The Renal Kallikrein-Kinin and Prostaglandin Systems Interaction

Nasjletti, A.; Malik, Kafait U.

doi:10.1146/annurev.ph.43.030181.003121

Cited by 44 publications

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“…Papillary necrosis in these cases is thought to result from obstruction of the medullary vasculature by amyloid, leading to ischemic necrosis of the * Inability to autoregulate medullary blood flow as a result of amyloid-induced damage to the prostaglandin-secreting medullary interstitial cells may also be an important factor. 20 In all cases, the affinity for the Congo red stain was eliminated by oxidation of tissue sections in potassium permanganate, indicating that the amyloid is of the AA type.24 Although immunohistochemical confirmation was not attempted in these cases, it has recently been shown that permanganate-sensitive systemic amyloid in the closely related mountain gazelle (Gazella gazella) cross-reacts strongly with murine monoclonal and bovine polyclonal anti-AA antibodies, l 7 suggesting that permanganate sensitivity is specific for amyloid A in gazelles, as in other species. It is interesting to note that the mountain gazelle of that report had heavy amyloid deposits in the glomeruli and tubular interstitium, but no mention is made of medullary involvement.…”

Section: Discussionmentioning

confidence: 99%

Renal Medullary Amyloidosis in Dorcas Gazelles

et al. 1989

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Abstract. Between January 1976 and September 1987 renal medullary amyloidosis (RMA) was diagnosed in 17 Dorcas gazelles; the necropsy prevalence rate was 17/32 (53%). The most severe amyloid deposits were in the renal medulla; glomeruli were spared. Renal cortical lesions of interstitial fibrosis and tubular atrophy and dilatation significantly correlated with RMA (P < 0.01) and were considered to be secondary changes.There were varying degrees of lymphoplasmacytic inflammation and tubular cast formation which did not significantly correlate with RMA. Amyloid was confirmed histochemically and by electron microscopy and was identified as AA type by the permanganate method. Progressive renal failure was the cause of death or necessitated euthanasia in 7/17 (4 1 Yo) gazelles. RMA in Dorcas gazelles does not appear to be familial. A high prevalence of chronic or recurring Actinomyces (Corynebacterium) pyogenes infections may be an important factor.Currently, classification of the amyloidoses is based in part on the nature of the fibril p r~t e i n .~ Reactive systemic amyloidosis, in which the fibril protein (AA) is believed to be derived by proteolytic cleavage from an acute phase protein (SAA), is the most common form in manZZ and is the only form of systemic amyloid reported in nonhumans.' Any organ can be involved in reactive systemic amyloidosis, but renal involvement occurs with greatest f r e q u e n~y . '~.~~ Renal amyloid also has the most serious consequences, since deposition of amyloid in glomeruli causes disruption of the glomerular filtration bamer, with resultant proteinuria and associated sequelae. l 5 In addition, deposition of amyloid in the pentubular interstitium can lead to ischemia and pressure atrophy of nephrons with subsequent interstitial scarring and loss of renal function.I5Involvement of the renal medulla with amyloid is rare in man26 and most animals,I5 but may be the predominant form of renal amyloidosis in cats3J5J8 and ~a t t l e .~J~J~ In cattle, there is a spectrum from predominantly glomerular to predominantly medullary amy10idosis;~~l~ the glomerular form can lead to the nephrotic ~y n d r o m e~~J~J~ as in other species, but the medullary form is usually subclinical.I0We have identified a syndrome of renal medullary amyloidosis (RMA) in a herd of Dorcas gazelles at the National Zoological Park (NZP). In contrast to medullary amyloidosis in cattle, RMA in Dorcas gazelles frequently leads to renal failure and death. This paper reports the occurrence and describes the gross and light microscopic features of renal medullary amyloidosis in Dorcas gazelles. The clinical aspects of the disease will be published elsewhere. Materials and MethodsDorcas gazelles are small ruminants indigenous to desert regions of Northeast Africa. Body weights in adults range from 10 to 15 kg. The National Zoological Park (NZP) maintains a herd of Dorcas gazelles with an average year-end population of about 20 animals. Twice yearly each animal is treated prophylactically with anthelminthics, and a complete...

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Section: Discussionmentioning

confidence: 99%

Renal Medullary Amyloidosis in Dorcas Gazelles

et al. 1989

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“…45 Prostaglandins (PGs) modulate the effects of vasoactive hormones by attenuating the renal actions of the renin-angiotensin system 6 and contributing to or mediating their effects on the kallikrein-kinin system (KKS). 7 Moreover, renal KKS is able to stimulate the renal prostaglandin system. 7 Evidence that the renal KKS and PGs are interrelated comes from the relationships between the urinary excretion rates of kailikrein and PGs, 8 the effect of alterations in KKS activity on renal PGs production, 9 ' I0 and the effect of PGs" or cyclooxygenase inhibitors (COIs) on the renal KKS.…”

Section: S Ince the Observation By Vanementioning

confidence: 99%

“…7 Moreover, renal KKS is able to stimulate the renal prostaglandin system. 7 Evidence that the renal KKS and PGs are interrelated comes from the relationships between the urinary excretion rates of kailikrein and PGs, 8 the effect of alterations in KKS activity on renal PGs production, 9 ' I0 and the effect of PGs" or cyclooxygenase inhibitors (COIs) on the renal KKS. 12 Therefore, we decided to evaluate if COIs, per se, can affect the KKS directly, since many studies analyzed the interaction between both systems by employing prostaglandin inhibition only.…”

Section: S Ince the Observation By Vanementioning

confidence: 99%

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Effects of cyclooxygenase inhibitors on plasma and urinary kallikrein.

Schor¹,

Voos²,

Stella³

et al. 1983

Hypertension

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SUMMARY In vitro studies were performed to investigate the direct effects of the cyclooxygenase inhibitors (COI), meclofenamate, imidazol, acetylsalicylic acid (ASA), indomethacin, and acetominophen on the plasma kailikrein system and on urinary kailikrein excretion. Biological (guinea pig ileum) and colorimetric (synthetic substrate) methods were used. Results showed that all COIs except ASA affected both the activation of pre-kallikrein in plasma and the direct activity of plasma kailikrein, but none of the COIs tested was able to alter the urinary kailikrein excretion. Additionally, in Wistar rats we studied the effects of chronic administration of ASA, meclofenamate, and indomethacin on the plasma kailikrein system and urinary kailikrein excretion. In contrast to the in vitro studies, administration of these COIs reduced the amount of total 24-hour urinary kailikrein excretion. Moreover, the pre-plasma kailikrein and total plasma kailikrein levels were diminished in all experimental groups. However, only ASA and meclofenamate increased the free-plasma kailikrein levels despite the fact the three COIs used reduced the high molecular weight kininogen. Thus, in vitro data suggest an important and direct effect of meclofenamate, imidazol, indomethacin, and acetominophen on the plasma kailikrein system, without any effect on urinary secretion. ASA was the only COI that showed no direct effect in these experiments. Chronic COI administration in Wistar rats suggests that ASA, meclofenamate, and indomethacin affect both the plasma kallikrein-kinin system and kailikrein excretion. When these drugs are used to evaluate the interactions between prostaglandins and the kallikrein-kinin system, their possible effects through both mechanisms, directly or via prostaglandin inhibition, should be considered. the circulation to the kidney was sustained by a major prostaglandin component; withdrawal of this component resulted in significant hemodynamic effects, particularly reduction in blood flow.45 Prostaglandins (PGs) modulate the effects of vasoactive hormones by attenuating the renal actions of the renin-angiotensin system 6 and contributing to or mediating their effects on the kallikrein-kinin system (KKS).7 Moreover, renal KKS is able to stimulate the renal prostaglandin system. 7 Evidence that the renal KKS and PGs are interrelated comes from the relationships between the urinary excretion rates of kailikrein and PGs, 8 the effect of alterations in KKS activity on renal PGs production, 9 ' I0 and the effect of PGs" or cyclooxygenase inhibitors (COIs) on the renal KKS.12 Therefore, we decided to evaluate if COIs, per se, can affect the KKS directly, since many studies analyzed the interaction between both systems by employing prostaglandin inhibition only.

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“…Furthermore, it has also been reported that mineralocorticoids increase urinary PGEZ excretion (Nasjletti et al 1978). Many efforts have been addressed to solve complex interactions between sodium intake, sodium excretion, prostaglandin and kallikrein excretion, and aldosterone (Nasjletti and Colina-Chourio 1975;Nasjletti and Malik 1981). However, the physiological relevance of mineralocorticoids to the regulation of renal kallikrein-kinin-PGE system has remained to be determined in detail.…”

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confidence: 99%

Long-term effects of aldosterone on kallikrein, prostaglandin E2 and sodium in rats.

Yasujima

Abe

Tanno

et al. 1987

Tohoku J. Exp. Med.

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To assess the long-term effects of mineralocorticoids on the regulation of the synthesis or release of kallikrein and prostaglandin E2 in the renal kallikrein-kininprostaglandin E system, we studied the effects of chronic infusion of aldosterone (50,ug/kg/day) on urinary excretion of total and active kallikrein, and prostaglandin E2 for 10 days in conscious rats on regular intakes of sodium and on sodium loading with 1% NaCI as a drinking water. Chronic infusion of aldosterone induced a prompt and transient decrease in the ratio of sodium to potassium and a sustained increase in urinary prostaglandin E2 excretion in rats on regular diets, whereas urinary total and active kallikrein excretion did not increase significantly until the 4th day of aldosterone infusion. In rats loaded with sodium, aldosterone did not induce any changes in urinary total and active kallikrein excretion, whereas it induced similar changes in the ratio of sodium to potassium and urinary prostaglandin E2 excretion to those in rats on regular diets. Thus, the present results suggest that aldosterone might stimulate the synthesis or release of renal prostaglandin E2 independent of sodium balance. Furthermore, it is also suggested that aldosterone might stimulate the synthesis or release of kallikrein, at least partly, via the same pathway as sodium loading does. mineralocorticoids ; inactive kallikrein ; trypsin-activated kallikrein ; renal prostaglandin E2 ; sodium balance It system 1977; is generally agreed that the renal kallikrein-kinin-prostaglandin (PG) E is involved in the regulation of electrolytes and water excretion (Dunn Levinsky 1979;Carretero and Scicli 1980). It is well established that

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The Renal Kallikrein-Kinin and Prostaglandin Systems Interaction

Cited by 44 publications

References 1 publication

Renal Medullary Amyloidosis in Dorcas Gazelles

Renal Medullary Amyloidosis in Dorcas Gazelles

Effects of cyclooxygenase inhibitors on plasma and urinary kallikrein.

Long-term effects of aldosterone on kallikrein, prostaglandin E2 and sodium in rats.

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