Dopaminergic Activity and Endorenal Dopamine Synthesis in Non-Insulin Dependent Diabetes Mellitus

In the present study we tried to clarify the differences of the cardiovascular and renal responses to feeding in relation to the peripheral dopamine system. In control subjects (C), ingestion of protein (100g) induced an increase in Ccr accompanied by an increase in tubular sodium excretion (FENa+)....

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Veröffentlicht in:Hypertension Research 1995, Vol.18(SupplementI), pp.S125-S130
Hauptverfasser: Shigetomi, Shuichi, Yamada, Zen-o, Ishii, Hajime, Sanada, Hironobu, Watanabe, Hidetsuna, Fukuchi, Soitsu
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Sprache:eng
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Zusammenfassung:In the present study we tried to clarify the differences of the cardiovascular and renal responses to feeding in relation to the peripheral dopamine system. In control subjects (C), ingestion of protein (100g) induced an increase in Ccr accompanied by an increase in tubular sodium excretion (FENa+). Patients with non-insulin dependent diabetic (NIDDM), a protein-induced increase in Ccr was comparable to that in C, while FENa+ did not change following protein. Since an increase in urinary 3, 4-dihydroxyphenylacetic acid was blunted in NIDDM, an impaired natriuretic response to high protein may be results from an insufficient synthesis of renal dopamine. Plasma dopamine and its metabolites in NIDDM following protein tended to be greater than in C. Protein induced a greater decrease in blood pressure (BP) in NIDDM, but no increase in pulse rate was observed. An ordinary diet containing 10g of protein also induced a decrease in BP. A reflex tachycardia was observed in C and normotensive NIDDM but not in hypertensive one. In normotensive NIDDM, plasma dopamine and norepinephrine increased after the diet, while in hypertensive NIDDM there were no increases in catecholamines. From these results it is suggested that the relatively elevated peripheral dopaminergic activity and the blunted dopamine synthesis in the kidney may be responsible for the abnormal cardiovascular and renal responses to feeding in patients with NIDDM. (Hypertens Res 1995; 18 Suppl. I: S125-S130)
ISSN:0916-9636
1348-4214
DOI:10.1291/hypres.18.SupplementI_S125