Phorbol myristate acetate and dioctanoylglycerol inhibit transport in rabbit proximal convoluted tubule

M. Baum, S. R. Hays

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Abstract

The present in vitro microperfusion study examined the effect of protein kinase C activation on transport in the rabbit proximal convoluted tubule (PCT). PCT were perfused with an ultrafiltrate-like solution and were bathed in a serumlike albumin solution. Addition of 5 x 10-8 and 5 x 10-7 M bath phorbol 12-myristate 13-acetate, an activator of protein kinase C, inhibited volume absorption from 1.06 ± 0.10 to 0.77 ± 0.07 nl·mm-1·min-1 (P < 0.05) and 0.76 ± 0.14 to 0.48 ± 0.08 nl·mm-1·min-1 (P < 0.01), respectively. Bath phorbol 12-myristate 13-acetate (5 x 10-9 M) had no effect on volume absorption (J(v), 0.82 ± 0.13 to 0.81 ± 0.12 nl·mm-1·min-1). In contrast, 5 x 10-8 M bath 4α-phorbol, an inactive phorbol that does not activate protein kinase C, had no effect on J(v) (0.95 ± 0.14 to 0.94 ± 0.11 nl·mm-1·min-1). Bath L-α-dioctanoylglycerol (10-4 M), another known activator of protein kinase C, inhibited volume absorption from 0.96 ± 0.08 to 0.71 ± 0.08 nl·mm-1·min-1 (P < 0.001). A 10-fold lower concentration of L-α-dioctanoylglycerol (10-5 M) had no effect on J(v) (0.81 ± 0.18 to 0.78 ± 0.17 nl·mm-1·min-1). Both 5 x 10-8 M phorbol 12-myristate 13-acetate and 10-4 M L-α-dioctanoylglycerol inhibited glucose, bicarbonate, and chloride transport in the PCT. These data are consistent with protein kinase C activation playing a role in the modulation of proximal tubular transport.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Volume254
Issue number1
StatePublished - 1988

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Tetradecanoylphorbol Acetate
Protein Kinase C
Baths
Rabbits
Acetates
Bicarbonates
Chlorides
Albumins
Glucose
phorbol-12-myristate
phorbol

ASJC Scopus subject areas

  • Physiology

Cite this

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title = "Phorbol myristate acetate and dioctanoylglycerol inhibit transport in rabbit proximal convoluted tubule",
abstract = "The present in vitro microperfusion study examined the effect of protein kinase C activation on transport in the rabbit proximal convoluted tubule (PCT). PCT were perfused with an ultrafiltrate-like solution and were bathed in a serumlike albumin solution. Addition of 5 x 10-8 and 5 x 10-7 M bath phorbol 12-myristate 13-acetate, an activator of protein kinase C, inhibited volume absorption from 1.06 ± 0.10 to 0.77 ± 0.07 nl·mm-1·min-1 (P < 0.05) and 0.76 ± 0.14 to 0.48 ± 0.08 nl·mm-1·min-1 (P < 0.01), respectively. Bath phorbol 12-myristate 13-acetate (5 x 10-9 M) had no effect on volume absorption (J(v), 0.82 ± 0.13 to 0.81 ± 0.12 nl·mm-1·min-1). In contrast, 5 x 10-8 M bath 4α-phorbol, an inactive phorbol that does not activate protein kinase C, had no effect on J(v) (0.95 ± 0.14 to 0.94 ± 0.11 nl·mm-1·min-1). Bath L-α-dioctanoylglycerol (10-4 M), another known activator of protein kinase C, inhibited volume absorption from 0.96 ± 0.08 to 0.71 ± 0.08 nl·mm-1·min-1 (P < 0.001). A 10-fold lower concentration of L-α-dioctanoylglycerol (10-5 M) had no effect on J(v) (0.81 ± 0.18 to 0.78 ± 0.17 nl·mm-1·min-1). Both 5 x 10-8 M phorbol 12-myristate 13-acetate and 10-4 M L-α-dioctanoylglycerol inhibited glucose, bicarbonate, and chloride transport in the PCT. These data are consistent with protein kinase C activation playing a role in the modulation of proximal tubular transport.",
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T1 - Phorbol myristate acetate and dioctanoylglycerol inhibit transport in rabbit proximal convoluted tubule

AU - Baum, M.

AU - Hays, S. R.

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N2 - The present in vitro microperfusion study examined the effect of protein kinase C activation on transport in the rabbit proximal convoluted tubule (PCT). PCT were perfused with an ultrafiltrate-like solution and were bathed in a serumlike albumin solution. Addition of 5 x 10-8 and 5 x 10-7 M bath phorbol 12-myristate 13-acetate, an activator of protein kinase C, inhibited volume absorption from 1.06 ± 0.10 to 0.77 ± 0.07 nl·mm-1·min-1 (P < 0.05) and 0.76 ± 0.14 to 0.48 ± 0.08 nl·mm-1·min-1 (P < 0.01), respectively. Bath phorbol 12-myristate 13-acetate (5 x 10-9 M) had no effect on volume absorption (J(v), 0.82 ± 0.13 to 0.81 ± 0.12 nl·mm-1·min-1). In contrast, 5 x 10-8 M bath 4α-phorbol, an inactive phorbol that does not activate protein kinase C, had no effect on J(v) (0.95 ± 0.14 to 0.94 ± 0.11 nl·mm-1·min-1). Bath L-α-dioctanoylglycerol (10-4 M), another known activator of protein kinase C, inhibited volume absorption from 0.96 ± 0.08 to 0.71 ± 0.08 nl·mm-1·min-1 (P < 0.001). A 10-fold lower concentration of L-α-dioctanoylglycerol (10-5 M) had no effect on J(v) (0.81 ± 0.18 to 0.78 ± 0.17 nl·mm-1·min-1). Both 5 x 10-8 M phorbol 12-myristate 13-acetate and 10-4 M L-α-dioctanoylglycerol inhibited glucose, bicarbonate, and chloride transport in the PCT. These data are consistent with protein kinase C activation playing a role in the modulation of proximal tubular transport.

AB - The present in vitro microperfusion study examined the effect of protein kinase C activation on transport in the rabbit proximal convoluted tubule (PCT). PCT were perfused with an ultrafiltrate-like solution and were bathed in a serumlike albumin solution. Addition of 5 x 10-8 and 5 x 10-7 M bath phorbol 12-myristate 13-acetate, an activator of protein kinase C, inhibited volume absorption from 1.06 ± 0.10 to 0.77 ± 0.07 nl·mm-1·min-1 (P < 0.05) and 0.76 ± 0.14 to 0.48 ± 0.08 nl·mm-1·min-1 (P < 0.01), respectively. Bath phorbol 12-myristate 13-acetate (5 x 10-9 M) had no effect on volume absorption (J(v), 0.82 ± 0.13 to 0.81 ± 0.12 nl·mm-1·min-1). In contrast, 5 x 10-8 M bath 4α-phorbol, an inactive phorbol that does not activate protein kinase C, had no effect on J(v) (0.95 ± 0.14 to 0.94 ± 0.11 nl·mm-1·min-1). Bath L-α-dioctanoylglycerol (10-4 M), another known activator of protein kinase C, inhibited volume absorption from 0.96 ± 0.08 to 0.71 ± 0.08 nl·mm-1·min-1 (P < 0.001). A 10-fold lower concentration of L-α-dioctanoylglycerol (10-5 M) had no effect on J(v) (0.81 ± 0.18 to 0.78 ± 0.17 nl·mm-1·min-1). Both 5 x 10-8 M phorbol 12-myristate 13-acetate and 10-4 M L-α-dioctanoylglycerol inhibited glucose, bicarbonate, and chloride transport in the PCT. These data are consistent with protein kinase C activation playing a role in the modulation of proximal tubular transport.

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