Mechanism of bradykinin, ADH, and cAMP interaction in rabbit cortical collecting duct

Research output: Chapter in Book/Report/Conference proceedingChapter

22 Citations (Scopus)

Abstract

Vasopressin (ADH) and bradykinin (BK) have been shown to stimulate prostaglandin synthesis in rabbit cortical collecting tubules. We studied ADH and BK effects on osmotic water flow (L(p)), Na transport (J(Na)), and transepithelial voltage (V(T)). Bath BK but not lumen BK blunted subsequent ADH hydroosmotic responses. This BK effect was prevented by ibuprofen or pertussigen pretreatment and was overcome with exogenous cAMP, suggesting that BK, via prostaglandins, interferes with ADH action on L(p) at the cAMP generation step. In contrast. bath BK had no effect on bath-to-lumen (J(b-1)(Na)) or lumen-to-bath (J(1-b)(Na)) Na flux or on V(T). As reported by others aDH lowered J(1-b)(Na)) and depolarized V(T); however, prostaglandin synthesis inhibitors neither prevented nor reversed these ADH effects. Together, these BK and ADH data do not support regulation of J(Na) by peptide-stimulated prostaglandins. Moreover, cAMP alone depolarized V(T) but had no effect on J(1-b)(Na). Therefore, ADH-induced depolarization of V(T) may at least partly owe to cAMP effects on V(T) independent of accompanying changes in J(Na). As with L(p), bath BK blunted subsequent ADH effects on V(T) and, to a lesser extent, J(1-b)(Na); these BK effects on ADH action were also prevented by ibuprofen or pertussigen pretreatment. The data are consistent with the following model: 1) ADH depolarizes V(T) and increases L(p) via cAMP; 2) ADH decreases J(Na) via neither cAMP nor prostaglandins; and 3) BK, via prostaglandins, inhibits the actions of ADH on L(p) and V(T) at the inhibitory guanyl-nucleotide regulatory subunit of adenylate cyclase.

Original languageEnglish (US)
Title of host publicationAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Volume18
Edition5
StatePublished - 1985
Externally publishedYes

Fingerprint

Bradykinin
Rabbits
Baths
Prostaglandins
Ibuprofen
Pertussis Toxin
Prostaglandin Antagonists
Vasopressins
Adenylyl Cyclases
Nucleotides
Peptides

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Schuster, V. L. (1985). Mechanism of bradykinin, ADH, and cAMP interaction in rabbit cortical collecting duct. In American Journal of Physiology - Renal Fluid and Electrolyte Physiology (5 ed., Vol. 18)

Mechanism of bradykinin, ADH, and cAMP interaction in rabbit cortical collecting duct. / Schuster, Victor L.

American Journal of Physiology - Renal Fluid and Electrolyte Physiology. Vol. 18 5. ed. 1985.

Research output: Chapter in Book/Report/Conference proceedingChapter

Schuster, VL 1985, Mechanism of bradykinin, ADH, and cAMP interaction in rabbit cortical collecting duct. in American Journal of Physiology - Renal Fluid and Electrolyte Physiology. 5 edn, vol. 18.
Schuster VL. Mechanism of bradykinin, ADH, and cAMP interaction in rabbit cortical collecting duct. In American Journal of Physiology - Renal Fluid and Electrolyte Physiology. 5 ed. Vol. 18. 1985
Schuster, Victor L. / Mechanism of bradykinin, ADH, and cAMP interaction in rabbit cortical collecting duct. American Journal of Physiology - Renal Fluid and Electrolyte Physiology. Vol. 18 5. ed. 1985.
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abstract = "Vasopressin (ADH) and bradykinin (BK) have been shown to stimulate prostaglandin synthesis in rabbit cortical collecting tubules. We studied ADH and BK effects on osmotic water flow (L(p)), Na transport (J(Na)), and transepithelial voltage (V(T)). Bath BK but not lumen BK blunted subsequent ADH hydroosmotic responses. This BK effect was prevented by ibuprofen or pertussigen pretreatment and was overcome with exogenous cAMP, suggesting that BK, via prostaglandins, interferes with ADH action on L(p) at the cAMP generation step. In contrast. bath BK had no effect on bath-to-lumen (J(b-1)(Na)) or lumen-to-bath (J(1-b)(Na)) Na flux or on V(T). As reported by others aDH lowered J(1-b)(Na)) and depolarized V(T); however, prostaglandin synthesis inhibitors neither prevented nor reversed these ADH effects. Together, these BK and ADH data do not support regulation of J(Na) by peptide-stimulated prostaglandins. Moreover, cAMP alone depolarized V(T) but had no effect on J(1-b)(Na). Therefore, ADH-induced depolarization of V(T) may at least partly owe to cAMP effects on V(T) independent of accompanying changes in J(Na). As with L(p), bath BK blunted subsequent ADH effects on V(T) and, to a lesser extent, J(1-b)(Na); these BK effects on ADH action were also prevented by ibuprofen or pertussigen pretreatment. The data are consistent with the following model: 1) ADH depolarizes V(T) and increases L(p) via cAMP; 2) ADH decreases J(Na) via neither cAMP nor prostaglandins; and 3) BK, via prostaglandins, inhibits the actions of ADH on L(p) and V(T) at the inhibitory guanyl-nucleotide regulatory subunit of adenylate cyclase.",
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AB - Vasopressin (ADH) and bradykinin (BK) have been shown to stimulate prostaglandin synthesis in rabbit cortical collecting tubules. We studied ADH and BK effects on osmotic water flow (L(p)), Na transport (J(Na)), and transepithelial voltage (V(T)). Bath BK but not lumen BK blunted subsequent ADH hydroosmotic responses. This BK effect was prevented by ibuprofen or pertussigen pretreatment and was overcome with exogenous cAMP, suggesting that BK, via prostaglandins, interferes with ADH action on L(p) at the cAMP generation step. In contrast. bath BK had no effect on bath-to-lumen (J(b-1)(Na)) or lumen-to-bath (J(1-b)(Na)) Na flux or on V(T). As reported by others aDH lowered J(1-b)(Na)) and depolarized V(T); however, prostaglandin synthesis inhibitors neither prevented nor reversed these ADH effects. Together, these BK and ADH data do not support regulation of J(Na) by peptide-stimulated prostaglandins. Moreover, cAMP alone depolarized V(T) but had no effect on J(1-b)(Na). Therefore, ADH-induced depolarization of V(T) may at least partly owe to cAMP effects on V(T) independent of accompanying changes in J(Na). As with L(p), bath BK blunted subsequent ADH effects on V(T) and, to a lesser extent, J(1-b)(Na); these BK effects on ADH action were also prevented by ibuprofen or pertussigen pretreatment. The data are consistent with the following model: 1) ADH depolarizes V(T) and increases L(p) via cAMP; 2) ADH decreases J(Na) via neither cAMP nor prostaglandins; and 3) BK, via prostaglandins, inhibits the actions of ADH on L(p) and V(T) at the inhibitory guanyl-nucleotide regulatory subunit of adenylate cyclase.

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M3 - Chapter

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