P<sub>2</sub>‐, but not P<sub>1</sub>‐purinoceptors mediate formation of 1,4,5‐inositol trisphosphate and its metabolites via a pertussis toxin‐insensitive pathway in the rat renal cortex

Nanoff, Christian; Freissmuth, Michael; Tuisl, Elisabeth; Schütz, Wolfgang

doi:10.1111/j.1476-5381.1990.tb12052.x

Cited by 37 publications

(15 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Prostacyclin is the major prostaglandin produced by most blood vessels and the stimulation of its release from aortic endothelial cells of porcine (Pearson et al, 1983) (Needham et al, 1987). Furthermore, PGI2 release may also result from an activation of nucleotide receptors located on smooth muscle cells (Demolle et al, 1988;O'Connor, 1992) and recent studies have demonstrated the presence of P2y-purinoceptors in the rat renal cortex (Nanoff et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

Effect of tienoxolol, a new diuretic β‐blocking agent, on urinary prostaglandin excretion in the rat

Caussade¹,

Cloarec²

1993

British J Pharmacology

View full text Add to dashboard Cite

1 The effects of tienoxolol, (ethyl 2-[3-[(1,1-dimethylethyl)amino]-2-hydroxypropoxy]-5-[(2-thienylcarbonyl) amino] benzoate, hydrochloride), a novel drug exhibiting both diuretic and Padrenoceptor blocking properties, were investigated on urinary 6-keto-prostaglandin Fl, (6-keto-PGFI,) and PGE2 excretion in the rat and compared to those of reference diuretic (furosemide) and Padrenoceptor antagonists (acebutolol, propranolol). Since tienoxolol was shown to bind to A, and A2 adenosine receptors, the action of theophylline was also evaluated.2 Tienoxolol (8-128mgkg-', p.o.) induced a dose-related increase of 6-keto-PGFI, excretion from 32 mg kg-' but a significant elevation of urinary PGE2 levels was only reached after administration of 128 mg kg-'. However, renal prostaglandin concentrations were not modified by tienoxolol.3 Furosemide (32 mg kg-') displayed a strong diuretic activity but did not enhance 6-keto-PGFI,, excretion. Likewise, the latter was unaffected by acebutolol and propranolol (128 mg kg-') and no significant diuresis was observed following administration of these two P-blocking agents. Theophylline (64 mg kg-1), like tienoxolol, was able to induce both diuresis and urinary prostaglandin excretion. Furthermore, they bound with similar affinities to A, and A2 adenosine receptors. This led to the suggestion that a relationship between P,-purinoceptors, prostaglandin release, diuresis and natriuresis could exist.4 Oral co-administration of NECA (0.2 mg kg-') with tienoxolol markedly reduced the urinary 6-keto-PGF,c, excretion observed when tienoxolol was administered alone. However, neither diuresis nor natriuresis were modified, demonstrating that the proposed relationship was untenable. 5 In conclusion, PGI2 probably does not participate in the diuretic and natriuretic activity of tienoxolol. The increase of urinary 6-keto-PGF,g excretion may result not only from the haemodynamic properties of the drug but also from the rise of the urinary flow induced by tienoxolol.

show abstract

Section: Discussionmentioning

confidence: 99%

Effect of tienoxolol, a new diuretic β‐blocking agent, on urinary prostaglandin excretion in the rat

Caussade¹,

Cloarec²

1993

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…It has been reported that the P2Y purinoceptors activate PI-PLC by PTX-insensitive mechanisms (Nanoff et al, 1990;Dubyak and el-Moatassim, 1993). Taylor et al (1991) demonstrated that the PI-PLCb1 isoform can be activated by asubunits of the Gq class of heterotrimeric G-proteins in liver membranes.…”

Section: Discussionmentioning

confidence: 99%

P2Y-Purinoceptor Mediated Inhibition of L-type Ca2+ Channels in Rat Pancreatic .BETA.-Cells.

Gong

Kakei

Koriyama

et al. 2000

Cell Struct. Funct.

View full text Add to dashboard Cite

ABSTRACT. We used the patch-clamp technique to study the effects of extracellular ATP on the activity of ion channels recorded in rat pancreatic b-cells. In cell-attached membrane patches, action currents induced by 8.3 mM glucose were inhibited by 0.1 mM ATP, 0.1 mM ADP or 15 mM ADPbS but not by 0.1 mM AMP or 0.1 mM adenosine. In perforated membrane patches, action potentials were measured in current clamp, induced by 8.3 mM glucose, and were also inhibited by 0.1 mM ATP with a modest hyperpolarization to -43 mV. In whole-cell clamp experiments, ATP dose-dependently decreased the amplitudes of L-type Ca 2+ channel currents (ICa) to 56.7±4.0% (p<0.001) of the control, but did not influence ATP-sensitive K + channel currents observed in the presence of 0.1 mM ATP and 0.1mM ADP in the pipette. Agonists of P2Y purinoceptors, 2-methylthio ATP (0.1 mM) or ADPbS (15 mM) mimicked the inhibitory effect of ATP on ICa, but PPADS (0.1 mM) and suramin (0.2 mM), antagonists of P2 purinoceptors, counteracted this effect. When we used 0.1 mM GTPgS in the pipette solution, ATP irreversibly reduced ICa to 58.4±6.6% of the control (p<0.001). In contrast, no inhibitory effect of ATP was observed when 0.2 mM GDPbS was used in the pipette solution. The use of either 20 mM BAPTA instead of 10 mM EGTA, or 0.1 mM compound 48/80, a blocker of phospholipase C (PLC), in the pipette solution abolished the inhibitory effect of ATP on ICa, but 1 mM staurosporine, a blocker of protein kinase C (PKC), did not. When the b-cells were pretreated with 0.4 mM thapsigargin, an inhibitor of the endoplasmic reticulum (ER) Ca 2+ pump, ATP lost the inhibitory effect on ICa. These results suggest that extracellular ATP inhibits action potentials by Ca 2+ -induced ICa inhibition in which an increase in cytosolic Ca 2+ released from thapsigargin-sensitive store sites was brought about by a P2Y purinoceptor-coupled G-protein, PI-PLC and IP3 pathway.

show abstract

“…Proximal convoluted tubules P2Y receptors were identified in the renal cortex over 20 years ago [254], and since then, a variety of approaches has begun to catalogue the distribution of specific receptor subtypes. P2Y 1 and P2X5 receptors have been immunolocalised to the apical membrane in the S3 segment of the rat pars recta and P2Y 4 and P2X6 receptor protein is found basolaterally in the proximal convoluted tubule (PCT).…”

Section: Renal Tubulesmentioning

confidence: 99%

Purinergic signalling in the kidney in health and disease

Burnstock

Evans

Bailey

2013

Purinergic Signalling

View full text Add to dashboard Cite

The involvement of purinergic signalling in kidney physiology and pathophysiology is rapidly gaining recognition and this is a comprehensive review of early and recent publications in the field. Purinergic signalling involvement is described in several important intrarenal regulatory mechanisms, including tuboglomerular feedback, the autoregulatory response of the glomerular and extraglomerular microcirculation and the control of renin release. Furthermore, purinergic signalling influences water and electrolyte transport in all segments of the renal tubule. Reports about purine-and pyrimidine-mediated actions in diseases of the kidney, including polycystic kidney disease, nephritis, diabetes, hypertension and nephrotoxicant injury are covered and possible purinergic therapeutic strategies discussed.

show abstract

P₂‐, but not P₁‐purinoceptors mediate formation of 1,4,5‐inositol trisphosphate and its metabolites via a pertussis toxin‐insensitive pathway in the rat renal cortex

Cited by 37 publications

References 30 publications

Effect of tienoxolol, a new diuretic β‐blocking agent, on urinary prostaglandin excretion in the rat

Effect of tienoxolol, a new diuretic β‐blocking agent, on urinary prostaglandin excretion in the rat

P2Y-Purinoceptor Mediated Inhibition of L-type Ca2+ Channels in Rat Pancreatic .BETA.-Cells.

Purinergic signalling in the kidney in health and disease

Contact Info

Product

Resources

About

P2‐, but not P1‐purinoceptors mediate formation of 1,4,5‐inositol trisphosphate and its metabolites via a pertussis toxin‐insensitive pathway in the rat renal cortex

Cited by 37 publications

References 30 publications

Effect of tienoxolol, a new diuretic β‐blocking agent, on urinary prostaglandin excretion in the rat

Effect of tienoxolol, a new diuretic β‐blocking agent, on urinary prostaglandin excretion in the rat

P2Y-Purinoceptor Mediated Inhibition of L-type Ca2+ Channels in Rat Pancreatic .BETA.-Cells.

Purinergic signalling in the kidney in health and disease

Contact Info

Product

Resources

About

P₂‐, but not P₁‐purinoceptors mediate formation of 1,4,5‐inositol trisphosphate and its metabolites via a pertussis toxin‐insensitive pathway in the rat renal cortex