Cellular Signalling in the Kidney: The Role of Inositol Lipids

Pfeilschifter, Josef

doi:10.1159/000173176

Cited by 15 publications

(15 citation statements)

References 95 publications

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“…In addition, the impaired ARNA responses to renal sensory receptor stimulation may be related to a defect in the substance P receptor-intracellular coupling mechanisms. Substance P is a known activator of phosphoinositidase C. 13 Numerous studies in kidney tissue have shown a defect in various receptor-intracellular coupling mechanisms involving activation of the phosphoinositidase C-PKC pathway (eg, References 43 to 48). Taken together, these studies may suggest a general defect in the activation of this intracellular pathway in kidney tissue.…”

Section: Discussionmentioning

confidence: 99%

“…11 Bradykinin is known to activate sensory receptors in various tissues by stimulating phosphoinositidase C, leading to increased intracellular calcium and activation of PKC. 12,13 Activation of PKC has been shown to stimulate the phospholipase A2-dependent formation of prostaglandins. 12,13 Recent in vitro studies in dorsal root ganglionic neurons showed that PKC activation also increases the release of substance P. 14 In the renal pelvis, activation of PKC increased ARNA and blockade of PKC activity reduced the ARNA response to bradykinin in normotensive rats, 15 suggesting an important role for PKC in renal sensory receptor activation.…”

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confidence: 99%

“…12,13 Activation of PKC has been shown to stimulate the phospholipase A2-dependent formation of prostaglandins. 12,13 Recent in vitro studies in dorsal root ganglionic neurons showed that PKC activation also increases the release of substance P. 14 In the renal pelvis, activation of PKC increased ARNA and blockade of PKC activity reduced the ARNA response to bradykinin in normotensive rats, 15 suggesting an important role for PKC in renal sensory receptor activation. Moreover, our studies in normotensive rats have shown that renal pelvic administration of bradykinin or increased renal pelvic pressure stimulates the release of PGE, leading to the release of substance P and an increase in ARNA.…”

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Renal Substance P–Containing Neurons and Substance P Receptors Impaired in Hypertension

et al. 1998

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Abstract-In normotensive rats, increased renal pelvic pressure stimulates the release of prostaglandin E and substance P, which in turn leads to an increase in afferent renal nerve activity (ARNA) and a contralateral natriuresis, a contralateral inhibitory renorenal reflex. In spontaneously hypertensive rats (SHR), increasing renal pelvic pressure failed to increase afferent renal nerve activity. The inhibitory nature of renorenal reflexes indicates that impaired renorenal reflexes could contribute to increased sodium retention in SHR. Phorbol esters, known to activate protein kinase C, increase afferent renal nerve activity in Wistar-Kyoto rats (WKY) but not in SHR. We examined the mechanisms involved in the impaired responses to renal sensory receptor activation in SHR. The phorbol ester 4␤-phorbol 12,13-dibutyrate increased renal pelvic protein kinase C activity similarly in SHR and WKY. Increasing renal pelvic pressure increased afferent renal nerve activity in WKY (27Ϯ2%) but not in SHR. Renal pelvic release of prostaglandin E increased similarly in WKY and SHR, from 0.8Ϯ0.1 to 2.0Ϯ0.4 ng/min and 0.7Ϯ0.1 to 1.4Ϯ0.2 ng/min. Renal pelvic release of substance P was greater (PϽ.01) in WKY, from 16.3Ϯ3.8 to 41.8Ϯ7.4 pg/min, than in SHR, from 9.9Ϯ1.7 to 17.0Ϯ3.2 pg/min. In WKY, renal pelvic administration of substance P at 0.8, 4, and 20 g/mL increased ARNA 382Ϯ69, 750Ϯ233, and 783Ϯ124% ⅐ second (area under the curve of afferent renal nerve activity versus time). In SHR, substance P at 0.8 to 20 g/mL failed to increase ARNA. These findings demonstrate that the impaired afferent renal nerve activity response to increased renal pelvic pressure is related to decreased release of substance P and/or impaired activation of substance P receptors. (Hypertension. 1998;31:815-822.)Key Words: afferent renal nerve activity Ⅲ receptors, sensory Ⅲ prostaglandins Ⅲ protein kinase C Ⅲ substance P Ⅲ rats, inbred SHR O bstruction to urine flow increases renal pelvic pressure and activates renal mechanoreceptors, resulting in an increase in ipsilateral ARNA.1-5 The increase in ARNA produces a fall in contralateral efferent renal sympathetic nerve activity (ER-SNA) and a contralateral diuresis and natriuresis, known as the contralateral inhibitory renorenal reflex. 2Accumulating evidence indicates that the renal nerves contribute to the pathogenesis of hypertension in SHR.6 Peripheral sympathetic nerve activity and, in particular, ERSNA is enhanced in SHR. The nature of the renorenal reflex, that is, a diuresis and natriuresis in association with decreased ERSNA, would suggest that an attenuation of this reflex would result in increased ERSNA leading to water and sodium retention, factors known to contribute to the hypertensive process. 7 Our previous studies in SHR demonstrated that increasing renal pelvic pressure failed to increase ARNA and thus failed to elicit a contralateral renorenal reflex in these rats. 8 The lack of an increase in ARNA in response to increased renal pelvic pressure suggested that the impairment of the reno...

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Section: Discussionmentioning

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Renal Substance P–Containing Neurons and Substance P Receptors Impaired in Hypertension

et al. 1998

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“…Furthermore, in protein kinase C-depleted mesangial cells the basal values of IPI, IP2, IP3 and IP4, as well as the values after stimulation with angiotensin 11, are increased as compared to control cells. Obviously, a constitutive protein kinase Cmediated inhibitory action on PIP, hydrolysis is removed on such down-regulated cells [71,130].…”

Section: How Mesangial Cells Relaxmentioning

confidence: 99%

Cross‐talk between transmembrane signalling systems: a prerequisite for the delicate regulation of glomerular haemodynamics by mesangial cells

Pfeilschifter

1989

Eur J Clin Investigation

105

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“…Also, individual phospholipids selectively regulate the activity of mem brane-bound enzymes as N a \ K -ATPase [16] by PtdSer and Ptdlns, and Ca: -ATPase by PtdEtn [17]. PtdC'ho and Ptdlns are also a substrate for endogenous phospholipases (phospholipase A; and C) leading to the generation of sec ond messengers [18,19], However, information on the role of phospholipid me tabolism in the pathogenesis of nephrotic injury is rather limited. Phospholipid pool undergoes turnover represented by the specific activity of 32P incorporation.…”

Section: Discussionmentioning

confidence: 99%

Is the Increase in Renal Papillary Phospholipid Biosynthesis a Protective Mechanism against Injury?

Setton-Avruj¹,

Fernández-Tomé²,

Negri

et al. 1996

Kidney Blood Press Res

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Mercuric chloride (HgCl₂) is a well-known renal toxic that causes acute renal failure. The effect of HgCl₂ treatment and the protection by thyroxine were studied in rat renal papilla (P), outer medullary inner stripe (OMIS), outer medullary outer stripe (OMOS) and cortical phospholipids (PhLs). HgCl₂ brought about an increase in the total phospholipid content in P and OMIS but a drop in OMOS and cortex. Only phosphatidylcholine (PtdCho) and phosphatidylethanolamine (PtdEtn) accounted for such changes. Thyroxine, injected on HgCl₂-treated rats, partially reversed the effect of the toxic metal in P and OMIS while completely reversed the PtdCho drop in OMOS and cortex. However, the hormone failed to recover the sphingomyelin increase in P, the PtdEtn shortage in OMIS, OMOS and partially reversed the drop in the cortex. When thyroxine was injected whith-out toxic treatment, no effect was observed in the phospholipid content of any kidney zone. Results obtained by using ³²P as a precursor to study the PhL de novo synthesis were consistent with those of the phospholipid content. Thus, a radioactivity increase – associated with PtdCho and PtdEtn – was observed in the kidney zones where said endogenous PhLs had risen. But in OMOS and cortex, where PtdCho and PtdEtn had dropped, they were also accompanied by a decrease in radioactivity. The thyroxine-induced recovery phase also paralleled the phospholipid content results with those of the de novo synthesis. We suggest that the decrease in the renal phospholipid de novo synthesis may constitute one biochemical explanation of the selective renal toxic effect exerted by HgCl₂ and that the increase observed in the renal phospholipid metabolism – induced by the toxic treatment in OMIS and P – may represent a protective mechanism of these zones against toxic injury. Moreover, recovery promoted by thyroxine treatment in OMOS and cortex was accompanied by the reversion of the corresponding PtdCho decrease induced by HgCl₂.

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Cellular Signalling in the Kidney: The Role of Inositol Lipids

Cited by 15 publications

References 95 publications

Renal Substance P–Containing Neurons and Substance P Receptors Impaired in Hypertension

Renal Substance P–Containing Neurons and Substance P Receptors Impaired in Hypertension

Cross‐talk between transmembrane signalling systems: a prerequisite for the delicate regulation of glomerular haemodynamics by mesangial cells

Is the Increase in Renal Papillary Phospholipid Biosynthesis a Protective Mechanism against Injury?

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