Hemodynamics of the Isolated Perfused Rat Kidney in the Absence and Presence of Kallikrein Substrate

Mair, Manfred; Zhegu, Zydi; Binder, Bernd R.

doi:10.1007/978-1-4684-5143-6_24

Cited by 4 publications

(2 citation statements)

References 5 publications

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“…Kinins infused into the renal artery in high doses increase glomerular plasma flow by reducing resistance of afferent and efferent arterioles, but GFR does not increase significantly because the ultrafiltration coefficient falls (39). Infusion of lower doses of kinin into the isolated perfused kidney raises both GFR and RPF (40). The disparity in GFR and RPF responses to high dose kinin is also seen with other potent vasodilators, such as PGE2, which raise RPF but not GRF when infused (39).…”

Section: Discussionmentioning

confidence: 99%

Evidence for renal kinins as mediators of amino acid-induced hyperperfusion and hyperfiltration in the rat.

Jaffa¹,

Vío²,

Silva³

et al. 1992

J. Clin. Invest.

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This study examined the role of tissue kallikrein and kinins in renal vasodilation produced by infusion of amino acids (AA). In rats fed a 9% protein diet for 2 wk, intravenous infusion of a 10% AA solution over 60-90 min reduced total renal vascular resistance and increased glomerular filtration rate (GFR) by 2540% and renal plasma flow (RPF) by 23-30% from baseline. This was associated with a two-to threefold increase in urinary kinin excretion rate. Acute treatment of rats with aprotinin, a kallikrein inhibitor, resulted in deposition of immunoreactive aprotinin in kallikrein-containing connecting tubule cells and inhibited renal kallikrein activity by 90%. Aprotinin pretreatment abolished the rise in urinary kinins and prevented significant increases in GFR and RPF in response to AA. In a second group of rats pretreated with a B2 kinin receptor antagonist, [DArg Hyp3, Thi"'8 D Phe71 bradykinin, AA infusion raised urinary kinins identically as in untreated controls, but GFR and RPF responses were absent. Aprotinin or the kinin antagonist produced no consistent change in renal function in rats that were not infused with AA. AA-induced increases in kinins were not associated with an increase in renal kallikrein activity. Notably, tissue active kallikrein level fell 50% in AA-infused rats.

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Section: Discussionmentioning

confidence: 99%

Evidence for renal kinins as mediators of amino acid-induced hyperperfusion and hyperfiltration in the rat.

Jaffa¹,

Vío²,

Silva³

et al. 1992

J. Clin. Invest.

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“…In the isolated perfused rat kidney, the addition of kininogen to the perfusate leads to an increase in renal plasma flow, glomerular filtration and sodium excretion [45], In patients with liver disease and the hepatorenal syndrome, the administration of fresh frozen plasma (presumably containing kininogen), but not albumin in creases renal blood flow and sodium excretion [46], In summary, our data indicate that a significant reduc tion in kinin excretion is present in patients with liver disease and ascites. A reduction in substrate excretion and enzyme activity are also present and may contribute to the reduction in kinin excretion.…”

Section: Discussionmentioning

confidence: 99%

The Kallikrein-Kininogen-Kinin System in Patients with Liver Disease and Ascites

Solomon

Azar

Trebbin

et al. 1988

Nephron

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The urinary excretion of kininogen, kallikrein (total and active), and kinins were measured in 7 men with severe liver disease and ascites. The results were compared with a group of normal controls matched for sodium excretion. Significant reductions in kinin excretion were noted in the patients with liver disease which could not be accounted for by differences in age, plasma renin, aldosterone excretion or sodium excretion. Both active kallikrein and kininogen excretion were reduced suggesting that deficiencies of enzyme and substrate contributed to the kinin deficiency. The importance of kininogen in the physiologic regulation of kinin excretion in this clinical state is discussed.

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Glomerular autacoids stimulated by bradykinin regulate efferent arteriole tone

Ren

Garvin

Falck

et al. 2003

Kidney International

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We concluded that in response to bradykinin, the glomerulus releases COX metabolites (probably prostaglandins) that have a vasodilator effect. When COXs are inhibited, the vasoconstrictor 20-HETE released by the glomerulus is able to oppose the vasodilator effect of bradykinin. This vasodilator effect is mediated by EETs released by the glomerulus and/or the efferent arteriole and does not involve nitric oxide. The balance between these opposing effects of various eicosanoids controls efferent arteriole resistance downstream from the glomerulus.

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Hemodynamics of the Isolated Perfused Rat Kidney in the Absence and Presence of Kallikrein Substrate

Cited by 4 publications

References 5 publications

Evidence for renal kinins as mediators of amino acid-induced hyperperfusion and hyperfiltration in the rat.

Evidence for renal kinins as mediators of amino acid-induced hyperperfusion and hyperfiltration in the rat.

The Kallikrein-Kininogen-Kinin System in Patients with Liver Disease and Ascites

Glomerular autacoids stimulated by bradykinin regulate efferent arteriole tone

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