Prostaglandin E2 regulation of ion transport is absent in medullary thick ascending limbs from SHR

David Good, Carlton R. Caflisch, Thampi George

Research output: Contribution to journalArticle

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Abstract

Regulation of HCO3 - and Cl- absorption by arginine vasopressin (AVP) and prostaglandin E2 (PGE2) was examined in isolated, perfused medullary thick ascending limbs (MTAL) from 4- to 7-wk-old spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. AVP inhibited HCO3 - absorption by 50% at 10-10 M and by 25% at 2 × 10-12 M in MTAL from both WKY and SHR. Cholera toxin (10-9 M) or forskolin (10-6 M) in the bath also inhibited HCO3 - absorption by 50% in the SHR. In MTAL from WKY, PGE2 (10-6 M in the bath) increased HCO3 - absorption from 7.1 ± 0.4 to 12.0 ± 0.4 pmol· min-1·mm-1 (P < 0.005) and decreased Cl- absorption from 65 ± 7 to 47 ± 6 pmol·min-1·mm-1 (P < 0.001) in the presence of 10-10 M AVP. Under the same conditions, PGE2 had no effect on HCO3 - or Cl- absorption in MTAL from SHR. PGE2 also reversed submaximal inhibition of HCO3 - absorption by 2 × 10-12 M AVP in WKY but not in SHR. With 10-10 M AVP in the bath, phorbol 12-myristate 13-acetate (10-6 M in the bath) increased HCO3 - absorption from 6.6 ± 0.5 to 12.3 ± 0.4 pmol·min-1·mm-1 in MTAL from WKY and from 7.6 ± 0.7 to 12.6 ± 1.2 pmol·min-1·mm-1 in MTAL from SHR (P < 0.005). These results demonstrate that 1) the effects of PGE2 to stimulate HCO3 - absorption and inhibit Cl- absorption in the presence of AVP are absent in MTAL from SHR, 2) the defect may involve an inability of PGE2 to stimulate protein kinase C, and 3) regulation of HCO3 - absorption by AVP via adenosine 3′,5′-cyclic monophosphate is similar in MTAL from WKY and SHR. The lack of PGE2 inhibition of NaCl absorption in the MTAL may contribute to renal salt retention during the development of hypertension in the SHR.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Volume269
Issue number1 38-1
StatePublished - Jul 1995

Fingerprint

Ion Transport
Dinoprostone
Extremities
Arginine Vasopressin
Baths
Inbred WKY Rats
Cholera Toxin
Colforsin
Adenosine
Protein Kinase C
Acetates
Salts
Hypertension

Keywords

  • Adenosine 3′,5′-cyclic monophosphate
  • Arginine vasopressin
  • Essential hypertension
  • Loop of Henle
  • Protein kinase C
  • Spontaneously hypertensive rat

ASJC Scopus subject areas

  • Physiology
  • Medicine(all)

Cite this

Prostaglandin E2 regulation of ion transport is absent in medullary thick ascending limbs from SHR. / Good, David; Caflisch, Carlton R.; George, Thampi.

In: American Journal of Physiology - Renal Fluid and Electrolyte Physiology, Vol. 269, No. 1 38-1, 07.1995.

Research output: Contribution to journalArticle

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abstract = "Regulation of HCO3 - and Cl- absorption by arginine vasopressin (AVP) and prostaglandin E2 (PGE2) was examined in isolated, perfused medullary thick ascending limbs (MTAL) from 4- to 7-wk-old spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. AVP inhibited HCO3 - absorption by 50{\%} at 10-10 M and by 25{\%} at 2 × 10-12 M in MTAL from both WKY and SHR. Cholera toxin (10-9 M) or forskolin (10-6 M) in the bath also inhibited HCO3 - absorption by 50{\%} in the SHR. In MTAL from WKY, PGE2 (10-6 M in the bath) increased HCO3 - absorption from 7.1 ± 0.4 to 12.0 ± 0.4 pmol· min-1·mm-1 (P < 0.005) and decreased Cl- absorption from 65 ± 7 to 47 ± 6 pmol·min-1·mm-1 (P < 0.001) in the presence of 10-10 M AVP. Under the same conditions, PGE2 had no effect on HCO3 - or Cl- absorption in MTAL from SHR. PGE2 also reversed submaximal inhibition of HCO3 - absorption by 2 × 10-12 M AVP in WKY but not in SHR. With 10-10 M AVP in the bath, phorbol 12-myristate 13-acetate (10-6 M in the bath) increased HCO3 - absorption from 6.6 ± 0.5 to 12.3 ± 0.4 pmol·min-1·mm-1 in MTAL from WKY and from 7.6 ± 0.7 to 12.6 ± 1.2 pmol·min-1·mm-1 in MTAL from SHR (P < 0.005). These results demonstrate that 1) the effects of PGE2 to stimulate HCO3 - absorption and inhibit Cl- absorption in the presence of AVP are absent in MTAL from SHR, 2) the defect may involve an inability of PGE2 to stimulate protein kinase C, and 3) regulation of HCO3 - absorption by AVP via adenosine 3′,5′-cyclic monophosphate is similar in MTAL from WKY and SHR. The lack of PGE2 inhibition of NaCl absorption in the MTAL may contribute to renal salt retention during the development of hypertension in the SHR.",
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T1 - Prostaglandin E2 regulation of ion transport is absent in medullary thick ascending limbs from SHR

AU - Good, David

AU - Caflisch, Carlton R.

AU - George, Thampi

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N2 - Regulation of HCO3 - and Cl- absorption by arginine vasopressin (AVP) and prostaglandin E2 (PGE2) was examined in isolated, perfused medullary thick ascending limbs (MTAL) from 4- to 7-wk-old spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. AVP inhibited HCO3 - absorption by 50% at 10-10 M and by 25% at 2 × 10-12 M in MTAL from both WKY and SHR. Cholera toxin (10-9 M) or forskolin (10-6 M) in the bath also inhibited HCO3 - absorption by 50% in the SHR. In MTAL from WKY, PGE2 (10-6 M in the bath) increased HCO3 - absorption from 7.1 ± 0.4 to 12.0 ± 0.4 pmol· min-1·mm-1 (P < 0.005) and decreased Cl- absorption from 65 ± 7 to 47 ± 6 pmol·min-1·mm-1 (P < 0.001) in the presence of 10-10 M AVP. Under the same conditions, PGE2 had no effect on HCO3 - or Cl- absorption in MTAL from SHR. PGE2 also reversed submaximal inhibition of HCO3 - absorption by 2 × 10-12 M AVP in WKY but not in SHR. With 10-10 M AVP in the bath, phorbol 12-myristate 13-acetate (10-6 M in the bath) increased HCO3 - absorption from 6.6 ± 0.5 to 12.3 ± 0.4 pmol·min-1·mm-1 in MTAL from WKY and from 7.6 ± 0.7 to 12.6 ± 1.2 pmol·min-1·mm-1 in MTAL from SHR (P < 0.005). These results demonstrate that 1) the effects of PGE2 to stimulate HCO3 - absorption and inhibit Cl- absorption in the presence of AVP are absent in MTAL from SHR, 2) the defect may involve an inability of PGE2 to stimulate protein kinase C, and 3) regulation of HCO3 - absorption by AVP via adenosine 3′,5′-cyclic monophosphate is similar in MTAL from WKY and SHR. The lack of PGE2 inhibition of NaCl absorption in the MTAL may contribute to renal salt retention during the development of hypertension in the SHR.

AB - Regulation of HCO3 - and Cl- absorption by arginine vasopressin (AVP) and prostaglandin E2 (PGE2) was examined in isolated, perfused medullary thick ascending limbs (MTAL) from 4- to 7-wk-old spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. AVP inhibited HCO3 - absorption by 50% at 10-10 M and by 25% at 2 × 10-12 M in MTAL from both WKY and SHR. Cholera toxin (10-9 M) or forskolin (10-6 M) in the bath also inhibited HCO3 - absorption by 50% in the SHR. In MTAL from WKY, PGE2 (10-6 M in the bath) increased HCO3 - absorption from 7.1 ± 0.4 to 12.0 ± 0.4 pmol· min-1·mm-1 (P < 0.005) and decreased Cl- absorption from 65 ± 7 to 47 ± 6 pmol·min-1·mm-1 (P < 0.001) in the presence of 10-10 M AVP. Under the same conditions, PGE2 had no effect on HCO3 - or Cl- absorption in MTAL from SHR. PGE2 also reversed submaximal inhibition of HCO3 - absorption by 2 × 10-12 M AVP in WKY but not in SHR. With 10-10 M AVP in the bath, phorbol 12-myristate 13-acetate (10-6 M in the bath) increased HCO3 - absorption from 6.6 ± 0.5 to 12.3 ± 0.4 pmol·min-1·mm-1 in MTAL from WKY and from 7.6 ± 0.7 to 12.6 ± 1.2 pmol·min-1·mm-1 in MTAL from SHR (P < 0.005). These results demonstrate that 1) the effects of PGE2 to stimulate HCO3 - absorption and inhibit Cl- absorption in the presence of AVP are absent in MTAL from SHR, 2) the defect may involve an inability of PGE2 to stimulate protein kinase C, and 3) regulation of HCO3 - absorption by AVP via adenosine 3′,5′-cyclic monophosphate is similar in MTAL from WKY and SHR. The lack of PGE2 inhibition of NaCl absorption in the MTAL may contribute to renal salt retention during the development of hypertension in the SHR.

KW - Adenosine 3′,5′-cyclic monophosphate

KW - Arginine vasopressin

KW - Essential hypertension

KW - Loop of Henle

KW - Protein kinase C

KW - Spontaneously hypertensive rat

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M3 - Article

VL - 269

JO - American Journal of Physiology - Endocrinology and Metabolism

JF - American Journal of Physiology - Endocrinology and Metabolism

SN - 0193-1849

IS - 1 38-1

ER -