Premium
DEVELOPMENT OF POLYURIA IN TSUKUBA HYPERTENSIVE MICE CARRYING HUMAN RENIN AND ANGIOTENSINOGEN GENES
Author(s) -
Uehara Sayuri,
Mino Nobuyuki,
Tsuchida Minoru,
Nishikibe Masaru,
Fukamizu Akiyoshi,
Murakami Kazuo,
Ikemoto Fumihiko
Publication year - 1995
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1995.tb02846.x
Subject(s) - polyuria , renin–angiotensin system , gene , endocrinology , medicine , physiology , biology , genetics , blood pressure , diabetes mellitus
Summary 1. Tsukuba hypertensive mice (THM) carry both human renin and angiotensinogen genes, and develop hypertension. The animal has high levels of renin activity and angiotensin II concentration in the plasma. 2. Urinary excretion in THM was greater than in the control animal, non‐transgenic C57/BL/6j. THM showed a greater amount of daily water intake. The osmolality of 24 h urine was lower than that of the control animal. 3. When water was deprived for 12h and then loaded with 0.25mL/10g bodyweight, the osmolality of urine at the first 0–3 h period was the same in THM and control, but significantly lower in THM at the following 3–6 h period, indicating that the urine concentrating activity is insufficient in THM compared with the control animal. 4. Urinary excretion of vasopressin was significantly higher in THM. Plasma aldosterone concentration and urinary excretion of aldosterone were also higher in THM. Plasma potassium level was significantly low. 5. The mechanism underlying the pathophysiology of polyuria is not totally explained; however, hypokalaemia, which was probably the result of hyperaldosteronism, may be at least partially involved, since hypokalaemia is considered to be a factor hampering the action of vasopressin for concentration of urine at the site of the collecting duct of the kidney.