IMPACT OF CYCLO‐OXYGENASE BLOCKADE ON JUXTAMEDULLARY MICROVASCULAR RESPONSES TO ANGIOTENSIN II IN RAT KIDNEY

L. M. Harrison-Bernard, Pamela K Carmines

Research output: Contribution to journalArticle

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Abstract

1. Experiments were designed to evaluate the hypothesis that cyclo‐oxygenase products modulate the influence of angiotensin II (AII) on the renal juxtamedullary microvasculature of enalaprilat‐treated rats. 2. The in vitro blood‐perfused juxtamedullary nephron technique was utilized to provide access to afferent arterioles, efferent arterioles and descending vasa recta located in the outer stripe of the outer medulla. 3. Baseline afferent arteriolar diameter was 20.8 ± 1.9 μm in kidneys subjected to cyclo‐oxygenase blockade (1μmol/L piroxicam), a value significantly lower than that observed in untreated kidneys (26.1 ± 1.0 μm). Baseline diameters of efferent arterioles and outer medullary descending vasa recta did not differ between untreated and piroxicam‐treated groups. 4. Topical application of 1 nmol/L AII reduced blood flow through outer medullary descending vasa recta by 22 ± 6% in untreated kidneys and by 24 ± 7% in piroxicam‐treated kidneys. 5. In untreated kidneys, AII (0.01–100nmol/L) produced concentration‐dependent afferent and efferent arteriolar constrictor responses of similar magnitudes. Neither afferent nor efferent arteriolar AII responsiveness was significantly altered in piroxicam‐treated kidneys, although afferent responses exceeded efferent responses at AII concentrations ≥ 10 nmol/L. 6. We conclude that endogenous cyclo‐oxygenase products exert a vasodilator influence on juxtamedullary afferent arterioles under baseline conditions. Although cyclo‐oxygenase inhibition had little effect on juxtamedullary microvascular responses to AII, the response to high AII concentrations may be modulated by cyclo‐oxygenase products in a manner which delicately alters the relative influence of the peptide on pre‐ vs postglomerular resistances.

Original languageEnglish (US)
Pages (from-to)732-738
Number of pages7
JournalClinical and Experimental Pharmacology and Physiology
Volume22
Issue number10
DOIs
StatePublished - Oct 1995

Fingerprint

Prostaglandin-Endoperoxide Synthases
Angiotensin II
Kidney
Arterioles
Rectum
Piroxicam
Nephrons
Microvessels
Vasodilator Agents
Peptides

Keywords

  • angiotensin II
  • arterioles
  • cyclo‐oxygenase inhibition
  • piroxicam
  • renal circulation.

ASJC Scopus subject areas

  • Physiology
  • Pharmacology
  • Physiology (medical)

Cite this

IMPACT OF CYCLO‐OXYGENASE BLOCKADE ON JUXTAMEDULLARY MICROVASCULAR RESPONSES TO ANGIOTENSIN II IN RAT KIDNEY. / Harrison-Bernard, L. M.; Carmines, Pamela K.

In: Clinical and Experimental Pharmacology and Physiology, Vol. 22, No. 10, 10.1995, p. 732-738.

Research output: Contribution to journalArticle

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abstract = "1. Experiments were designed to evaluate the hypothesis that cyclo‐oxygenase products modulate the influence of angiotensin II (AII) on the renal juxtamedullary microvasculature of enalaprilat‐treated rats. 2. The in vitro blood‐perfused juxtamedullary nephron technique was utilized to provide access to afferent arterioles, efferent arterioles and descending vasa recta located in the outer stripe of the outer medulla. 3. Baseline afferent arteriolar diameter was 20.8 ± 1.9 μm in kidneys subjected to cyclo‐oxygenase blockade (1μmol/L piroxicam), a value significantly lower than that observed in untreated kidneys (26.1 ± 1.0 μm). Baseline diameters of efferent arterioles and outer medullary descending vasa recta did not differ between untreated and piroxicam‐treated groups. 4. Topical application of 1 nmol/L AII reduced blood flow through outer medullary descending vasa recta by 22 ± 6{\%} in untreated kidneys and by 24 ± 7{\%} in piroxicam‐treated kidneys. 5. In untreated kidneys, AII (0.01–100nmol/L) produced concentration‐dependent afferent and efferent arteriolar constrictor responses of similar magnitudes. Neither afferent nor efferent arteriolar AII responsiveness was significantly altered in piroxicam‐treated kidneys, although afferent responses exceeded efferent responses at AII concentrations ≥ 10 nmol/L. 6. We conclude that endogenous cyclo‐oxygenase products exert a vasodilator influence on juxtamedullary afferent arterioles under baseline conditions. Although cyclo‐oxygenase inhibition had little effect on juxtamedullary microvascular responses to AII, the response to high AII concentrations may be modulated by cyclo‐oxygenase products in a manner which delicately alters the relative influence of the peptide on pre‐ vs postglomerular resistances.",
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