Effect of metabolic alkalosis and metabolic acidosis on urinary kallikrein excretion of anaesthetized rats: evidence for a role of blood pH as regulator of renal kallikrein secretion

1996 ◽  
Vol 432 (2) ◽  
pp. 202-206 ◽  
Author(s):  
Marcos Marin-Grez ◽  
Patricia Vallés
Keyword(s):  
Metabolic Acidosis ◽  
Metabolic Alkalosis ◽  
Urinary Kallikrein ◽  
Blood Ph ◽  
Urinary Kallikrein Excretion ◽  
Anaesthetized Rats ◽  
Renal Kallikrein

Role of renal kallikrein in control of renin release in conscious rats

1983 ◽  
Vol 244 (3) ◽  
pp. E262-E265 ◽  
Author(s):  
M. Kobayashi ◽  
S. Suzuki ◽  
K. Hashiba
Keyword(s):  
Renin Release ◽  
Protease Production ◽  
Urinary Kallikrein ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Urinary Kallikrein Excretion ◽  
Renal Kallikrein

Renal kallikrein was reported to activate human inactive renin and to release active renin from rat renal cortical slices. To evaluate the role of renal kallikrein in the control of renin release in vivo, Trasylol and soybean trypsin inhibitor (SBTI) were used to determine whether they can inhibit renin release stimulated by the administration of furosemide and a 2-wk low-sodium diet. Plasma renin activity (PRA) was increased by furosemide and also by the low-sodium diet. Urinary kallikrein excretion was increased by the sodium depletions. Trasylol did not affect basal PRA; however, it inhibited PRA and urinary kallikrein excretion, when stimulated by furosemide and by a low-sodium diet. These results suggest that furosemide and low-sodium diet act on the kidney to release renin via protease production. Because SBTI affected neither PRA nor urinary kallikrein excretion stimulated by these sodium depletions, it is suggested that renal kallikrein may play an important role in the control of renin release stimulated by furosemide and by low-sodium diet.

Changes in Renal and Urinary Kallikrein Activity by Mannitol-Induced Osmotic Diuresis

1981 ◽  
Vol 61 (1) ◽  
pp. 47-51 ◽  
Author(s):  
G. Bönner ◽  
M. Marin-Grez ◽  
D. Beck ◽  
M. Deeg ◽  
F. Gross
Keyword(s):  
Renal Cortex ◽  
Plasma Aldosterone ◽  
Urinary Kallikrein ◽  
Osmotic Diuresis ◽  
Plasma Aldosterone Concentration ◽  
Urinary Kallikrein Excretion ◽  
Short Period ◽  
Urinary Potassium ◽  
Renal Kallikrein ◽  
Kallikrein Activity

1. Osmotic diuresis was induced in male Sprague-Dawley rats by a 30% (w/v) mannitol solution injected three times at 15-min intervals. Kallikrein excretion increased for a short period after the first two injections, but, despite marked diuresis, the increment of kallikrein excretion after the second injection was less marked than after the first and no enhanced kallikrein excretion was observed after the third injection of mannitol. 2. Urinary kallikrein excretion correlated only with urinary potassium excretion. No correlation was found with either urine volume or urinary sodium excretion. 3. At the end of the osmotic diuresis kallikrein activity was significantly reduced both in the urine and in the renal cortex. At that time plasma aldosterone concentration was slightly greater in the mannitol-treated than that in the control group, but the difference did not reach statistical significance. 4. In this experiment no relationship was observed between the activity of the renal kallikrein-kinin system and the plasma aldosterone concentration. 5. The transient increase in urinary kallikrein excretion is interpreted as a wash-out effect of renal kallikrein, which is followed by a diminished kallikrein activity in urine and in renal cortex.

Effect of vasopressin on renal kallikrein excretion

1980 ◽  
Vol 239 (4) ◽  
pp. F388-F392 ◽  
Author(s):  
Géza Fejes-TÓth ◽  
Tibor Zahajszky ◽  
János Filep
Keyword(s):  
Technical Assistance ◽  
Free Water ◽  
Urinary Kallikrein ◽  
Water Diuresis ◽  
Free Water Clearance ◽  
Kinin System ◽  
Urinary Kallikrein Excretion ◽  
Renal Kallikrein ◽  
Kallikrein Kinin System ◽  
Induced Changes

In an attempt to investigate a possible interaction between vasopressin and the renal kallikrein-kinin system, renal function and urinary kallikrein excretion were monitored in trained conscious dogs and in anesthetized rats in water diuresis and in vasopressin-induced antidiuresis. Vasopressin elevated urinary kallikrein excretion in a dose-dependent way in both species, with concomitant increases in urinary osmolality and electrolyte excretion. A significant increase in kallikrein excretion was observed with a dose of vasopressin as low as 2 mU·kg-1·h-1 in the dog and 3 mU·kg-1·h-1 in the rat without a change in renal hemodynamics. In the rat vasopressin-induced changes in kallikrein excretion were positively correlated with changes in sodium and potassium excretion and negatively correlated with changes in free water clearance. It is concluded that vasopressin over its normal physiological range of concentration stimulates renal kallikrein secretion. Note: With the Technical Assistance of Klára Peres and Edit Spitzár water diuresis; antidiuresis; natriuresis; kinins; dog; rat Submitted on October 8, 1979 Accepted on May 21, 1980

Renal Kallikrein Activity and Urinary Kallikrein Excretion in Rats with Experimental Renal Hypertension

1982 ◽  
Vol 63 (4) ◽  
pp. 349-354 ◽  
Author(s):  
M. Marin-Grez ◽  
G. Schaechtelin ◽  
G. Bönner ◽  
G. Speck ◽  
D. Ganten ◽  
...  
Keyword(s):  
Renal Hypertension ◽  
Plasma Renin ◽  
Renin Activity ◽  
Urinary Kallikrein ◽  
Hypertensive Rats ◽  
Control Value ◽  
Urinary Kallikrein Excretion ◽  
Renal Kallikrein ◽  
Experimental Renal Hypertension ◽  
Kallikrein Activity

1. Rats were made hypertensive by ligating the aorta between the origins of both renal arteries. Sham-operated animals served as controls. Urinary and renal kallikrein activities, as well as plasma and renal renin activities, were measured 8 and 90 days after surgery. 2. Blood pressure was 155 ± 6 mmHg on day 8 after aortic ligature and 142 ± 6 mmHg on day 90; in controls pressures were 107 ± 3 and 110 ± 5 mmHg respectively. 3. Eight days after aortic ligature, kallikrein activity in the ischaemic kidneys was about 6·5 times, and in the non-ischaemic kidneys almost 2 times, that in controls. After 90 days the kallikrein activity was reduced to one-half of that in the controls in the ischaemic kidneys and it was normal in the contralateral. 4. The urinary kallikrein excretion of hypertensive rats was about one-third of that of the controls at both 8 and 90 days after aortic ligature. 5. The plasma renin activity in hypertensive rats was approximately seven times that in control animals 8 days after aortic ligature and did not differ from the control value after 90 days. Renin activity in the kidneys showed the same pattern as in other models of renovascular hypertension: elevation in the ischaemic kidney and reduction in the non-ischaemic one.

Effect of pH and amiloride on the intrarenal formation of kinins

1983 ◽  
Vol 245 (2) ◽  
pp. F198-F203
Author(s):  
A. G. Scicli ◽  
M. A. Diaz ◽  
O. A. Carretero
Keyword(s):  
Urinary Kallikrein ◽  
Urinary Ph ◽  
Kinin System ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Urinary Kallikrein Excretion ◽  
Renal Kallikrein ◽  
Kallikrein Kinin System ◽  
Lower Urinary

Changes in urinary kallikrein excretion are assumed to reflect changes in intrarenal formation of kinins. Yet factors that alter the enzymatic activity of renal kallikrein and kininases may alter the concentration of kinins in the nephron independent of amount of kallikrein excreted. In anesthetized rats, we measured excretion of urinary kallikrein (kininogenase activity) and kinin excretion during altered urinary pH and after amiloride, which reportedly inhibits urinary kallikrein. In rats fed a low sodium diet, urine was acidified by intravenous 0.28 M sodium sulfate. This decreased urinary pH from 6.1 +/- 0.09 to 5.3 +/- 0.17 and urinary kinin excretion from 28.0 +/- 9.0 to 10.5 +/- 5.0 pg/min. Urinary kallikrein excretion doubled from 43.0 +/- 5.0 to 82.5 +/- 13.5 ng/min. The optimum pH of kallikrein is congruent to 8.5, so the decreased excretion of urinary kinins is probably secondary to decreased kininogenase activity at lower urinary pH. Amiloride decreased urinary kinins from 35.5 +/- 7.3 to 18.2 +/- 2.5 pg/min and kallikrein from 18.7 +/- 4.9 to 9.3 +/- 1.8 ng/min, while urinary pH increased from 6.7 +/- 0.07 to 7.3 +/- 0.07. The depressed excretion of kallikrein and kinins with amiloride may not have been due to inhibition of kallikrein, since amiloride (1 mM) did not inhibit the kininogenase activity of rat urinary kallikrein (congruent to 1.2 nM) on dog or rat kininogen in vitro. We conclude that changes in urinary kallikrein may not reflect changes in intrarenal formation of kinins. These data also indicate that kallikrein excretion increases and kinin formation decreases when urine is acidified in the distal nephron and that there may be a link between the kallikrein-kinin system and the renal mechanisms affected by amiloride.

scholarly journals High serum bicarbonate and adverse outcomes in hemodialysis patients

2021 ◽  
Vol 35 (1) ◽  
pp. 35-38
Author(s):  
Gonçalo Ávila ◽  
◽  
Ivo Laranjinha ◽  
Patrícia Matias ◽  
◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Metabolic Alkalosis ◽  
Hemodialysis Patients ◽  
High Serum ◽  
Adverse Outcomes ◽  
Morbidity And Mortality ◽  
Main Concern ◽  
Serum Bicarbonate ◽  
Acid Base ◽  
Blood Ph

Metabolic acidosis is a usual complication of progressive chronic kidney disease and is associated with morbidity and mortality. The correction of metabolic acidosis is a main goal of dialysis. In prevalent hemodialysis patients, acid-base homeostasis depends on many factors, mainly net acid production, amount of alkali given by the dialysate bath and duration of the interdialytic period. At present, the main concern in prevalent hemodialysis patients is not over patients with metabolic acidosis, but rather about the growing numbers of patients with metabolic alkalosis. Several large cohort studies have shown significant associations between high predialysis bicarbonate, as well as blood pH, and morbidity and mortality risk. Based on recent guidelines, we should keep predialysis serum bicarbonate concentrations at 24-26 mEq/L, although this is opinion-based and there is no consensus on the issue. Furthermore, there should be specific focus on the patient´s nutritional status and reversible comorbidities.

Increased Excretion of Kallikrein during Dexamethasone Administrationl in Normal Man on Low and Normal Salt Intake

1983 ◽  
Vol 65 (5) ◽  
pp. 487-490 ◽  
Author(s):  
José M. López ◽  
Eugenio Arteaga ◽  
José A. Rodriguez ◽  
Héctor Croxatto
Keyword(s):  
Salt Intake ◽  
Sodium Intake ◽  
Direct Action ◽  
Urinary Kallikrein ◽  
Kinin System ◽  
Sodium Potassium ◽  
Urinary Kallikrein Excretion ◽  
Renal Kallikrein ◽  
Normal Men ◽  
Kallikrein Kinin System

1. The effect of dexamethasone administration for 3 days on urinary kallikrein excretion was studied in 12 normal men with normal sodium intake (n=6) or low sodium intake (n=6). Urinary excretion of sodium, potassium, 17-hydroxycorticosteroids, aldosterone and water was also measured in all subjects. 2. Dexamethasone administration was associated with a significant increase in urinary kallikrein excretion (F3, 30 = 6.9; P < 0.001) regardless of sodium intake. No significant correlation could be established between the increase in urinary kallikrein excretion and changes in urinary sodium, potassium, 17-hydroxycorticosteroids, aldosterone or water. 3. These results suggest that dexamethasone can exert a direct action on the renal kallikrein-kinin system.

The Mechanism of Urinary Kallikrein Excretion in the Rat

1982 ◽  
Vol 63 (2) ◽  
pp. 217-218 ◽  
Author(s):  
A. Martínez Seeber ◽  
S. B. Vila ◽  
O. L. Catanzaro
Keyword(s):  
Wistar Rats ◽  
Filtration Rate ◽  
Glucose Solution ◽  
Urine Flow ◽  
Urinary Flow ◽  
Urinary Kallikrein ◽  
Osmotic Diuresis ◽  
Urinary Kallikrein Excretion ◽  
Renal Kallikrein ◽  
Male Wistar Rats

1. In male Wistar rats urinary kallikrein excretion was positively correlated with urinary flow and glomerular filtration rate (GFR). 2. Osmotic diuresis produced by a 30% (w/v) glucose solution increased urinary kallikrein, and a positive correlation between this variable and urine flow was observed. No correlation was observed with GFR. 3. The mechanism of urinary kallikrein excretion is interpreted as a wash-out effect of renal kallikrein.

Respiratory acidosis in carbonic anhydrase II-deficient mice

1998 ◽  
Vol 274 (2) ◽  
pp. L301-L304 ◽  
Author(s):  
Yeong-Hau H. Lien ◽  
Li-Wen Lai
Keyword(s):  
Metabolic Acidosis ◽  
Carbonic Anhydrase ◽  
Respiratory Acidosis ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Arterial Blood ◽  
Blood Ph ◽  
Type Ii Pneumocytes ◽  
Deficient Mice

To investigate the role of carbonic anhydrase (CA) II on pulmonary CO2 exchange, we analyzed arterial blood gases from CA II-deficient and normal control mice. CA II-deficient mice had a low arterial blood pH (7.18 ± 0.06) and[Formula: see text] concentration ([[Formula: see text]]; 17.5 ± 1.9 meq/l) and a high [Formula: see text](47.4 ± 5.3 mmHg), consistent with mixed respiratory and metabolic acidosis. To eliminate the influence of metabolic acidosis on arterial blood gases, NaHCO3 (4 mmol/kg body weight) was given intraperitoneally, and arterial blood gases were analyzed 4 h later. Normal mice had a small increase in pH and were able to maintain [Formula: see text] and [[Formula: see text]]. The metabolic acidosis in CA II-deficient mice was corrected ([[Formula: see text]], 22.9 ± 2.4 meq/l), and respiratory acidosis became more profound ([Formula: see text], 50.4 ± 2.4 mmHg). These results indicate that CA II-deficient mice have a partial respiratory compensation for metabolic acidosis. We conclude that CA II-deficient mice have a mixed respiratory and metabolic acidosis. It is most likely that CO2 retention in these animals is due to CA II deficiency in both red blood cells and type II pneumocytes.

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