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The changes in active and inactive renin after captopril (n = 29) or furosemide administration (n = 10) were studied in hypertensive patients. Furthermore, after percutaneous transluminal angioplasty (PTA) in 3 cases of renovascular hypertension (RVH), and after nephrectomy in a case of juxtaglomerular cell tumor, the time course of the changes in these two types of renin was investigated. Inactive renin was activated by trypsin treatment. Plasma renin concentration was measured by using an excess of sheep substrate. In patients with essential hypertension or primary aldosteronism, inactive renin was unchanged, irrespective of response in active renin, after the administration of captopril and furosemide. In patients with RVH, inactive renin was markedly decreased by furosemide but unchanged by captopril, in spite of significant increase in active renin. After PTA and nephrectomy, inactive renin decreased slower than active renin. These data support the idea that in patients with RVH, the increase in active renin by furosemide is at least partly due to the activation of inactive renin. It is also suggested that the increase in active renin by captopril is mainly due to the promoted release of active renin from the kidney. Furthermore, it seems likely that the metabolic clearance of inactive renin is slower than that in active renin.
T Goto, and
K Abe, and
K Tsunoda, and
M Seino, and
M Yasujima, and
Y Imai, and
S Chiba, and
M Sato, and
T Haruyama, and
K Omata
September 1991,
Canadian journal of physiology and pharmacology,
T Goto, and
K Abe, and
K Tsunoda, and
M Seino, and
M Yasujima, and
Y Imai, and
S Chiba, and
M Sato, and
T Haruyama, and
K Omata
January 1982,
Clinical and experimental hypertension. Part A, Theory and practice,
T Goto, and
K Abe, and
K Tsunoda, and
M Seino, and
M Yasujima, and
Y Imai, and
S Chiba, and
M Sato, and
T Haruyama, and
K Omata
May 1982,
The Journal of clinical endocrinology and metabolism,
T Goto, and
K Abe, and
K Tsunoda, and
M Seino, and
M Yasujima, and
Y Imai, and
S Chiba, and
M Sato, and
T Haruyama, and
K Omata
July 1985,
Nihon Sanka Fujinka Gakkai zasshi,
T Goto, and
K Abe, and
K Tsunoda, and
M Seino, and
M Yasujima, and
Y Imai, and
S Chiba, and
M Sato, and
T Haruyama, and
K Omata
January 1982,
Nephron,
T Goto, and
K Abe, and
K Tsunoda, and
M Seino, and
M Yasujima, and
Y Imai, and
S Chiba, and
M Sato, and
T Haruyama, and
K Omata
April 1982,
The American journal of cardiology,
T Goto, and
K Abe, and
K Tsunoda, and
M Seino, and
M Yasujima, and
Y Imai, and
S Chiba, and
M Sato, and
T Haruyama, and
K Omata
January 1982,
Clinical and experimental hypertension. Part A, Theory and practice,
T Goto, and
K Abe, and
K Tsunoda, and
M Seino, and
M Yasujima, and
Y Imai, and
S Chiba, and
M Sato, and
T Haruyama, and
K Omata
January 1982,
Clinical and experimental hypertension. Part A, Theory and practice,
T Goto, and
K Abe, and
K Tsunoda, and
M Seino, and
M Yasujima, and
Y Imai, and
S Chiba, and
M Sato, and
T Haruyama, and
K Omata
January 1985,
Clinical and experimental pharmacology & physiology,
T Goto, and
K Abe, and
K Tsunoda, and
M Seino, and
M Yasujima, and
Y Imai, and
S Chiba, and
M Sato, and
T Haruyama, and
K Omata
August 1977,
Japanese circulation journal,
