inhibition of acid secretion.
• These drugs stimulated HCO3- secretion, suggesting a different transport mechanism.

Conclusions:

• Turtle bladder acid secretion is not mediated by H(+)/K(+)-ATPase due to K+ independence.
• Omeprazole and SCH 28080 likely inhibit the vacuolar H(+)-ATPase in turtle bladders.
• HCO3- secretion utilizes a distinct H+ transport mechanism separate from acid secretion.