The effect of bradykinin on proximal tubular sodium reabsorption in the dog: evidence for functional nephron heterogeneity

Stein, Janice Gross; Congbalay, Rolando C.; Karsh, Dennis L.; Osgood, Richard W.; Ferris, Thomas F.

doi:10.1172/jci106972

Cited by 136 publications

(50 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, there are other factors which regulate GFR, for example, the mean transcapillary hydrostatic pressure (d P), the mean transcapillary oncotic pressure difference, renal plasma flow (RPF) and glomerular ultrafiltration coefficient (Kf). In acute dog experiments, RPF is not a major determinant of GFR, because vasodilators such as acetylcholine and bradykinin increase RPF but do not affect GFR (3,4). In the present experiment, the filtration fraction in dog kidney during forskolin infusion did not change because of the parallel increases in RBF and GFR.…”

Section: Table 1 Effects Of Forskolin On Urine Flow and Excretion Ofcontrasting

confidence: 43%

“…These results suggest that these renal vasodilators show preferential action for dilating the preglomerular arteriole over the postglomerular arteriole. On the other hand, intrarenal infusion of acetylcholine or bradykinin increase RBF but do not alter GFR (3,4), indicating that acetylcholine and bradykinin dilate both arterioles equally. These findings suggest that the different responses of the afferent and efferent arterioles result from stimulation of a different adenylate cyclase-cAMP system in each arteriole.…”

mentioning

confidence: 91%

See 1 more Smart Citation

Forskolin preferentially dilates the afferent arteriole in the canine kidney.

et al. 1991

View full text Add to dashboard Cite

ABSTRACT-Intrarenal infusion of forskolin (0.2,ug/kg/min) in anesthetized dogs increased renal blood flow (RBF) and glomerular filtration rate (GFR) to the same degree but did not change the mean arterial pressure or heart rate. Forskolin also increased urine flow and urinary sodium excretion. The proportional increases in RBF and GFR may result from a preferential action of forskolin to dilate the afferent arteriole.The role of adenosine 3'5'-cyclic monophosphate (cAMP) as a second messenger of hormone-or drug-induced vasodilation has been investigated. A rise in intracellular cAMP concentration is believed to be responsible for the relaxation of vascular smooth muscle by certain drugs. We previously reported that isoproterenol and glucagon, both stimulators of adenylate cyclase, increased not only renal blood flow (RBF) but also glomerular filtration rate (GFR) (1, 2). These results suggest that these renal vasodilators show preferential action for dilating the preglomerular arteriole over the postglomerular arteriole. On the other hand, intrarenal infusion of acetylcholine or bradykinin increase RBF but do not alter GFR (3, 4), indicating that acetylcholine and bradykinin dilate both arterioles equally. These findings suggest that the different responses of the afferent and efferent arterioles result from stimulation of a different adenylate cyclase-cAMP system in each arteriole.Forskolin is a powerful adenylate cyclase stimulator and a good pharmacological tool for investigating the role of cAMP in vasodilation (5). We have reported that forskolin stimulates the accumulation of cAMP in the isolated afferent arterioles (6). In the present study, we examined the effects of intrarenal infusion of forskolin on renal hemodynamics and renal function and discussed the role of cAMP on the regulation of renal hemodynamics.Experiments were performed on adult mongrel dogs of both sexes, weighing 9 -13 kg, which were maintained on standard laboratory diet for I week. The animals were anesthetized with sodium pentobarbital (30 mg/kg i.v.) and were given additional doses as required. After tracheotomy, the dogs were mechanically ventilated with room air. Catheters were inserted into the right brachial vein and artery for infusion of saline and for arterial blood sampling. Renal arterial pressure was measured from a catheter inserted into the right femoral artery and advanced into the abdominal aorta just below the left renal artery. The left kidney was exposed through a retroperitoneal flank incision. The kidney was denervated by carefully sectioning all visible nerve fibers associated with the renal vessels.

show abstract

Section: Table 1 Effects Of Forskolin On Urine Flow and Excretion Ofcontrasting

confidence: 43%

mentioning

confidence: 91%

Forskolin preferentially dilates the afferent arteriole in the canine kidney.

et al. 1991

View full text Add to dashboard Cite

show abstract

“…Because renal medullary interstitial bradykinin infusion increased sodium and water excretion but did not change glomerular filtration rate or renal blood flow, the significant increase in fractional sodium excretion indicates that the natriuresis and diuresis during bradykinin were due to direct or indirect effects of bradykinin to alter tubular transport. Micropuncture studies indicate no direct effect of bradykinin to alter proximal tubular sodium and water reabsorption, 10 although direct infusion of bradykinin into the distal nephron appears to inhibit the distal nephron reabsorption of radiolabeled sodium. 16 In addition, bradykinin has been demonstrated to oppose the hydroosmotic effects of vasopressin in the rabbit cortical collecting duct 17 and to inhibit sodium reabsorption in the rat cortical collecting duct.…”

Section: Discussionmentioning

confidence: 92%

“…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

View full text Add to dashboard Cite

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...

show abstract

“…It has been suggested that the hemodynamic effect of these agents alters Starling forces in the peritubular capillary circulation leading to a fall in the proximal tubular reabsorption of sodium (1). Direct micropuncture studies have shown that neither bradykinin nor prostaglandin E2 alters proximal tubular sodium reabsorption (2). Earley and Friedler (3) suggested that renal vasodilatation may cause a natriuresis as a consequence of the washout of the hypertonic medullary interstitium occurring in this setting.…”

Section: Introductionmentioning

confidence: 99%

Studies on the Mechanism of Sodium Excretion during Drug-induced Vasodilatation in the Dog

Fadem¹,

Hernandez-Llamas²,

Patak³

et al. 1982

J. Clin. Invest.

Self Cite

View full text Add to dashboard Cite

A B S T R A C T The administration of vasodilating agents such as bradykinin and acetylcholine cause an increase in urinary sodium excretion. Yet the mechanisms involved in this natriuretic effect are not clear. Recent studies with another renal vasodilator, secretin have shown this drug also causes a profound increase in renal blood flow but without major changes in sodium excretion. To attempt to delineate the basis of this difference in sodium excretion with these drugs, the renal functional effects of secretin and bradykinin were compared at an equivalent vasodilating dose. Bradykinin increased renal blood flow from 222 to 342 ml/min, urine volume from 0.2 to 1.2 ml/min, and urine sodium excretion from 28 to 115,ueq/min. Urine osmolality fell from 1,230 to 401 mosmol/kg. Secretin caused a comparable increase in renal blood flow (216 to 325 ml/min) while changes in urine flow, sodium excretion, and urine osmolality were significantly less.In further studies papillary plasma flow was estimated using the albumin accumulation technique. Control papillary plasma flow was 29 ml/min per 100 g. Bradykinin increased urinary sodium excretion 108 seq/min and decreased urinary osmolality from 1,254 to 516 mosmol/kg in association with a rise in papillary plasma flow to 62 ml/min per 100 g. Urine sodium excretion, urinary osmolality, and urine flow rate, as well as papillary plasma flow rate (32 ml/min per 100 g) were unchanged from control when secretin was administered. Studies with acetylcholine were qualitatively similar to those of bradykinin. Renal blood flow increased from 150 to 248 ml/min, urinary sodium excretion increased from 20 to 243 geq/min, urinary osmolality decreased from 1,237 to 411 mos-

show abstract

The effect of bradykinin on proximal tubular sodium reabsorption in the dog: evidence for functional nephron heterogeneity

Cited by 136 publications

References 14 publications

Forskolin preferentially dilates the afferent arteriole in the canine kidney.

Forskolin preferentially dilates the afferent arteriole in the canine kidney.

Kinin actions on renal papillary blood flow and sodium excretion.

Studies on the Mechanism of Sodium Excretion during Drug-induced Vasodilatation in the Dog

Contact Info

Product

Resources

About