scholarly journals Activation of phospholipase C and prostaglandin synthesis by [arginine] vasopressin in cultures

1985 ◽  
Vol 225 (3) ◽  
pp. 835-835
Keyword(s):  
Phospholipase C ◽  
Arginine Vasopressin ◽  
Prostaglandin Synthesis

scholarly journals Activation of phospholipase C and prostaglandin synthesis by [arginine]vasopressin in cultures

1984 ◽  
Vol 223 (3) ◽  
pp. 855-859 ◽  
Author(s):  
J Pfeilschifter ◽  
A Kurtz ◽  
C Bauer
Keyword(s):  
Arachidonic Acid ◽  
Phosphatidic Acid ◽  
Prostaglandin E2 ◽  
Phospholipase C ◽  
Arginine Vasopressin ◽  
Mesangial Cells ◽  
Significant Loss ◽  
Prostaglandin Synthesis ◽  
Phosphatidylinositol 4 ◽  
In Cells

[Arginine]vasopressin (AVP) stimulates maximal prostaglandin E2 production in cultured rat renal mesangial cells within 2 min. As early as 10s after addition of AVP (10(-6)M) a significant loss of radioactivity from phosphatidylinositol 4,5-bisphosphate but not from phosphatidylinositol 4-phosphate and phosphatidylinositol was observed in cells prelabelled with 32Pi. Cells labelled with [14C]arachidonic acid showed an increase of label in 1,2-diacylglycerol after 15 s and in phosphatidic acid after 30 s upon stimulation with AVP. Pretreatment of the cells with indomethacin (10(-5)M) did not abolish the effect of AVP on the increased labelling of phosphatidic acid.

Tolbutamide and diazoxide modulate phospholipase C-linked Ca2+ signaling and insulin secretion in β-cells

2000 ◽  
Vol 278 (4) ◽  
pp. E639-E647 ◽  
Author(s):  
Christof Schöfl ◽  
Julia Börger ◽  
Thilo Mader ◽  
Mark Waring ◽  
Alexander von zur Mühlen ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Phospholipase C ◽  
Insulin Release ◽  
Arginine Vasopressin ◽  
Bay K 8644 ◽  
Free Medium ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Activating Receptors

Arginine vasopressin (AVP), bombesin, and ACh increase cytosolic free Ca2+ and potentiate glucose-induced insulin release by activating receptors linked to phospholipase C (PLC). We examined whether tolbutamide and diazoxide, which close or open ATP-sensitive K+ channels (KATP channels), respectively, interact with PLC-linked Ca2+ signals in HIT-T15 and mouse β-cells and with PLC-linked insulin secretion from HIT-T15 cells. In the presence of glucose, the PLC-linked Ca2+ signals were enhanced by tolbutamide (3–300 μM) and inhibited by diazoxide (10–100 μM). The effects of tolbutamide and diazoxide on PLC-linked Ca2+ signaling were mimicked by BAY K 8644 and nifedipine, an activator and inhibitor of L-type voltage-sensitive Ca2+channels, respectively. Neither tolbutamide nor diazoxide affected PLC-linked mobilization of internal Ca2+ or store-operated Ca2+ influx through non-L-type Ca2+ channels. In the absence of glucose, PLC-linked Ca2+ signals were diminished or abolished; this effect could be partly antagonized by tolbutamide. In the presence of glucose, tolbutamide potentiated and diazoxide inhibited AVP- or bombesin-induced insulin secretion from HIT-T15 cells. Nifedipine (10 μM) blocked both the potentiating and inhibitory actions of tolbutamide and diazoxide on AVP-induced insulin release, respectively. In glucose-free medium, AVP-induced insulin release was reduced but was again potentiated by tolbutamide, whereas diazoxide caused no further inhibition. Thus tolbutamide and diazoxide regulate both PLC-linked Ca2+signaling and insulin secretion from pancreatic β-cells by modulating KATP channels, thereby determining voltage-sensitive Ca2+ influx.

scholarly journals Phorbol ester inhibits arginine vasopressin activation of phospholipase C and promotes contraction of, and prostaglandin production by, cultured mesangial cells

1988 ◽  
Vol 251 (3) ◽  
pp. 907-912 ◽  
Author(s):  
D A Troyer ◽  
O F Gonzalez ◽  
J G Douglas ◽  
J I Kreisberg
Keyword(s):  
Phospholipase C ◽  
Phorbol Ester ◽  
Arginine Vasopressin ◽  
Contractile Response ◽  
Mesangial Cells ◽  
Pge2 Production ◽  
Intact Cells ◽  
Kinase C ◽  
Acid Release ◽  
Activate Protein Kinase

We have previously shown that arginine vasopressin (AVP) causes a rapid (5-10 min) contractile response in cultured mesangial cells plated onto slippery substrata such as poly(hydroxyethyl methacrylate)-coated dishes. This contraction is associated with an increase in the levels of inositol trisphosphate (InsP3), diacylglycerol and prostaglandin E2 (PGE2). We now report that agents which are known to activate protein kinase C, i.e. phorbol 12-myristate 13-acetate (PMA) and oleolylacetylglycerol (OAG), also contract mesangial cells; however, the contractile response is slow to develop (15-30 min). The inactive phorbol ester, 4 alpha -phorbol 12,13-didecanoate, did not elicit contraction. PMA and OAG did not increase InsP3 release in mesangial cells. However, pretreatment of mesangial cells with PMA inhibited the formation of InsP3. This inhibition could not be explained by a reduction in AVP binding since PMA treatment did not influence the number or affinity of [3H]AVP binding sites in intact cells. PMA alone stimulated PGE2 production in mesangial cells to a degree similar to AVP. Contrary to what was seen with InsP3, pretreatment of cells with PMA before AVP had an additive effect on arachidonic acid release and PGE2 production. Thus, there is an apparent dissociation of phospholipase C activity from that of phospholipase A2.

PROSTAGLANDIN A2 AT LOW RATES OF INFUSION RESTORES THE ANTIDIURETIC EFFECT OF VASOPRESSIN IN LITHIUM-TREATED RATS

1977 ◽  
Vol 73 (1) ◽  
pp. 31-36 ◽  
Author(s):  
J. P. MTABAJI ◽  
C. J. ROBINSON ◽  
M. S. MANKU ◽  
D. CRONIN ◽  
D. F. HORROBIN
Keyword(s):  
Renal Function ◽  
Arginine Vasopressin ◽  
Prostaglandin Synthesis ◽  
Urine Flow ◽  
Male Rats ◽  
Urinary Volume ◽  
Antidiuretic Effect ◽  
Pre Treatment ◽  
Prostaglandin A2 ◽  
Antidiuretic Action

SUMMARY To test the effect of prostaglandin A2 (PGA2) on renal function, infusions of PGA2 (0·7 ng/ kg/min), arginine-vasopressin (AVP) (1·25 ng/kg/min) and PGA2 plus AVP were administered to male rats made resistant to the antidiuretic effect of AVP by pre-treatment with lithium. In non-lithium-treated control rats, AVP had its expected antidiuretic action but in lithium-treated rats neither urinary volume nor osmolarity was changed. Prostaglandin A2 alone had no effect on urine output in lithium-treated rats; AVP plus PGA2 infused together evoked a near normal antidiuretic response. This antidiuretic action of PGA2 contrasts with the diuretic action reported by others. However, our infusion rates were 300–4000 times lower than those of other workers and it is suggested that PGs may have opposite actions on the kidney depending on their concentration. The effect of indomethacin (a blocker of prostaglandin synthesis) on urine flow was tested in five groups of rats on different régimes of liquid intake. Urine flow was reduced in the three groups with the highest urine volumes before treatment, and increased in the two groups with the lowest urinary volumes, again indicating that PGs may have both diuretic and antidiuretic actions.

Presence of pituitary adenylate cyclase-activating polypeptide 38-immuno-like material in the brain and ovary of the female crested newt, Triturus carnifex: its involvement in the ovarian synthesis of prostaglandins and steroids

1997 ◽  
Vol 152 (1) ◽  
pp. 141-146 ◽  
Author(s):  
A Gobbetti ◽  
M Zerani ◽  
A Miano ◽  
M Bramucci ◽  
O Murri ◽  
...  
Keyword(s):  
Adenylate Cyclase ◽  
Phospholipase C ◽  
Prostaglandin Synthesis ◽  
Prostaglandin E ◽  
Ovarian Steroidogenesis ◽  
Pituitary Adenylate Cyclase ◽  
Crested Newt ◽  
The Brain

Abstract The presence of pituitary adenylate cyclase-activating peptide (PACAP) 38-immuno-like material (PACAP 38-IL) in the brain and ovary of the crested newt, Triturus carnifex, and its action on ovarian steroidogenesis and prostaglandin synthesis were evaluated. The HPLC brain and ovary extract peaks that eluted like PACAP 38 were considered PACAP 38-like material. The concentrations of PACAP 38-IL in the HPLC extracts were measured by RIA. T. carnifex ovary was incubated with PACAP 38, brain and ovary PACAP 38-IL, and inhibitors of cyclooxygenase (COX), adenylate cyclase (AC) and phospholipase C (PLC) for 30 and 60 min. PACAP 38, and brain and ovary PACAP 38-IL increased prostaglandin E2 (PGE2) (30 and 60 min), and progesterone and corticosterone (60 min), but decreased oestradiol-17β (60 min). COX and PLC inhibitors counteracted the increases in PGE2, progesterone and corticosterone and the decrease in oestradiol-17β, and the AC inhibitor also counteracted them except for PGE2. These results suggest that PACAP 38-IL, present in T. carnifex brain and ovary, acts on PLC, inducing the increase of PGE2 which, in turn, acting on AC, induces increases in progesterone and corticosterone and a decrease in oestradiol-17β. Journal of Endocrinology (1997) 152, 141–146

scholarly journals Somatostatin-induced paradoxical increase in intracellular Ca2+ concentration and insulin release in the presence of arginine vasopressin in clonal HIT-T15 β-cells

2002 ◽  
Vol 364 (1) ◽  
pp. 33-39 ◽  
Author(s):  
Henrique CHENG ◽  
Sirintorn YIBCHOK-ANUN ◽  
Seung-Chun PARK ◽  
Walter H. HSU
Keyword(s):  
Phospholipase C ◽  
Insulin Release ◽  
Arginine Vasopressin ◽  
Receptor Agonist ◽  
Calcium Concentration ◽  
Somatostatin Receptors ◽  
Rapid Decline ◽  
Atpase Inhibitor ◽  
Β Cells ◽  
Induced Changes

Somatostatin, a hormone that signals via Gi/Go, usually inhibits increases in intracellular calcium concentration ([Ca2+]i) and insulin release from β-cells. We have found that in the presence of arginine vasopressin (AVP), which signals via Gq, somatostatin increased [Ca2+]i, leading to insulin release in HIT-T15 cells. The increase in [Ca2+]i by somatostatin was observed even after 60min of AVP treatment. Somatostatin alone failed to increase [Ca2+]i and insulin release. Somatostatin induced changes in [Ca2+]i in a biphasic pattern, characterized by a sharp and transient increase followed by a rapid decline to sub-basal levels. Pretreatment with pertussis toxin, which inactivates Gi/Go, abolished the effects of somatostatin. U-73122, an inhibitor of phospholipase C, antagonized the somatostatin-induced increase in [Ca2+]i. In Ca2+-free medium, somatostatin still increased [Ca2+]i. Depletion of intracellular Ca2+ stores with thapsigargin, a microsomal Ca2+-ATPase inhibitor, abolished somatostatin's effect. In the presence of bradykinin, another Gq-coupled receptor agonist, somatostatin also increased [Ca2+]i, but not in the presence of isoproterenol (a Gs-coupled receptor agonist) or medetomidine (a Gi/Go-coupled receptor agonist). Our findings suggest that somatostatin signals through Gi/Go, and involves phospholipase C and Ca2+ release from the endoplasmic reticulum. The increase in [Ca2+]i by somatostatin leads to insulin release. This cross-talk is specific to Gq and Gi/Go, and is not limited to the AVP and somatostatin receptors.

The role of phospholipase C in arginine vasopressin secretion by rat hypothalami in vitro

Neuroreport ◽  
1997 ◽  
Vol 8 (5) ◽  
pp. 1277-1281 ◽  
Author(s):  
J Wayte ◽  
J C. Buckingham ◽  
A M. Cowell
Keyword(s):  
Phospholipase C ◽  
Arginine Vasopressin ◽  
Vasopressin Secretion

Vasoconstrictor-evoked prostaglandin synthesis in cultured vascular smooth muscle

1983 ◽  
Vol 245 (3) ◽  
pp. C278-C282 ◽  
Author(s):  
A. Hassid ◽  
C. Williams
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Arginine Vasopressin ◽  
Muscle Cells ◽  
Prostaglandin Synthesis ◽  
Mesenteric Arteries ◽  
Pressor Activity

We investigated the hypothesis that vasopressin, angiotensin II, and norepinephrine stimulate the synthesis of vasodilatory prostaglandins in cultured vascular smooth muscle cells from rat mesenteric arteries. The major prostaglandin synthesized by subcultured vascular smooth muscle cells was PGI2 (measured as its stable metabolite 6-keto-PGF1 alpha) followed by 1/20th to 1/40th as much PGF2 alpha and PGE2. Vasopressin and angiotensin II dose dependently increased prostaglandin synthesis with a half-maximal stimulatory concentration of the order of 1 X 10(-8) M for both peptides. However, vasopressin could provoke the synthesis of two to three times as much PGI2 as angiotensin II, at maximally effective concentrations. Vasopressin's ability to provoke prostaglandin synthesis depended on its pressor activity as demonstrated by the ability of a potent antipressor analogue of vasopressin, [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine] arginine vasopressin, to completely inhibit vasopressin-provoked prostaglandin synthesis. Moreover, 1-desamino-8-D-arginine vasopressin, an analogue having full antidiuretic but no pressor activity was much less effective than vasopressin as a prostaglandin-stimulatory agent. Unlike peptide vasoconstrictors, norepinephrine (10(-9) to 10(-5) M) had no ability to stimulate prostaglandin synthesis in vascular smooth muscle cells. We conclude that the potent vasodilator PGI2, released from vascular smooth muscle cells, may buffer the peptide-induced vasoconstriction.

Increased phospholipase C activity after experimental brain injury

1982 ◽  
Vol 56 (5) ◽  
pp. 695-698 ◽  
Author(s):  
Enoch P. Wei ◽  
Robert G. Lamb ◽  
Hermes A. Kontos
Keyword(s):  
Brain Injury ◽  
Phospholipase C ◽  
Prostaglandin Synthesis ◽  
Content Type ◽  
Free Arachidonic Acid ◽  
Membrane Bound ◽  
Cell Fractions ◽  
Cytidine Diphosphate ◽  
The Brain ◽  
Experimental Fluid

✓ Phospholipase C activity was measured in 1000 × G centrifuged cellular fractions isolated from cerebral cortical homogenates obtained from either control cats or cats subjected to experimental fluid-percussion brain injury. Phospholipase C activity was determined directly by measuring the Ca++-dependent conversion of membrane-bound, labeled phosphatidate to diacylglycerol or indirectly by measuring the diacylglycerol-dependent (brain diacylglycerol content) formation of phosphatidylcholine in the presence of labeled cytidine diphosphate (CDP) choline. Phospholipase C activity determined by either method was about two times greater in cell fractions isolated from animals subjected to brain injury than in controls (p < 0.01). The brain injury-induced rise in phospholipase C activity may be responsible, at least in part, for generating diacylglycerol that may be a source of free arachidonic acid that stimulates prostaglandin synthesis. These changes may account for the rise in brain prostaglandin levels that has been demonstrated earlier to occur after this type of brain injury.

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