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ONLINEISSN:1348-4214
PRINTISSN:0916-9636
Hypertension Research
Vol. 27 (2004) , No. 7 July 501-508
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The Role of Renal Natriuretic and Depressor Systems in Insulin-Resistant Hypertensive Rats
Koichi HASEGAWA1), Hideaki YOSHIDA1), Nobuyuki URA1), Hideyuki MURAKAMI1), Makoto HAGIWARA1) and Kazuaki SHIMAMOTO1)
1) Second Department of Internal Medicine, Sapporo Medical University School of Medicine
(Received November 14, 2003)
(Accepted April 5, 2004)

Insulin resistance and impairment of the renal depressor system have been thought to be involved in the development of essential hypertension. However, the relationship between insulin resistance and this system is still unclear. To clarify this relationship, we investigated the role of the renal depressor system in a rat model of insulin-resistant hypertension. Sprague-Dawley rats were fed a standard diet (control) or a fructose-rich diet (FFR), and their blood pressures were measured every week. Urinary dopamine (uDA), urinary kallikrein (uKAL) activity and urinary nitric oxide (uNOx) levels were also measured each week, and the renal mRNA expression levels of endothelial nitric oxide synthase (eNOS), aromatic-L-amino-acid decarboxylase (AADC), and kallikrein (KAL) activity were compared at the end of the study. The blood pressure of FFR was elevated significantly from 2 weeks after the start of fructose loading. The uDA level was lower in FFR than in control rats throughout the study period (p <0.01), and the expression level of AADC mRNA was enhanced in FFR (p <0.05). There was a tendency of negative correlation between uDA level and systolic blood pressure (SBP) (r =-0.49, p =0.056). uNOx level was lower in FFR throughout the study period (p <0.05), and the eNOS mRNA expression level in the kidney was lower in FFR than in control rats (p <0.05). There was a negative correlation between uNOx level and SBP (r =-0.68, p <0.01). On the other hand, there was no significant difference in the kallikrein-kinin system between FFR and control rats. In conclusion, impairment in functions of the renal dopamine and NO systems occur in FFR, and this impairment may be caused by insulin resistance and may contribute to the development of hypertension. (Hypertens Res 2004; 27: 501-508)
Key Words:insulin resistance, hypertension, dopamine, nitric oxides, kallikrein

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To cite this article:
Koichi HASEGAWA, Hideaki YOSHIDA, Nobuyuki URA, Hideyuki MURAKAMI, Makoto HAGIWARA and Kazuaki SHIMAMOTO: “The Role of Renal Natriuretic and Depressor Systems in Insulin-Resistant Hypertensive Rats”. Hypertens Res; Vol. 27: 501-508 (2004) .
doi:10.1291/hypres.27.501
JOI  JST.JSTAGE/hypres/27.501
Copyright (c) 2004 by the Japanese Society of Hypertension

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