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(Circulation Research. 1995;76:592-599.)
© 1995 American Heart Association, Inc.

Articles

Arginine Vasopressin–Induced Potentiation of Unitary L-Type Ca²⁺ Channel Current in Guinea Pig Ventricular Myocytes

Shetuan Zhang, Yuji Hirano, Masayasu Hiraoka

From the Department of Cardiovascular Diseases, Medical Research Institute, Tokyo (Japan) Medical and Dental University.

Correspondence to Yuji Hirano, MD, PhD, Department of Cardiovascular Diseases, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo 113, Japan.

Abstract The effects of arginine vasopressin (AVP) on L-type Ca²⁺ channels were studied by recording single-channel activity from cell-attached patches on isolated guinea pig ventricular myocytes, with 100 mmol/L Ba²⁺ used as the charge carrier. Bath application of AVP (100 nmol/L) reversibly increased channel open probability by a factor of 2.92±1.43 (n=15) because of the increased number of channel openings and increased open times. AVP did not change the amplitudes of single-channel currents (1.17±0.10 pA in the control condition and 1.12±0.11 pA after AVP, at +20 mV; n=6). In our experimental conditions, in which myocytes were bathed in Ca²⁺-free high-potassium solutions, AVP-induced potentiation was observed without changes in [Ca²⁺]_i measured by fura 2 fluorescence signals (estimated [Ca²⁺]_i, 80 nmol/L). The AVP-induced increase in channel open probability was abolished by OPC-21268 (8 µmol/L), a specific blocker of V₁ receptor, but not by a V₂ blocker, OPC-31260 (5 µmol/L). AVP-induced potentiation was also suppressed by a broad-spectrum protein kinase inhibitor, H7 (100 µmol/L, bath application), but not by H89 (1 µmol/L), a blocker with high specificity to protein kinase A. AVP application after the treatment by phorbol ester (phorbol 12-myristate 13-acetate, 100 nmol/L for 1 hour) failed to potentiate the channel activity. These results raised the possibility that protein kinase C might be involved during signal transduction. Our results provide direct evidence that AVP potentiates cardiac L-type Ca²⁺ currents via V₁ receptor stimulation.

Key Words: arginine vasopressin • L-type Ca²⁺ channel • V₁ receptor • protein kinase C

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