Role of intracellular calcium in renal proximal tubule cell volume regulation

Abstract

Osmoregulatory Ca2+ signaling in hypotonic solutions was studied with videometric techniques in 158 proximal renal tubules isolated from the teleost Carassius auratus. Absence of extracellular Ca2+, hypoxia (23 mmHg), or NaCN (3 mM) did not alter regulatory volume decreases (RVD). Nevertheless, decrements of intracellular Ca2+ via the A23187 ionophore or after intracellular Ca2+ chelation with indo-1/AM (5 microM) inhibited RVD. In tubules depleted of Ca2+, RVD could only be fully elicited when intracellular Ca2+ pulses were given within 1 min after hypotonic stimulation. While inhibition of Ca2+ release from the endoplasmic reticulum (ER) with 8-(diethylamino)octyl 3,4,5-trimethoxybenzoate hydrochloride (TMB-8, 50 microM) blunted RVD, some of its effects could be reversed with the anion carrier tributyltin (1 microM). Dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP, 0.5 and 1.0 mM) and forskolin (0.25 mM) also impeded RVD; however, their effects could be partially reversed with the K+ ionophore gramicidin (0.5 microM). In conclusion, in Carassius auratus proximal renal tubule cells, RVD is activated by an intracellular Ca2+ signal that likely emanates from the ER and not from the extracellular media or the mitochondrial Ca2+ pool. Ca2+ activation of a cAMP-modulated osmoregulatory K+ channel appears to play an important role.

Metabolic and ionic responses of trout hepatocytes to anisosmotic exposure

“…In fish, a strict dependence of RVD on [Ca 2+ ]i has been reported for goldfish renal proximal tubule cells (Terreros and Kanli, 1992), whereas no requirement for Ca 2+ has been documented in trout tubule cells (Kanli and Norderhus, 1998). In the present study, the importance of [Ca 2+ ]i changes for RVD and RVI has not been specifically addressed, but our results clearly showed that anisosmotic conditions evoke alterations of [Ca 2+ ]i in trout hepatocytes (Figs·5,·6).…”

Cell swelling increases intracellular calcium in Necturuserythrocytes

“…In some instances, RVD strictly depends on Ca 2+ influx across the plasma membrane (Montrose-Rafizadeh and Guggino, 1991;Wong et al, 1990), whereas in other cell types the Ca 2+ response is mediated by Ca 2+ release from intracellular stores (Negulescu et al, 1992;Terreros and Kanli, 1992). In addition, although it has been suggested that Ca 2+ can directly activate ion channels during RVD (Hazama and Okada, 1990;McCarty and O'Neil, 1992), there also is evidence that several Ca 2+ -This study examined the role of Ca 2+ in regulatory volume decrease by Necturus erythrocytes.…”

Calcium-induced calcium release participates in cell volume regulation of rabbit TALH cells

“…In these systems, the volume regulation can be inhibited by removing extracellular calcium or by the presence of calcium channel blockers [45,47]. In other cell types, RVD is mainly dependent on calcium release from intracellular stores [2,29,38]. For example, in rat inner medullary collecting duct cells (IMCD), cell swelling in hyposmotic solutions leads to a biphasic calcium response, in which the early transient phase is due to the mobilization of calcium from intracellular stores while the later sustained phase represents entry of extracellular calcium across the plasma membrane [39,40].…”