Bradykinin-induced renal hemodynamic alterations: renin and prostaglandin relationships

Flamenbaum, Walter; Gagnon, John A.; Ramwell, Peter W.

doi:10.1152/ajprenal.1979.237.6.f433

Cited by 24 publications

(14 citation statements)

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“…Previous studies examining the renal hemodynamic and excretory effects of exogenous bradykinin were performed by renal arterial infusion. 8 " 10 This route of infusion may not mimic a physiological route of kinin delivery, because intrarenally formed kinins must reach the vasculature via the interstitium. To address this problem, we have recently developed an infusion technique in our From laboratory by which compounds can be infused and localized in the renal medullary interstitium.…”

Section: Orphological and Functional Data Indicate Thatmentioning

confidence: 99%

Kinin actions on renal papillary blood flow and sodium excretion.

Mattson

Cowley

1993

Hypertension

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Infusion of bradykinin into the renal medullary interstitium (0.1 /ig/min, n=6) significantly increased renal papillary blood flow as measured by laser-Doppler flowmetry to 117±3% of control without altering cortical blood flow or blood pressure in anesthetized Munich-Wistar rats. In animals prepared for clearance studies, renal medullary bradykinin infusion did not alter total renal blood flow, glomerular filtration rate, or renal interstitial hydrostatic pressure but increased urine flow by 100%, sodium excretion by 111%, and fractional sodium excretion by 107%. No changes occurred in mean arterial pressure or contralateral kidney function during the interstitial bradykinin infusion. Blockade of endogenous kinin degradation by interstitial infusion of captopril (1 mg/hr) significantly increased papillary blood flow by 21 ±5% without altering cortical blood flow. Pretreatment with the nitric oxide inhibitor jV c -nltro-L-arginine-methyI ester (2 fig/mia, n=l) eliminated the increase in papillary blood flow associated with either bradykinin or captopril infusion. We conclude that renal medullary interstitial infusion of bradykinin increases sodium and water excretion, which is associated with a selective increase in papillary blood flow by a nitric oxide-dependent mechanism. kinins may act as paracrine agents in the renal medulla. 1 " 3 Intravenous administration of an inhibitor of neutral endopeptidase, the major kininase in the rat kidney, 4 selectively increased renal inner medullary (papillary) blood flow in anesthetized rats.3 This effect was blocked by a kinin receptor antagonist, indicating that an elevation of endogenous kinins can alter medullary blood flow. Similar results have been demonstrated during angiotensin converting enzyme inhibition. Although cortical blood flow increases during inhibition of converting enzyme because of decreased angiotensin II levels, renal medullary blood flow increases because of increased kinins. 6 ' 7 These data indicate that kinins have a primary influence on the renal medullary circulation in the rat. In support of these functional data, morphological data indicate that the intrarenal site of kinin formation and release is in the distal connecting tubule and collecting duct. 1 -3 It is therefore thought that the peptide exerts its physiological effects from the luminal or the interstitial side of the collecting duct in the renal medulla. Previous studies examining the renal hemodynamic and excretory effects of exogenous bradykinin were performed by renal arterial infusion. "10 This route of infusion may not mimic a physiological route of kinin delivery, because intrarenally formed kinins must reach the vasculature via the interstitium. To address this problem, we have recently developed an infusion technique in our laboratory by which compounds can be infused and localized in the renal medullary interstitium. 1112The purpose of the present study was to characterize the effects of renal medullary interstitial infusion of bradykinin on the intrarenal distribution o...

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Section: Orphological and Functional Data Indicate Thatmentioning

confidence: 99%

Kinin actions on renal papillary blood flow and sodium excretion.

Mattson

Cowley

1993

Hypertension

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“…[1][2][3][4][5][6][7][8] Previous studies have shown that kallikrein from the connecting tubule enters the vascular space 9 -11 as well as the interstitium, 8 where it produces bradykinin. Thus, both plasma bradykinin and interstitial bradykinin may be significant regulators of afferent arteriole resistance.…”

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Biphasic Effect of Bradykinin on Rabbit Afferent Arterioles

Carretero

Juncos

et al. 1998

Hypertension

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Abstract-Bradykinin plays an important role in the regulation of renal hemodynamics. However, there have been few studies of the effect of bradykinin on isolated afferent arterioles, vascular segments that are important for the regulation of renal blood flow and glomerular filtration rate. Our purpose was to study (1) the effects of bradykinin on isolated perfused rabbit afferent arterioles and (2) the mechanisms of actions. Afferent arterioles dissected from rabbits were perfused in vitro at 60 mm Hg. In afferent arterioles preconstricted with phenylephrine, 10 Ϫ12 to 10 Ϫ10 mol/L bradykinin increased luminal diameter from 9.0Ϯ1.0 to 14.3Ϯ1.2 m (PϽ0.003). In contrast, 10 Ϫ9 and 10 Ϫ8 mol/L bradykinin decreased luminal diameter to 10.8Ϯ1.4 and 9.7Ϯ1.2 m, respectively (PϽ0.001). Bradykinin added to the bath had no effect on preconstricted afferent arterioles. The addition of [des-Arg 9 ]-bradykinin (10 Ϫ9 and 10 Ϫ8 mol/L), a B 1 receptor agonist, to the lumen decreased diameter from 9.7Ϯ1.2 to 6.7Ϯ1.2 m at 10 Ϫ8 mol/L (PϽ0.002). Icatibant (Hoe 140), a B 2 receptor antagonist, blocked both the vasodilation and vasoconstriction induced by bradykinin as well as the vasoconstriction induced by [des-Arg 9 ]-bradykinin. L-NAME had no effect on bradykinin-induced dilation or constriction. Indomethacin blocked both the dilation induced by 10 Ϫ12 to 10 Ϫ10 mol/L bradykinin and the constriction induced by 10 Ϫ9 to 10 Ϫ8 mol/L bradykinin. In fact, in the presence of indomethacin, 10 Ϫ9 and 10 Ϫ8 mol/L bradykinin increased luminal diameter from 6.2Ϯ0.7 to 10.7Ϯ0.6 m at 10 Ϫ8 mol/L (PϽ0.001), which was attenuated by L-NAME. Finally, in the presence of SQ29548, a prostaglandin H 2 /thromboxane A 2 receptor antagonist, bradykinin caused dilation at all concentrations tested. In conclusion, bradykinin has a biphasic effect on afferent arterioles. Both dilation and constriction may be mediated by bradykinin B 2 receptors. The mechanisms of vasodilation and vasoconstriction are due to cyclooxygenase products, not nitric oxide. (Hypertension. 1998;32:287-292.)

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“…Key Words • bradykinin • kallikrein • angiotensins • blood pressure • mineralocorticoids lease, 13 whereas an opposite effect reportedly occurs after administration of aprotinin, a nonspecific inhibitor of renal kallikrein. 14 In the vasculature, the intrinsic kallikrein-kinin system 8 19 Although these data need to be confirmed, it is tempting to speculate that in vivo stimulation of kinin generation by Ang II could restore the balance between these functionally opposite hormones.…”

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Chronic inhibition of bradykinin B2-receptors enhances the slow vasopressor response to angiotensin II.

et al. 1994

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The contribution of endogenous kinins in the regulation of blood pressure of angiotensin-treated rats was evaluated using the new bradykinin I^-receptor antagonist Hoe 140 (D-Arg^Hyp'.Thi'.D-Tic'.Oic^-bradykinin). Chronic infusion of Hoe 140 at 75 nmol/d (a dose able to inhibit the vasodepressor effect of an intra-aortic bolus injection of 0.85 nmol/kg bradykinin) did not alter systolic blood pressure (tail-cuff plethysmography). Chronic infusion of angiotensin II (Ang II) induced a dose-related increase in systolic blood pressure and plasma Ang II levels. The vasopressor effect of 40 or 100 nmol/d Ang II was enhanced in rats given chronic infusion of Hoe 140 (by 12 and 14 mm Hg, respectively), whereas the increase in plasma Ang II levels remained unaltered. Furthermore, a low nonpressor dose of Ang II (20 nmol/d) was then able to increase blood pressure during chronic blockade of bradykinin receptors by Hoe 140 (from K inins are endogenous vasodilators that act as local hormones by activating the release of endothelium-derived relaxing factors and prostaglandins.

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Bradykinin-induced renal hemodynamic alterations: renin and prostaglandin relationships

Cited by 24 publications

References 0 publications

Kinin actions on renal papillary blood flow and sodium excretion.

Kinin actions on renal papillary blood flow and sodium excretion.

Biphasic Effect of Bradykinin on Rabbit Afferent Arterioles

Chronic inhibition of bradykinin B2-receptors enhances the slow vasopressor response to angiotensin II.

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