Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 2000;36:872-877

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bursztyn, M.
Right arrow Articles by Bernheim, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bursztyn, M.
Right arrow Articles by Bernheim, J.
Related Collections
Right arrow Animal models of human disease
Right arrow Other hypertension
Right arrow Hypertension - basic studies
Right arrow Mechanism of atherosclerosis/growth factors

(Hypertension. 2000;36:872.)
© 2000 American Heart Association, Inc.


Scientific Contributions

Subpressor Dose of L-NAME Unmasks Hypertensive Effect of Chronic Hyperinsulinemia

Michael Bursztyn; Judith Mekler; Edna Peleg; Jacques Bernheim

From the Hypertension Unit, Department of Medicine, Hadassah University Hospital, Mount Scopus, Jerusalem (M.B., J.M.); Hypertension Institute, Sheba Medical Center, Tel Hashomer (E.P.); and Department of Nephrology, Sapir Medical Center, Meir Hospital, Kfar Saba (J.B.), Israel.

Correspondence to Michael Bursztyn, MD, Hypertension Unit, Department of Medicine, Hadassah University Hospital, Mount Scopus, PO Box 24035, Jerusalem 91240, Israel. E-mail bursz{at}cc.huji.ac.il

Abstract—We previously found that chronic exogenous hyperinsulinemia without sugar supplementation does not elevate blood pressure. This may be partially explained by the ability of insulin to release nitric oxide and cause vasodilatation. To test this hypothesis, we studied 4 groups of rats: 9 rats (body weight, 213±14 g) treated with a gradual increase of a sustained-release subcutaneous insulin pellet; 9 rats (body weight, 213±9 g) treated with NG-nitro-L-arginine methyl ester (L-NAME) in drinking water 50 mg/L; 19 rats (body weight, 217±11 g) treated with the combination of L-NAME and insulin; and 9 control rats (body weight, 218±11 g). Blood pressure was followed weekly for 6 weeks, and then rats were studied in metabolic cages. Weight gain was not different during the 6 weeks. Renal function did not differ between the 4 groups, but 24-hour urinary nitrite/nitrate excretion was lower (P<0.02) in L-NAME–treated and higher in insulin-treated rats. Plasma insulin doubled (P<0.002) in the insulin-treated rats, but there was no hypoglycemia and, by week 6, fructosamine levels were 2.1±0.2, 2.1±0.2, 2.3±0.1, and 2.3±0.2 mmol/L in control rats and rats treated with L-NAME, insulin, and L-NAME plus insulin, respectively. Systolic blood pressure, which did not differ at baseline, at week 3 was 122±17, 118±17, and 118±24 mm Hg in the control, L-NAME, and insulin groups and 136±14 mm Hg (P<0.03) in the combination group. At week 6, systolic blood pressure was 128±14, 127±15, and 118±13 mm Hg in the control, L-NAME, and insulin groups, respectively, and 150±14 mm Hg (P<0.0005) in the combination group. In a subsequent experiment, L-arginine 2 g/L abrogated the effects of L-NAME and insulin combination. In conclusion, chronic exogenous hyperinsulinemia does not affect blood pressure but may cause hypertension when endothelial function is compromised.


Key Words: insulin • nitric oxide • sodium • nitrites • nitrates