The renal kallikrein-kinin system.

Abe

Tanno

et al. 1985

To assess possible interactions of circulating vasopressin with the synthesis or activation of renal kallikrein, we studied the effect of chronic infusion of vasopressin (7.2 U/kg/day i.p.) for 6 days on the urinary excretion of total and active kallikrein in conscious rats. We determined urinary total, active and inactive kallikrein by measuring kallikrein activity using a kininogenase assay before and after the treatment with trypsin (200pg/ml). Chronic infusion of vasopressin induced sustained decreases in urinary total, active and inactive kallikrein excretion, but did not affect the ratio of active to total kallikrein. The infusion of vasopressin induced significant increases in circulating levels of vasopressin (248.1± 35.2 pg/ml in vasopressin-infused rats (n = 7) compared to 95.5± 14.6 pg/ml in vehicle-infused rats (n = 7), p <0.001) and in weight gain (39.6± 1.3 g in vasopressin-infused rats (n = 7) compared to 29.1 ± 3.3 g in vehicle-infused rats (n = 7), p <0.05), and also sustained decreases in water intake and urine volume, but it did not induce any change in urinary sodium excretion. Circulating levels of angiotensin II was decreased by chronic infusion of vasopressin. Thus, the present study suggests that the elevation of circulating vasopressin levels induces a decrease in the synthesis of renal kallikrein. total kallikrein ; trypsinactivated kallikrein ; renal kallikrein system ; antidiuretic hormone Kallikrein is a serine protease which is synthesized by the kidney and excreted in the urine (Nustad et al. 1975). It liberates kinins, potent vasodilator peptides, from its natural substrate kininogen. Several previous studies have examined the response of urinary kallikrein excretion to altered water metabolism and infused vasopressin in experimental animals and humans (Levinsky 1979;Carretero and Scicli 1980). Previously we have also shown that the infusion of Med

Section: Discussionmentioning

confidence: 93%

“…It liberates kinins, potent vasodilator peptides, from its natural substrate kininogen. Several previous studies have examined the response of urinary kallikrein excretion to altered water metabolism and infused vasopressin in experimental animals and humans (Levinsky 1979;Carretero and Scicli 1980). Previously we have also shown that the infusion of Med…”

mentioning

confidence: 99%

Decreased urinary active and inactive kallikrein by chronic infusion of vasopressin in conscious rats.

Abe

Tanno

et al. 1985

“…The kallikrein-kinin system has been proposed as a contributor to the regulatory control of blood pressure, renal blood flow, and excretion of sodium and water (Levinsky 1979;Carretero and Scicli 1980;Margolius 1983). Studies suggest that impaired renal kallikrein and kinins system is relevant to hypertensive and renal diseases (hayfield and Margolius 1983), and diabetes mellitus (Jaffa et al 1987; Harvey et al 1990).…”

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confidence: 99%

Urinary Active Kallikrein Excretion and Diabetic Renal Impairments in Streptozotocin-Treated Rats.

Yoshida

Kanazawa

et al. 1993

To assess possible roles of the renal kallikrein-kinin system in the development of renal impairments in diabetes mellitus, we determined daily excretion of urinary total and active kallikrein in uninephrectomized Wistar-Kyoto rats made diabetic by streptozotocin (45 mg/kg) as a bolus injection. We also evaluated the effect of captopril (50 mg/kg/day) administered orally on the development of diabetic renal impairments in the streptozotocin-treated rats. Active kallikrein was determined by its kininogenase activity, and generated kinins were radioimmunologically measured. Total kallikrein was also determined by measuring kininogenase activity after inactive kallikrein had been activated with trypsin (200,ag/ml). Urinary active kallikrein excretion was significantly reduced in streptozotocin-treated rats whereas urinary total kallikrein excretion was unchanged, resulting in the decreased ratio of active to total kallikrein compared to that in the controls. These reductions were preceded by the increased excretion of urine protein measured as an ilidex of renal impairments. The administration of captopril for 12 weeks attenuated the development of diabetic renal impairments evaluated by urine protein excretion in streptozotocin-treated rats, although it did not induce significant changes in urinary total and active kallikrein excretion, and the ratio of active to total kallikrein. Thus the results of this study indicate that the renal kallikrein-kinin system might not play major roles in the development of diabetic renal impairments in the rat, although the pathophysiological relevance of impaired activation of renal kallikrein system to the development of diabetic renal impairments remains to be determined. In addition, they suggest that the renoprotective effects of captopril may , be independent of the activation of renal kallikrein system in streptozotocin-treated rats.renal kallikrein-kinin system; active kalli-

“…mineralocorticoids ; inactive kallikrein ; trypsin-activated kallikrein ; renal prostaglandin E2 ; sodium balance It system 1977; is generally agreed that the renal kallikrein-kinin-prostaglandin (PG) E is involved in the regulation of electrolytes and water excretion (Dunn Levinsky 1979;Carretero and Scicli 1980). It is well established that kallikrein in the urine arises within the kidney and its rate of excretion is a function of renal kallikrein synthesis (Nustad et al 1975 ;Levinsky 1979;Carretero and Scicli 1980) although it cannot be excluded that glandular kallikrein from various origin is excreted in the urine. In addition, urinary PGEZ excretion is also regarded as an indicator of the synthesis of renal PGEZ (Frolich et al 1975).…”

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confidence: 99%

“…In addition, urinary PGEZ excretion is also regarded as an indicator of the synthesis of renal PGEZ (Frolich et al 1975). Several previous studies have demonstrated that mineralocorticoids could have a major regulatory influence on renal kallikrein and increase urinary kallikrein excretion (Levinsky 1979;Carretero and Scicli 1980). That mineralocorticoids enhance the activity of the renal kallikrein-kinin system has been inferred from the finding of increased urinary kallikrein excretion in patients with primary aldosteronism and in patients and animals receiving sodium-retaining mineralocorticoids.…”

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confidence: 99%

Long-term effects of aldosterone on kallikrein, prostaglandin E2 and sodium in rats.

Abe

Tanno

et al. 1987

To assess the long-term effects of mineralocorticoids on the regulation of the synthesis or release of kallikrein and prostaglandin E2 in the renal kallikrein-kininprostaglandin E system, we studied the effects of chronic infusion of aldosterone (50,ug/kg/day) on urinary excretion of total and active kallikrein, and prostaglandin E2 for 10 days in conscious rats on regular intakes of sodium and on sodium loading with 1% NaCI as a drinking water. Chronic infusion of aldosterone induced a prompt and transient decrease in the ratio of sodium to potassium and a sustained increase in urinary prostaglandin E2 excretion in rats on regular diets, whereas urinary total and active kallikrein excretion did not increase significantly until the 4th day of aldosterone infusion. In rats loaded with sodium, aldosterone did not induce any changes in urinary total and active kallikrein excretion, whereas it induced similar changes in the ratio of sodium to potassium and urinary prostaglandin E2 excretion to those in rats on regular diets. Thus, the present results suggest that aldosterone might stimulate the synthesis or release of renal prostaglandin E2 independent of sodium balance. Furthermore, it is also suggested that aldosterone might stimulate the synthesis or release of kallikrein, at least partly, via the same pathway as sodium loading does. mineralocorticoids ; inactive kallikrein ; trypsin-activated kallikrein ; renal prostaglandin E2 ; sodium balance It system 1977; is generally agreed that the renal kallikrein-kinin-prostaglandin (PG) E is involved in the regulation of electrolytes and water excretion (Dunn Levinsky 1979;Carretero and Scicli 1980). It is well established that