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BAY K 8644-induced oscillations in rabbit gall-bladder transepithelial potential difference.
Pflugers Archiv : European Journal of Physiology
|May 1, 1986
Summary
The calcium channel activator BAY K 8644 causes oscillations in rabbit gallbladder potential difference. It also inhibits sodium absorption by affecting the mucosa-to-serosa flux.
Area of Science:
- Physiology
- Pharmacology
- Cell Biology
Background:
- The rabbit gallbladder is a model for studying epithelial transport.
- Calcium channels play a crucial role in regulating cellular functions, including ion transport.
Purpose of the Study:
- To investigate the effects of the calcium channel activator BAY K 8644 on rabbit gallbladder epithelial transport.
- To determine the impact of BAY K 8644 on transepithelial potential difference, electrical resistance, and sodium fluxes.
Main Methods:
- Experiments were conducted on isolated rabbit gallbladders.
- Transepithelial potential difference (Pd), electrical resistance (Rt), and unidirectional Na+-fluxes were measured.
- The effects of BAY K 8644 at various concentrations were analyzed.
- Nifedipine was used to block calcium channels.
Main Results:
- BAY K 8644 induced regular oscillations in transepithelial Pd (18 mHz, 30-35 microV) without altering mean Pd or Rt.
- Oscillations were primarily elicited from the serosal side.
- A concentration of 10(-5) M BAY K 8644 reduced net Na+ absorption by 16% by inhibiting the mucosa-to-serosa flux.
- Nifedipine blocked the Pd oscillations but did not reverse the Na+ transport inhibition.
Conclusions:
- BAY K 8644 activates calcium channels, leading to increased intracellular calcium concentration.
- This activation results in oscillatory changes in gallbladder potential difference and reduced sodium absorption.
- The findings suggest a role for calcium signaling in regulating gallbladder epithelial transport.