Vasopressin increases cytosolic free calcium in LLC-PK1 cells through a V1-receptor.
We examined the effects of arginine vasopressin (AVP), parathyroid hormone (PTH), and bradykinin (BK) on the cytosolic free calcium concentration ([Ca]i) in cultured LLC-PK1 and MDCK kidney cell lines by use of the fluorescent Ca chelator fura-2. In LLC-PK1 cells, the addition of AVP but not [1-desamino-8-D-arginine]vasopressin (dDAVP, V2 agonist), PTH, or BK (10(-6) M) caused a significant increase in [Ca]i. The AVP-induced increase in [Ca]i from 61 +/- 6 to 225 +/- 44 nM (n = 7, P less than 0.01) was rapid and transient, returning to base line in 2 to 3 min. The effect of AVP was dose dependent and was present at 1 (61% increase) but not 5 min after extracellular Ca was removed. The effect of 10(-6) M AVP could be blocked with the pressor (V1) antagonist, d(CH2)5Tyr(Me)AVP, but not dDAVP. In MDCK cells, BK, but not AVP and PTH, increased [Ca]i from 146 +/- 11 to 281 +/- 31 nM (n = 9, P less than 0.001). The removal of extracellular Ca (5 min), reduced but did not abolish this effect. These results indicate that [Ca]i mobilized by activation of V1-receptors may mediate AVP-regulated function in some transporting epithelia.
D001127:Arginine Vasopressin / Q000494:pharmacology; D001920:Bradykinin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D002460:Cell Line; D003600:Cytosol / Q000378:metabolism*; D007668:Kidney / Q000166:cytology / Q000378:metabolism*; D010281:Parathyroid Hormone / Q000494:pharmacology; D011945:Receptors, Angiotensin / Q000502:physiology*; D017483:Receptors, Vasopressin; D014667:Vasopressins / Q000378:metabolism / Q000494:pharmacology*
D010281:Parathyroid Hormone; D011945:Receptors, Angiotensin; D017483:Receptors, Vasopressin; D014667:Vasopressins; D001127:Arginine Vasopressin; D001920:Bradykinin; D002118:Calcium