Urinary Excretion of Free Dopamine and Digoxinlike Substances Correlates with Endogenous Secretion of Insulin in Normotensive Adults, but Not in Hypertensive Subjects
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- Nishimura Masato
- Department of Clinical Laboratory and Medicine, Kyoto Prefectural University of Medicine
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- Takahashi Hakuo
- Department of Clinical Sciences and Laboratory Medicine, Kansai Medical University
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- Nanbu Akira
- Department of Clinical Laboratory and Medicine, Kyoto Prefectural University of Medicine
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- Habuchi Yoshizumi
- Department of Clinical Laboratory and Medicine, Kyoto Prefectural University of Medicine
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- Fujita Naohisa
- Department of Clinical Laboratory and Medicine, Kyoto Prefectural University of Medicine
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- Nakanishi Tadashi
- Department of Clinical Laboratory and Medicine, Kyoto Prefectural University of Medicine
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- Yoshimura Manabu
- Department of Clinical Laboratory and Medicine, Kyoto Prefectural University of Medicine
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We investigated whether urinary excretion of free dopamine is related with the humoral factors which affect Na+, K+ ATPase activity in the kidneys. Subjects were 51 adults admitted in a hospital without renal insufficiency: they were divided into normotensive (n=36, 60±3 years old, 122±3/73±2mmHg) and hypertensive groups (n=15, 65±5 years old, 157±6/91±2mmHg). Urinary excretion of free dopamine was significantly and positively correlated with urinary excretion of C-peptide immunoreactivity of insulin (CPR) (r=0.451, p=0.014) in normotensive subjects, but not in hypertensive subjects (r= 0.155, p=0.668). Urinary excretion of endogenous digoxinlike substances (EDLS) was also significantly and positively correlated with urinary CPR (r=0.500, p=0.006) in normotensive subjects, but not in hypertensive subjects (r=0.275, p=0.363). In normotensive subjects, urinary excretion of free dopamine and EDLS may be regulated at least in part by insulin secreted endogenously. In hypertensive subjects, however, this regulatory mechanism of the diuretic factors, such as insulin, EDLS and dopamine, is thought to be deranged, which might result in decompensation of a diuretic and antidiuretic balance leading to blood pressure elevation. (Hypertens Res 1995; 18 Suppl. I: S191-S192)
収録刊行物
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- Hypertension Research
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Hypertension Research 18 (SupplementI), S191-S192, 1995
日本高血圧学会
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詳細情報 詳細情報について
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- CRID
- 1390282679696253568
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- NII論文ID
- 10008736090
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- NII書誌ID
- AA10847079
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- ISSN
- 13484214
- 09169636
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- Crossref
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可