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Research ArticleArticle

Pressor and Renal Vasoconstrictor Responses to Acute Systemic Nitric Oxide Synthesis Inhibition Are Independent of the Sympathetic Nervous System and Angiotensin II

Chris Baylis, Jeff Harvey, Beth R. Santmyire and Kevin Engels
Journal of Pharmacology and Experimental Therapeutics February 1999, 288 (2) 693-698;
Chris Baylis
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Jeff Harvey
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Beth R. Santmyire
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Kevin Engels
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Abstract

Acute systemic, nonselective nitric oxide synthesis inhibition (NOSI) causes a marked pressor and renal vasoconstrictor response in the normal conscious chronically catheterized rat. The present studies directly address the question of how these vasoconstrictor responses are related to the combined vasoconstrictor activities of the sympathetic nervous system and angiotensin II. When thealpha adrenoceptors are blocked (with prazosin) the pressor and renal hemodynamic responses to NOSI are unaffected. Combined alpha adrenoceptor and angiotensin II receptor blockade at the same time as NOSI results in no net change in blood pressure while leaving the renal vasoconstrictor response intact. However, when the NOSI is delayed, a substantial and unblunted pressor response is seen. In contrast to the vasoconstrictor responses, the natriuretic and diuretic responses to acute NOSI are prevented by simultaneous alpha adrenoceptor blockade alone and combined with angiotensin II receptor blockade. These findings suggest that the hemodynamic actions of acute NOSI in the unstressed rat are independent of the sympathetic nervous system and angiotensin II. In contrast, the natriuretic/diuretic response to acute NOSI is apparently partly the result of some interaction with the sympathetic nervous system, not, as we had previously suggested, exclusively the result of a pressure natriuresis.

Footnotes

  • ↵1 These studies were supported by National Institutes of Health Grant DK-45517 and NIH RR-94-1.

  • Abbreviations:
    NOSI
    nitric oxide synthase inhibition
    GFR
    glomerular filtration rate
    RPF
    renal plasma flow
    RVR
    renal vascular resistance
    V
    urine flow
    UNaV
    urinary excretion of Na
    UKV
    urinary excretion of K
    FENa
    fractional excretion of Na
    nNOS
    neuronal NOS
    PAH
    paraaminohippuric acid
    • Received May 22, 1998.
    • Accepted September 15, 1998.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 288 (2)
Journal of Pharmacology and Experimental Therapeutics
Vol. 288, Issue 2
1 Feb 1999
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Research ArticleArticle

Pressor and Renal Vasoconstrictor Responses to Acute Systemic Nitric Oxide Synthesis Inhibition Are Independent of the Sympathetic Nervous System and Angiotensin II

Chris Baylis, Jeff Harvey, Beth R. Santmyire and Kevin Engels
Journal of Pharmacology and Experimental Therapeutics February 1, 1999, 288 (2) 693-698;

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Research ArticleArticle

Pressor and Renal Vasoconstrictor Responses to Acute Systemic Nitric Oxide Synthesis Inhibition Are Independent of the Sympathetic Nervous System and Angiotensin II

Chris Baylis, Jeff Harvey, Beth R. Santmyire and Kevin Engels
Journal of Pharmacology and Experimental Therapeutics February 1, 1999, 288 (2) 693-698;
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