Effects of Aldosterone and Deoxycorticosterone on the Urinary Excretion of Kallikrein and of Prostaglandin E-Like Substance in the Rat

2015 ◽  
pp. 126-131 ◽  
Author(s):  
J. Coiina-Chourio ◽  
J. C. McGiff ◽  
A. Nasjletti
Keyword(s):  
Urinary Excretion ◽  
Prostaglandin E

Urinary Excretion and Glomerular Synthesis of Prostaglandin E2 and Prostaglandin F2α in Cirrhotic, Non-Ascitic Rats: The Effects of Sodium Overload

Nephron ◽  
1988 ◽  
Vol 49 (4) ◽  
pp. 322-327 ◽  
Author(s):  
Juan Carlos Santos ◽  
Diego Rodríguez-Puyol ◽  
Alicia Blanchart ◽  
Luis Hernando ◽  
José Miguel López-Novoa
Keyword(s):  
Urinary Excretion ◽  
Prostaglandin E ◽  
Prostaglandin F ◽  
Sodium Overload

Effect of propranolol on the urinary excretion of prostaglandin E and plasma benin activity in hypertensive patients

1980 ◽  
Vol 5 (1) ◽  
pp. 1-9 ◽  
Author(s):  
M. Sato ◽  
K. Abe ◽  
M. Yasujima ◽  
Y. Otsuka ◽  
S. Chiba ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Prostaglandin E ◽  
Hypertensive Patients

The Role of Intrarenal Vasoactive Substances in the Pathogenesis of Essential Hypertension

1978 ◽  
Vol 55 (s4) ◽  
pp. 363s-366s ◽  
Author(s):  
K. Abe ◽  
M. Yasujima ◽  
N. Irokawa ◽  
M. Seino ◽  
S. Chiba ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Urinary Excretion ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Prostaglandin E ◽  
Plasma Aldosterone Concentration ◽  
Renin Angiotensin ◽  
Vasoactive Substances ◽  
Angiotensin Ii Antagonist ◽  
Renal Kallikrein

To investigate the role of renal vasoactive substances in the pathogenesis of essential hypertension, urinary prostaglandin E excretion, urinary kallikrein excretion, plasma renin activity, plasma aldosterone concentration and urinary Na excretion were measured in normal subjects and patients with essential hypertension after stimulation of the renin—angiotensin—aldosterone system by the intravenous injection of frusemide or a low Na diet; after the inhibition of renin—angiotensin—aldosterone by an angiotensin II antagonist and after the inhibition of renal prostaglandin E synthesis by indomethacin. The urinary excretions of prostaglandin E and kallikrein, plasma renin activity and plasma aldosterone concentration increased after frusemide administration. The urinary excretion of kallikrein increased after frusemide or a low Na diet but decreased after the angiotensin II antagonist and indomethacin during Na depletion. Changes in urinary kallikrein excretion paralleled those in the renin—angiotensin—aldosterone system after various stimuli. The urinary excretion of prostaglandin E increased after frusemide. However, a dissociation between the urinary excretions of prostaglandin E and kallikrein was found during the low Na diet: the former decreased and the latter increased. The urinary excretion of prostaglandin E was closely related to urinary Na output after various stimuli. Basal levels of urinary prostaglandin E and kallikrein excretion were lower in essential hypertension than in normal subjects. The release of renal prostaglandin E and kallikrein after frusemide was also suppressed in essential hypertension compared with that in normal subjects. The data indicate that renal kallikrein—kinin and renin—angiotensin—aldosterone may interact in a dynamic fashion to maintain blood pressure, that renal prostaglandin E may be involved in renal Na handling and that the suppression of renal kallikrein—kinin and prostaglandin E in essential hypertension may be an etiological factor in essential hypertension.

Role of the renal kinin-prostaglandin system in diltiazem-induced natriuresis

1986 ◽  
Vol 250 (2) ◽  
pp. F197-F202
Author(s):  
M. Seino ◽  
K. Abe ◽  
N. Nushiro ◽  
K. Omata ◽  
K. Sato ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Significant Relationship ◽  
Intravenous Infusion ◽  
Renal Hemodynamics ◽  
Prostaglandin E ◽  
Drug Induced ◽  
Entry Blocker ◽  
Prostaglandin System

Intravenous infusion of the Ca2+ entry blocker diltiazem (10 micrograms . kg-1 . min-1 for 30 min) induced an increase in urinary excretion of sodium (UNaV) from 209 +/- 42 to 922 +/- 311 mueq without significant alterations in renal hemodynamics in anesthetized rabbits. Urinary excretion of kinin (UkinV) and prostaglandin E (UPGEV) were also increased by diltiazem, from 14.3 +/- 2.5 to 25.9 +/- 4.8 ng and 1.33 +/- 0.20 to 2.44 +/- 0.34 ng, respectively. Moreover, there was a significant correlation between UkinV and UNaV (r = 0.81, P less than 0.05). A significant relationship between UPGEV and UNaV (r = 0.83, P less than 0.05) was also observed. However, no correlation between urinary excretion of kallikrein (UkallV) and UNaV was found after infusion of diltiazem. Further, to examine a possible contribution of renal kinins and prostaglandins in diltiazem-induced natriuresis, aprotinin (50,000 KIU/kg bolus + 1,000 KIU . kg-1 . min-1 infusion) and indomethacin (8 mg/kg) were used. Aprotinin pretreatment attenuated diltiazem-induced natriuresis, accompanied by suppression of UkallV, UkinV, and UPGEV. However, indomethacin pretreatment did not affect this drug-induced natriuresis, although UPGEV was significantly decreased. Furthermore, under the indomethacin pretreatment, a significant increase in UkinV was produced by diltiazem. These results suggest that renal kinins rather than renal prostaglandin E, at least in part, play a role in diltiazem-induced natriuresis.

Reduced urinary excretion of prostaglandin E in essential hypertension

1983 ◽  
Vol 11 (2) ◽  
pp. 189-197 ◽  
Author(s):  
K. Sato ◽  
K. Abe ◽  
M. Seino ◽  
M. Yasujima ◽  
S. Chiba ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Urinary Excretion ◽  
Prostaglandin E

Exaggerated Fractional Sodium Excretion in Hypertension with Advanced Renal Disease: The Role of Renal Prostaglandin and Kallikrein

1981 ◽  
Vol 61 (s7) ◽  
pp. 327s-330s ◽  
Author(s):  
Keishi Abe ◽  
Yutaka Imai ◽  
Makito Sato ◽  
Toshiaki Haruyama ◽  
KO Sato ◽  
...  
Keyword(s):  
Renal Disease ◽  
Urinary Excretion ◽  
Creatinine Clearance ◽  
Sodium Excretion ◽  
Prostaglandin E ◽  
Borderline Hypertension ◽  
Fractional Sodium Excretion ◽  
Sustained Hypertension ◽  
Renal Tubular

1. The role of renal prostaglandin E (PGE) and kallikrein in the mechanism of the exaggerated fractional sodium excretion in hypertensive patients with advanced renal disease was investigated. 2. Urinary excretion of PGE and kallikrein was significantly decreased in patients with sustained hypertension. 3. Four times higher values for fractional sodium excretion and four or five times higher values for the urinary excretion of PGE corrected for creatinine clearance were found in patients with sustained hypertension. There was a significant positive correlation (r = 0.677) between the two, suggesting that PGE in the renal tubular compartment may be involved in the mechanism of the exaggerated fractional Na excretion in patients with advanced renal disease. 4. The urinary excretion rate of kallikrein corrected for creatinine clearance was three times greater in patients with borderline hypertension, but not significantly increased in those with sustained hypertension, compared with that in healthy volunteers.

Potassium homeostasis in chronic experimental diabetes mellitus in rats

1984 ◽  
Vol 105 (2) ◽  
pp. 239-244 ◽  
Author(s):  
Matsuhiko Hayashi ◽  
Shigetoshi Senba ◽  
Ikuo Saito ◽  
Waichi Kitajima ◽  
Takao Saruta
Keyword(s):  
Diabetes Mellitus ◽  
Renal Function ◽  
Urinary Excretion ◽  
Plasma Potassium ◽  
Diabetic Rats ◽  
Prostaglandin E ◽  
Potassium Homeostasis ◽  
Dietary Potassium ◽  
Urinary Potassium ◽  
Potassium Loading

Abstract. To examine potassium homeostasis in diabetes mellitus, we observed the effect of dietary potassium loading on the renin-angiotensin-aldosterone system and potassium balance in streptozotocin-induced diabetic rats. In diabetic rats with 26.51 ± 1.89 mmol/l of serum glucose, the plasma renin activity (PRA), plasma aldosterone (PA), immunoreactive insulin (IRI) and urinary excretion of prostaglandin E2 (PGE2) were all significantly lower than in control rats, but the plasma potassium and renal function were not significantly different. With potassium loading, both control and diabetic rats showed a similar increase in plasma potassium and urinary potassium excretion and a decrease in PRA, but the IRI, plasma corticosterone and urinary excretion of PGE2 exhibited no significant change. On the other hand, the PA was significantly increased only in the control rats, and not in the diabetic rats on potassium loading. Based up on these results, it is suggested that potassium homeostasis is well maintained in diabetic rats with normal renal function in spite of an attenuated response of aldosterone secretion to dietary potassium loading and insulin deficiency.

scholarly journals 103 URINARY EXCRETION OF PROSTAGLANDIN E FOLLOWING THE ADMINISTRATION OF FUROSEMIDE AND INDOMETHACIN TO SICK LOW BIRTHUEIGHT INFANTS

1978 ◽  
Vol 12 ◽  
pp. 381-381
Author(s):  
Zvi Friedman ◽  
Laurence M Demers ◽  
Susan B Uhrmann ◽  
Keith H Marks ◽  
M Jeffrey Maisels
Keyword(s):  
Urinary Excretion ◽  
Prostaglandin E

scholarly journals Effect of Spironolactone on Urinary Excretion of Immunoreactive Prostaglandin E in Essential Hypertension and Primary Aldosteronism

1978 ◽  
Vol 124 (4) ◽  
pp. 297-305 ◽  
Author(s):  
SATORU CHIBA ◽  
KEISHI ABE ◽  
MINORU YASUJIMA ◽  
NOBUO IROKAWA ◽  
MASAHIDE SEINO ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Urinary Excretion ◽  
Primary Aldosteronism ◽  
Prostaglandin E
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