Basal nitric oxide production curtails arteriolar vasoconstrictor responses to ANG II in rat kidney

Hideki Ikenaga, Rachel W. Fallet, Pamela K. Carmines

Research output: Contribution to journalArticlepeer-review

45 Scopus citations

Abstract

Experiments were performed to test the hypothesis that renal arteriolar vasoconstrictor responses to angiotensin II(ANG II) are curtailed through a mechanism that involves stimulation of endogenous nitric oxide(NO) synthesis. The in vitro blood-perfused juxtamedullary nephron technique was exploited to monitor arteriolar lumen diameter responses to exogenous ANG II before and during treatment with the NO synthase inhibitor Nω-nitro-L-arginine(L-NNA). Under control conditions, 1 nM ANG II reduced afferent and efferent arteriolar diameters by 13 and 11%, respectively. In the presence of L-NNA, 1 nM ANG II decreased afferent diameter by 26% and efferent diameter by 35%. This augmentation could not be attributed to the L-NNA-induced decrease in baseline diameter. L-NNA also augmented vasopressin responses, indicating a lack of agonist specificity in this interaction. ANG II reactivity during L-NNA treatment was not enhanced when tissue NO activity was fixed at basal levels(exposure to 1 μM sodium nitroprusside). These results indicate that endogenous NO modulates the vasoconstrictive impact of ANG II on both afferent and efferent arterioles of juxtamedullary nephrons and that this process does not require stimulation of NO synthesis.

Original languageEnglish (US)
Pages (from-to)F365-F373
JournalAmerican Journal of Physiology
Volume271
Issue number2 PART 2
DOIs
StatePublished - 1996

Keywords

  • Afferent arteriole
  • Arginine vasopressin
  • Efferent arteriole
  • Nitro-l-arginine
  • Norepinephrine

ASJC Scopus subject areas

  • Physiology (medical)

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