Inhibition of nitric oxide synthesis enhances insulin-hypertension in conscious rats

B. W. Shek, H. L. Keen, Michael W Brands, J. E. Hall

Research output: Contribution to journalArticle

4 Scopus citations

Abstract

We have previously shown that chronic hypcrinsulinemia causes hypertension in rats and acute studies suggest that endothelial-derived nitric oxide (EDNO) may modulate the vascular actions of insulin. The present study was designed to determine whether blockade of EDNO synthesis with nitro-L-arginine methyl ester (L-NAME) exacerbates the hypertensive actions of insulin in conscious rats. Male Sprague-Dawley rats were instrumented with arterial and venous catheters and mean arterial pressure (MAP) was monitored continuously 24 hr/day. After 7 days of control measurments, rats were given either vehicle (C rats, n=4) or L-NAME (10 μg/kg/min, i.V., n=4) throughout the entire experiment After 4 days of L-NAME or vehicle infusion, a 5 day infusion of insulin (1.5 mU/kg/min, i.v.) was initiated while euglycemia was maintained with glucose infusion (22 mg/kg/min, i.v.). After 4 days of L-NAME infusion, MAP increased from 91±1 to 122±2 mmHg. Vehicle infusion did not significantly alter MAP in C rats. After 5 days of insulin infusion, MAP increased to a greater extent in L-NAME rats than in C rats (21±4 vs 8±0.3 mmHg). Thus, blockade of EDNO synthesis significantly enhanced the chronic hypertensive effects of insulin in rats. These observations suggest that EDNO may help to minimize the rise in blood pressure during chronic hyperinsulinemia in rats. (Supported by HL51971, HL39399, and HL23502).

Original languageEnglish (US)
JournalFASEB Journal
Volume10
Issue number3
StatePublished - Dec 1 1996
Externally publishedYes

    Fingerprint

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

Cite this