Changes in blood pressure, urinary kallikrein, and urinary prostaglandin E2 in rats with streptozotocin-induced diabetes

Matsuhiko Hayashi, Shigetoshi Senba, Ikuo Saito, Waichi Kitajima, Takao Saruta

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

To reveal the mechanism of hypertension in diabetes mellitus, changes in blood pressure were measured in streptozotocin (STZ)-induced diabetes mellitus in male Wistar rats. Development of diabetes mellitus and elevation of blood pressure were observed in rats which received 60 mg/kg STZ, but not in rats which received 20 mg/kg STZ. In the rats which developed diabetes mellitus after STZ, the plasma renin activity, renal renin content, plasma aldosterone, and urinary kallikrein activity were all significantly reduced. The urinary excretion of prostaglandin E2 (PGE2) was significantly increased at 1 week after STZ in diabetic rats, but it gradually returned to control values and showed a tendency to decrease at 4 weeks after the treatment compared to the rats of the control groups. The pressor responsiveness to norepinephrine in the conscious unrestrained state in the STZ-induced diabetic rats was not remarkably changed compared to that of control rats. These results indicate that blood pressure gradually increases with the progress of diabetes. It is suggested that the changes in urinary excretion of PGE2 and urinary kallikrein activity may be related to the regulation of blood pressure in STZ-induced diabetic rats. On the other hand, it is considered unlikely that the reninangiotensin system and vascular responsiveness play an important role in the occurrence of hypertension in diabetes mellitus.

Original languageEnglish
Pages (from-to)290-294
Number of pages5
JournalNaunyn-Schmiedeberg's Archives of Pharmacology
Volume322
Issue number4
DOIs
Publication statusPublished - 1983 May

Fingerprint

Tissue Kallikreins
Experimental Diabetes Mellitus
Dinoprostone
Streptozocin
Blood Pressure
Diabetes Mellitus
Renin
Plasma Kallikrein
Hypertension
Aldosterone
Blood Vessels
Wistar Rats
Norepinephrine
Kidney
Control Groups

Keywords

  • Experimental diabetes
  • Experimental hypertension
  • Kallikrein
  • Prostaglandins
  • Reninangiotensin system

ASJC Scopus subject areas

  • Pharmacology

Cite this

Changes in blood pressure, urinary kallikrein, and urinary prostaglandin E2 in rats with streptozotocin-induced diabetes. / Hayashi, Matsuhiko; Senba, Shigetoshi; Saito, Ikuo; Kitajima, Waichi; Saruta, Takao.

In: Naunyn-Schmiedeberg's Archives of Pharmacology, Vol. 322, No. 4, 05.1983, p. 290-294.

Research output: Contribution to journalArticle

Hayashi, Matsuhiko ; Senba, Shigetoshi ; Saito, Ikuo ; Kitajima, Waichi ; Saruta, Takao. / Changes in blood pressure, urinary kallikrein, and urinary prostaglandin E2 in rats with streptozotocin-induced diabetes. In: Naunyn-Schmiedeberg's Archives of Pharmacology. 1983 ; Vol. 322, No. 4. pp. 290-294.
@article{b4d1d538219d43f8820891d51a80ac6b,
title = "Changes in blood pressure, urinary kallikrein, and urinary prostaglandin E2 in rats with streptozotocin-induced diabetes",
abstract = "To reveal the mechanism of hypertension in diabetes mellitus, changes in blood pressure were measured in streptozotocin (STZ)-induced diabetes mellitus in male Wistar rats. Development of diabetes mellitus and elevation of blood pressure were observed in rats which received 60 mg/kg STZ, but not in rats which received 20 mg/kg STZ. In the rats which developed diabetes mellitus after STZ, the plasma renin activity, renal renin content, plasma aldosterone, and urinary kallikrein activity were all significantly reduced. The urinary excretion of prostaglandin E2 (PGE2) was significantly increased at 1 week after STZ in diabetic rats, but it gradually returned to control values and showed a tendency to decrease at 4 weeks after the treatment compared to the rats of the control groups. The pressor responsiveness to norepinephrine in the conscious unrestrained state in the STZ-induced diabetic rats was not remarkably changed compared to that of control rats. These results indicate that blood pressure gradually increases with the progress of diabetes. It is suggested that the changes in urinary excretion of PGE2 and urinary kallikrein activity may be related to the regulation of blood pressure in STZ-induced diabetic rats. On the other hand, it is considered unlikely that the reninangiotensin system and vascular responsiveness play an important role in the occurrence of hypertension in diabetes mellitus.",
keywords = "Experimental diabetes, Experimental hypertension, Kallikrein, Prostaglandins, Reninangiotensin system",
author = "Matsuhiko Hayashi and Shigetoshi Senba and Ikuo Saito and Waichi Kitajima and Takao Saruta",
year = "1983",
month = "5",
doi = "10.1007/BF00508345",
language = "English",
volume = "322",
pages = "290--294",
journal = "Naunyn-Schmiedeberg's Archives of Pharmacology",
issn = "0028-1298",
publisher = "Springer Verlag",
number = "4",

}

TY - JOUR

T1 - Changes in blood pressure, urinary kallikrein, and urinary prostaglandin E2 in rats with streptozotocin-induced diabetes

AU - Hayashi, Matsuhiko

AU - Senba, Shigetoshi

AU - Saito, Ikuo

AU - Kitajima, Waichi

AU - Saruta, Takao

PY - 1983/5

Y1 - 1983/5

N2 - To reveal the mechanism of hypertension in diabetes mellitus, changes in blood pressure were measured in streptozotocin (STZ)-induced diabetes mellitus in male Wistar rats. Development of diabetes mellitus and elevation of blood pressure were observed in rats which received 60 mg/kg STZ, but not in rats which received 20 mg/kg STZ. In the rats which developed diabetes mellitus after STZ, the plasma renin activity, renal renin content, plasma aldosterone, and urinary kallikrein activity were all significantly reduced. The urinary excretion of prostaglandin E2 (PGE2) was significantly increased at 1 week after STZ in diabetic rats, but it gradually returned to control values and showed a tendency to decrease at 4 weeks after the treatment compared to the rats of the control groups. The pressor responsiveness to norepinephrine in the conscious unrestrained state in the STZ-induced diabetic rats was not remarkably changed compared to that of control rats. These results indicate that blood pressure gradually increases with the progress of diabetes. It is suggested that the changes in urinary excretion of PGE2 and urinary kallikrein activity may be related to the regulation of blood pressure in STZ-induced diabetic rats. On the other hand, it is considered unlikely that the reninangiotensin system and vascular responsiveness play an important role in the occurrence of hypertension in diabetes mellitus.

AB - To reveal the mechanism of hypertension in diabetes mellitus, changes in blood pressure were measured in streptozotocin (STZ)-induced diabetes mellitus in male Wistar rats. Development of diabetes mellitus and elevation of blood pressure were observed in rats which received 60 mg/kg STZ, but not in rats which received 20 mg/kg STZ. In the rats which developed diabetes mellitus after STZ, the plasma renin activity, renal renin content, plasma aldosterone, and urinary kallikrein activity were all significantly reduced. The urinary excretion of prostaglandin E2 (PGE2) was significantly increased at 1 week after STZ in diabetic rats, but it gradually returned to control values and showed a tendency to decrease at 4 weeks after the treatment compared to the rats of the control groups. The pressor responsiveness to norepinephrine in the conscious unrestrained state in the STZ-induced diabetic rats was not remarkably changed compared to that of control rats. These results indicate that blood pressure gradually increases with the progress of diabetes. It is suggested that the changes in urinary excretion of PGE2 and urinary kallikrein activity may be related to the regulation of blood pressure in STZ-induced diabetic rats. On the other hand, it is considered unlikely that the reninangiotensin system and vascular responsiveness play an important role in the occurrence of hypertension in diabetes mellitus.

KW - Experimental diabetes

KW - Experimental hypertension

KW - Kallikrein

KW - Prostaglandins

KW - Reninangiotensin system

UR - http://www.scopus.com/inward/record.url?scp=0020598553&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0020598553&partnerID=8YFLogxK

U2 - 10.1007/BF00508345

DO - 10.1007/BF00508345

M3 - Article

VL - 322

SP - 290

EP - 294

JO - Naunyn-Schmiedeberg's Archives of Pharmacology

JF - Naunyn-Schmiedeberg's Archives of Pharmacology

SN - 0028-1298

IS - 4

ER -