This is different to the case for animal models, because only NBCn1 (SLC4A7) mediates the Na [sup]+ -dependent bicarbonate transport that is, important for acid extrusion in the smooth muscle cells of mice mesenteric, coronary, and cerebral small arteries.
sup],, It has been demonstrated that Na [sup]+ -dependent bicarbonate transport include five members of the SLC4 family, including two electrogenic NBC (NBCe1/SLC4A4 and NBCe2/SLC4A5), 1 electroneutral Na [sup]+-HCO[sub]3 [sup]− cotransporter (NBCn1/SLC4A7) and 2 Na [sup]+ -dependent Cl[sup]− /HCO[sub]3 [sup]− exchangers (NCBE/SLC4A10 and NDCBE/SLC4A8).
NBCn1 (slc4a7) mediates the Na+-dependent bicarbonate transport important for regulation of intracellular pH in mouse vascular smooth muscle cells.
These results led to speculation that chloride-dependent bicarbonate transport might be involved in fluid alkalinization.
After a new alkalinization rate was established, a bicarbonate transport inhibitor, SITS (4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid, [10.
Two experiments investigating dependent and independent bicarbonate transport mechanisms are shown in Table III.
3] M), a bicarbonate transport inhibitor, when applied to the luminal medium, had no statistically significant effect on the alkalinization rate after luminal exposure to chloride (Table III).
Addition of the bicarbonate transport inhibitor, SITS ([10.
Such a scenario has been observed in the rat parotid acini: SITS, an inhibitor of bicarbonate transport, increased intracellular pH and was thought to stimulate bicarbonate secretion via anion channels (Pirani et al.
Such mechanisms for bicarbonate transport have been demonstrated in renal proximal tubule (Yoshitomi et al.