Synthesis of Kallikreins by Rat Kidney Slices

Nustad, Kjell; Vaaje, Kirsten; Pierce, Jack V.

doi:10.1111/j.1476-5381.1975.tb07353.x

Cited by 151 publications

(43 citation statements)

References 20 publications

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“…It preferentially acts on low molecular weight kininogen substrate to release lysyl-BK. Tissue kallikrein has also been reported to be present in plasma [22,23] Plasma kallikrein preferentially acts on high molecular weight kininogen substrate to release BK. BK promotes both cardiovascular and renal functions, for example, vasodilation, naturesis and diuresis [24,25] BK is rapidly (< 15 sec) inactivated by circulating kinases [26] BK acts on B1receptor (B1R) and B2 receptor (B2R) [27] to elicit physiological and pharmacological actions.…”

Section: The Bradykinin System and Diabetesmentioning

confidence: 99%

The Role of Bradykinin System in Type 2 Diabetes

Sharma¹

2016

J Diabetes Metab

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Section: The Bradykinin System and Diabetesmentioning

confidence: 99%

The Role of Bradykinin System in Type 2 Diabetes

Sharma¹

2016

J Diabetes Metab

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“…Renal kallikrein is synthesized by the kidney (Nustad et al, 1975) and has been found to be released into the urine and perfusion fluid of isolated perfused 'Author for correspondence. 2Present address: University of Tirana, Albania.…”

Section: Introductionmentioning

confidence: 99%

Urinary kallikrein excretion during inhibition of endogenous angiotensin II in the pig

Binder¹,

Maier²,

Rana³

et al. 1986

British J Pharmacology

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1 This study was performed to assess the possible contribution ofendogenous angiotensin II (All) to the regulation of urinary kallikrein excretion. The All antagonist saralasin or the saline vehicle was infused into the aorta above the renal arteries of pigs under halothane-02/N20 anaesthesia. Systemic and renal functional parameters were followed for 140 min and during stimulation of the reninangiotensin system by haemorrhage. 2 Urinary kallikrein excretion, determined as kininogenase activity, was increased immediately upon both initiation and termination of the 2 h saralasin infusion into pigs not subjected to haemorrhage. Renal cortical blood flow (RCBF) was maintained in both saline and saralasin-treated animals at blood pressures as low as 70 mm Hg, while glomerular filtration rate was dissociated during saralasin infusion. As long as RCBF was maintained, urinary kallikrein excretion rate was elevated during the progressive hypotension in both saline and saralasin-treated animals. 3 These findings confirm a close relationship between the maintenance of RCBF and increased activity of the kallikrein-kinin system whether or not All is antagonized, and indicate that during haemorrhage the kallikrein-kinin system is stimulated by a mechanism not involving All.

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“…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.…”

mentioning

confidence: 99%

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

Yasujima

Abe

Tanno

et al. 1985

Tohoku J. Exp. Med.

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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

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Synthesis of Kallikreins by Rat Kidney Slices

Cited by 151 publications

References 20 publications

The Role of Bradykinin System in Type 2 Diabetes

The Role of Bradykinin System in Type 2 Diabetes

Urinary kallikrein excretion during inhibition of endogenous angiotensin II in the pig

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

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