Stimulation of arachidonic acid metabolism in rat kidney mesangial cells by bradykinin, antidiuretic hormone, and their analogues

Uglesity, A.; Kreisberg, Jeffrey I.; Levine, Lawrence

doi:10.1016/s0262-1746(83)80023-7

Cited by 33 publications

(10 citation statements)

References 11 publications

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“…Other data are beginning to suggest that renal kallikrein and kinins participate in tubuloglomerular feedback mechanisms (1)(2)(3)(4)(5)(6)(7)(8), and our preliminary studies support the possibility that the abnormalities of renal kallikrein we have discovered may contribute to abnormalities in renal hemodynamics and glomerular filtration. In the untreated STZ-diabetic rat, reduced renal and urinary active kallikrein are associated with reduced glomerular filtration rate and renal plasma flow, and both the kallikrein and renal function abnormalities are reversed by treatment with insulin (39).…”

Section: Discussionsupporting

confidence: 60%

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Abnormal regulation of renal kallikrein in experimental diabetes. Effects of insulin on prokallikrein synthesis and activation.

Jaffa

Miller²,

Bailey³

et al. 1987

J. Clin. Invest.

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The effects of streptozotocin (STZ) diabetes and insulin on regulation of renal kallikrein were studied in the rat. 1 and 2 wk after STZ injection, diabetic rats had reduced renal levels and urinary excretion of active kallikrein. Tissue and urinary prokallikrein levels were unchanged, but the rate of renal prokallikrein synthesis relative to total protein synthesis was reduced 3045% in diabetic rats. Treatment of diabetic rats with insulin prevented or reversed the fall in tissue level and excretion rate of active kallikrein and normalized prokallikrein synthesis rate. To further examine insulin's effects, nondiabetic rats were treated with escalating insulin doses to produce hyperinsulinemia. In these rats, renal active kallikrein increased. Although renal prokallikrein was not increased significantly by hyperinsulinemia, its synthesis was increased. As this was accompanied by proportionally increased total protein synthesis, relative kallikrein synthesis rate was not changed. Excretion of active kallikrein was unchanged, but prokallikrein excretion was markedly reduced. Therefore, increased tissue active kallikrein seen with hyperinsulinemia can be explained not only by increased synthesis but also by retention and increased activation of renal prokallikrein. These studies show that STZ diabetes produces an impairment in renal kallikrein synthesis and suggest that this disease state also impairs renal prokallikrein activation. The findings also suggest that insulin modulates renal kallikrein production, activation, and excretion.

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Section: Discussionsupporting

confidence: 60%

“…arterioles and glomerular mesangial cells support the possibility that the renal kallikrein-kinin system may be a participant in the tubuloglomerular feedback mechanisms that regulate glomerular function (5)(6)(7)(8). Kinins can also cause marked changes in electrolyte and water transport in renal tubules and in other transporting epithelia (9)(10)(11)(12).…”

mentioning

confidence: 99%

Abnormal regulation of renal kallikrein in experimental diabetes. Effects of insulin on prokallikrein synthesis and activation.

Jaffa

Miller²,

Bailey³

et al. 1987

J. Clin. Invest.

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“…At 10-8moll-P of Hoe 140, BK-induced cyclic GMP formation was reduced by about 50% and totally suppressed at (Regoli, 1984). (Terragno et at., 1975;Uglesity et al, 1983;Zusmann, 1987). The stimulatory effect of BK on vascular PGI2 synthesis could be explained by an increase in kinin activity.…”

Section: Introductionmentioning

confidence: 99%

Hoe 140 a new potent and long acting bradykinin‐antagonist: in vitro studies

Hock¹,

Wirth²,

Albus³

et al. 1991

British J Pharmacology

659

330

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Hoe 140 (d‐Arg‐[Hyp3, Thi5, d‐Tic7, Oic8]bradykinin) is a new bradykinin (BK)‐antagonist. It was tested in several in vitro assays and compared with d‐Arg‐[Hyp2, Thi5,8,d‐Phe7]BK. In receptor binding studies in guinea‐pig ileum preparations, Hoe 140 showed an IC50 of 1.07 × 10−9mol l−1 and a KI value of 7.98 × 10−10 mol l−1. In isolated organ preparations Hoe 140 and d‐Arg‐[Hyp2, Thi5,8, d‐Phe7]BK inhibited bradykinin‐induced contractions concentration dependently, with IC50‐values in the guinea‐pig ileum preparation of 1.1 × 10−8 mol l−1 and 3 × 10−5 mol l−1, respectively. pA2 values in this tissue were 8.42 and 6.18, respectively. In the rat uterus preparation the IC50 value was 4.9 × 10−9 mol l−1 for Hoe 140. d‐Arg‐[Hyp2, Thi5,8, d‐Phe7]BK showed an IC50 of 4.0 × 10−6 mol l−1. The IC50 values in the guinea‐pig isolated pulmonary artery were 5.4 × 10−9 mol l−1 and 6.4 × 10−6 mol l−1, respectively. In the rabbit aorta no inhibitory effects on Des‐Arg9‐BK induced contractions were observed. In cultured bovine endothelial cells, Hoe 140 antagonized (IC50 = 10−8 mol l−1) bradykinin‐induced endothelium‐derived relaxing factor (EDRF) release and the bradykinin‐induced increase in cytosolic free calcium (IC50 = 10−9 mol l−1). Hoe 140 (10−7 mol l−1) totally suppressed the bradykinin‐induced (10−8 to 10−4mol l−1) prostacyclin (PGI2) release from cultured endothelial cells of bovine aorta. d‐Arg‐[Hyp2, Thi5,8, d‐Phe7]BK (10−7 mol l−1) showed a weaker antagonism. Taken together these results show that Hoe 140 is a highly potent bradykinin antagonist. It was two to three orders of magnitude more potent than d‐Arg‐[Hyp2, Thi5,8, d‐Phe7]BK.

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“…Accumulated data suggest that the renal kallikrein-kinin system has a paracrine function to regulate glomerular hemodynamics (10)(11)(12), and interactions have been described between renal kallikrein, kinins, eicosanoids, ANP, and the renin-angiotensin system (13)(14)(15)(16)(17). We previously reported that insulin-treated IDDM patients show increased kidney excretion of active kallikrein (18), whereas untreated severely hyperglycemic streptozocin-induced diabetic (STZ-KALUKREIN IN THE DIABETIC KIDNEY SD) rats show reduced renal kallikrein synthesis and active kallikrein excretion (19,20).…”

mentioning

confidence: 99%

Renal Kallikrein and Hemodynamic Abnormalities of Diabetic Kidney

Harvey

Jaffa²,

Margolius³

et al. 1990

Diabetes

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The relationship between renal hemodynamic abnormalities and renal kallikrein activity was studied in streptozocin-induced diabetic rats. Diabetic rats were either not treated with insulin and had plasma glucose levels greater than 400 mg/dl (severely hyperglycemic diabetic [SD]) or were treated with 1.5-1.75 U/day protamine zinc insulin and had glucose levels of 200-300 mg/dl (moderately hyperglycemic diabetic [MD]). In SD rats, kidney tissue level and excretion of active kallikrein were reduced after 3 wk compared with age-matched nondiabetic control rats (tissue, 11.7 +/- 1.9 vs. 20.5 +/- 1.8 ng/mg protein, P less than 0.005; urine, 126 +/- 12 vs. 179 +/- 10 micrograms/24 h, P less than 0.005). Despite increased kidney size, renal plasma flow (RPF) was reduced in SD rats (5.38 +/- 0.23 vs. 6.37 +/- 0.20 ml/min, P less than 0.05). Glomerular filtration rate (GFR) was not significantly lower (2.77 +/- 0.60 vs. 3.02 +/- 0.56 ml/min). In MD rats, kidney tissue level and excretion of active kallikrein were increased after 5 wk compared with age-matched nondiabetic control rats (tissue, 28.4 +/- 1.3 vs. 23.3 +/- 1.7 ng/mg protein, P less than 0.05; urine, 289 +/- 16 vs. 196 +/- 13 micrograms/24 h, P less than 0.001). In MD rats, GFR and RPF were increased (3.80 +/- 0.11 and 8.04 +/- 0.17 ml/min, respectively) compared with control rats (3.22 +/- 0.05 and 7.28 +/- 0.09 ml/min, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

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Stimulation of arachidonic acid metabolism in rat kidney mesangial cells by bradykinin, antidiuretic hormone, and their analogues

Cited by 33 publications

References 11 publications

Abnormal regulation of renal kallikrein in experimental diabetes. Effects of insulin on prokallikrein synthesis and activation.

Abnormal regulation of renal kallikrein in experimental diabetes. Effects of insulin on prokallikrein synthesis and activation.

Hoe 140 a new potent and long acting bradykinin‐antagonist: in vitro studies

Renal Kallikrein and Hemodynamic Abnormalities of Diabetic Kidney

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