Role of calcium in cAMP-mediated effects in the elasmobranch rectal gland

1983 ◽  
Vol 245 (6) ◽  
pp. R894-R900
Author(s):  
T. J. Shuttleworth
Keyword(s):  
Oxygen Consumption ◽  
Secretory Activity ◽  
Rectal Gland ◽  
Ouabain Binding ◽  
Calcium Dependent ◽  
Mediated Effects ◽  
Cotransport System ◽  
Vasodilatory Action ◽  
Potent Vasoconstrictor ◽  
Stimulation Of

The effects of A23187 and verapamil on the vasomotor and secretory effects of adenosine 3',5'-cyclic monophosphate (cAMP) in the rectal gland were investigated in Scyliorhinus canicula and Squalus acanthias. A23187 was a potent vasoconstrictor in the gland and reversed the vasodilatory action of cAMP in glands constricted with norepinephrine. Verapamil, like cAMP, prevented the vasoconstriction induced in the gland by norepinephrine. A23187 had no effect on the secretory activity (measured as ouabain binding and ouabain-sensitive oxygen consumption) of the glands. Verapamil inhibited the stimulation of ouabain binding, ouabain-sensitive oxygen consumption, and sodium secretion rate induced by cAMP plus theophylline, but did not affect the stimulation of ouabain binding and ouabain-sensitive oxygen consumption induced by amphotericin B. These data indicate that it is the cAMP-induced stimulation of the sodium-chloride cotransport system that is verapamil sensitive, and it is suggested that this stimulation is a calcium-dependent process. This emphasizes the independent nature of the secretory and vasomotor effects of the nucleotide in the gland.

Thrombin stimulation of platelet oxygen consumption rate

1964 ◽  
Vol 19 (2) ◽  
pp. 297-300 ◽  
Author(s):  
Qamar Zafar Hussain ◽  
Thomas F. Newcomb
Keyword(s):  
Oxygen Consumption ◽  
Oxygen Consumption Rate ◽  
Consumption Rate ◽  
Human Platelets ◽  
Intermediary Metabolism ◽  
Calcium Dependent ◽  
Two Phases ◽  
Hank’S Solution ◽  
Stimulation Of

Oxygen consumption of human platelets was measured by O2 cathode. Platelets were prepared by collecting blood into ACD solution, and isolation and washing in buffer by centrifugation. O2 consumption was measured by vibrating cathode at 25 C in Hank's solution. The Qo2 was 14.5 ± 4.8 mμmoles/min 109 platelets with added glucose and 21.4 ± 5.0 with added glycerol. Thrombin addition resulted in increase in Qo2 of elevenfold lasting 3–5 min followed by clumping of the platelets. EDTA blocked the thrombin effect. Similar effects were noted when prothrombin was activated to form thrombin. 5-Hydroxytryptamine was without effect. With EDTA the reaction had two phases, a phase of thrombin effect and a calcium-dependent clumping phase. The observations are compatible with the hypothesis that thrombin alters platelet permeability. platelet clumping; viscous metamorphosis of platelets; platelet respiration measurement by O2 cathode; thrombin effect on platelet respiration; platelet respiration; platelet intermediary metabolism Submitted on September 20, 1963

scholarly journals Calcium-dependent phosphodiesterase 1C inhibits renin release from isolated juxtaglomerular cells

2009 ◽  
Vol 297 (5) ◽  
pp. R1469-R1476 ◽  
Author(s):  
M. Cecilia Ortiz-Capisano ◽  
Tang-Dong Liao ◽  
Pablo A. Ortiz ◽  
William H. Beierwaltes
Keyword(s):  
Western Blot ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Renin Release ◽  
Calcium Sensing Receptor ◽  
Calcium Dependent ◽  
Calcium Sensing ◽  
Inhibitory Modulation ◽  
Camp Formation ◽  
Stimulation Of

Renin release from the juxtaglomerular (JG) cell is stimulated by the second messenger cAMP and inhibited by calcium. We previously showed JG cells contain a calcium sensing receptor (CaSR), which, when stimulated, decreases cAMP formation and inhibits renin release. We hypothesize CaSR activation decreases cAMP and renin release, in part, by stimulating a calcium calmodulin-activated phosphodiesterase 1 (PDE1). We incubated our primary culture of JG cells with two selective PDE1 inhibitors [8-methoxymethil-IBMX (8-MM-IBMX; 20 μM) and vinpocetine (40 μM)] and the calmodulin inhibitor W-7 (10 μM) and measured cAMP and renin release. Stimulation of the JG cell CaSR with the calcimimetic cinacalcet (1 μM) resulted in decreased cAMP from a basal of 1.13 ± 0.14 to 0.69 ± 0.08 pM/mg protein ( P < 0.001) and in renin release from 0.89 ± 0.16 to 0.38 ± 0.08 μg ANG I/ml·h−1·mg protein−1 ( P < 0.001). However, the addition of 8-MM-IBMX with cinacalcet returned both cAMP (1.10 ± 0.19 pM/mg protein) and renin (0.57 ± 0.16 μg ANG I/ml·h−1·mg protein−1) to basal levels. Similar results were obtained with vinpocetine, and also with W-7. Combining 8-MM-IBMX and W-7 had no additive effect. To determine which PDE1 isoform is involved, we performed Western blot analysis for PDE1A, B, and C. Only Western blot analysis for PDE1C showed a characteristic band apparent at 80 kDa. Immunofluorescence showed cytoplasmic distribution of PDE1C and renin in the JG cells. In conclusion, PDE1C is expressed in isolated JG cells, and contributes to calcium's inhibitory modulation of renin release from JG cells.

Stimulation of oxygen consumption at the cytochrome A3 level inhibits aldosterone biosynthesis from 18-hydroxycorticosterone

1986 ◽  
Vol 884 (2) ◽  
pp. 270-275 ◽  
Author(s):  
Brigitte Aupetit ◽  
Nicole Emeric ◽  
Renée Toury ◽  
Odile Racadot ◽  
Jean Racadot ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Stimulation Of

Short-term stimulation of the thiazide-sensitive Na+-Cl− cotransporter by vasopressin involves phosphorylation and membrane translocation

2010 ◽  
Vol 298 (3) ◽  
pp. F502-F509 ◽  
Author(s):  
K. Mutig ◽  
T. Saritas ◽  
S. Uchida ◽  
T. Kahl ◽  
T. Borowski ◽  
...  
Keyword(s):  
Fold Increase ◽  
Short Term ◽  
Nephron Segments ◽  
Mediated Effects ◽  
Effector System ◽  
Apical Trafficking ◽  
Fine Regulation ◽  
Combined Action ◽  
Effective Site ◽  
Stimulation Of

Vasopressin influences salt and water transport in renal epithelia. This is coordinated by the combined action of V2 receptor-mediated effects along distinct nephron segments. Modulation of NaCl reabsorption by vasopressin has been established in the loop of Henle, but its role in the distal convoluted tubule (DCT), an effective site for fine regulation of urinary electrolyte composition and the target for thiazide diuretics, is largely unknown. The Na+-Cl− cotransporter (NCC) of DCT is activated by luminal trafficking and phosphorylation at conserved NH2-terminal residues. Here, we demonstrate the effects of short-term vasopressin administration (30 min) on NCC activation in Brattleboro rats with central diabetes insipidus (DI) using the V2 receptor agonist desmopressin (dDAVP). The fraction of NCC abundance in the luminal plasma membrane was significantly increased upon dDAVP as shown by confocal microscopy, immunogold cytochemistry, and Western blot, suggesting increased apical trafficking of the transporter. Changes were paralleled by augmented phosphorylation of NCC as detected by antibodies against phospho-threonine and phospho-serine residues (2.5-fold increase at Thr53 and 1.4-fold increase at Ser71). dDAVP-induced phosphorylation of NCC, studied in tubular suspensions in the absence of systemic effects, was enhanced as well (1.7-fold increase at Ser71), which points to the direct mode of action of vasopressin in DCT. Changes were more pronounced in early (DCT1) than in late DCT as distinguished by the distribution of 11β-hydroxysteroid dehydrogenase 2 in DCT2. These results suggest that the vasopressin-V2 receptor-NCC signaling cascade is a novel effector system to adjust transepithelial NaCl reabsorption in DCT.

Relation between duodenal alkaline secretion and motility in fasted and sham-fed dogs

1986 ◽  
Vol 251 (5) ◽  
pp. G591-G596 ◽  
Author(s):  
S. J. Konturek ◽  
P. Thor
Keyword(s):  
Motor Activity ◽  
Vagal Stimulation ◽  
Secretory Activity ◽  
Phase Iii ◽  
Plasma Gastrin ◽  
Marked Rise ◽  
Sham Feeding ◽  
Duodenal Motility ◽  
Alkaline Secretion ◽  
Stimulation Of

A relation between duodenal myoelectric and motor activity and alkaline secretion has been investigated in conscious dogs under basal conditions and following vagal excitation with and without pretreatment with atropine or indomethacin. It was found that duodenal alkaline secretion shows typical periodicity in phase with the myoelectric or motor activity of the duodenum, reaching a peak during phase III and a nadir during phase I of the migrating motor complex (MMC). Sham feeding interrupted the motor and secretory MMC cycle and caused a prolonged increase in duodenal myoelectric or motor activity as well as a sudden and marked rise in duodenal alkaline secretion accompanied by a significant elevation in plasma gastrin and pancreatic polypeptide. Atropine and indomethacin abolished the motor and secretory duodenal cycles and reduced basal alkaline secretion significantly. Atropine abolished, whereas indomethacin increased duodenal myoelectric or motor activity during basal conditions and after vagal stimulation. Neither atropine nor indomethacin abolished sham feeding-induced duodenal alkaline secretion. We conclude that duodenal alkaline secretion fluctuates cyclically in phase with duodenal motility, vagal excitation results in a potent stimulation of duodenal motor and secretory activity, and the mechanism of vagally induced duodenal alkaline secretion is only partly cholinergic and does not involve endogenous generation of prostaglandins.

Stimulation of growth of a colon cancer cell line by gastrin

1986 ◽  
Vol 251 (5) ◽  
pp. G597-G601 ◽  
Author(s):  
C. J. Kusyk ◽  
N. O. McNiel ◽  
L. R. Johnson
Keyword(s):  
Motor Activity ◽  
Cancer Cell Line ◽  
Secretory Activity ◽  
Colon Cancer Cell Line ◽  
Phase Iii ◽  
Marked Rise ◽  
Sham Feeding ◽  
Duodenal Motility ◽  
Alkaline Secretion ◽  
Stimulation Of

A relation between duodenal myoelectric and motor activity and alkaline secretion has been investigated in conscious dogs under basal conditions and following vagal excitation with and without pretreatment with atropine or indomethacin. It was found that duodenal alkaline secretion shows typical periodicity in phase with the myoelectric or motor activity of the duodenum, reaching a peak during phase III and a nadir during phase I of the migrating motor complex (MMC). Sham feeding interrupted the motor and secretory MMC cycle and caused a prolonged increase in duodenal myoelectric or motor activity as well as a sudden and marked rise in duodenal alkaline secretion accompanied by a significant elevation in plasma gastrin and pancreatic polypeptide. Atropine and indomethacin abolished the motor and secretory duodenal cycles and reduced basal alkaline secretion significantly. Atropine abolished, whereas indomethacin increased duodenal myoelectric or motor activity during basal conditions and after vagal stimulation. Neither atropine nor indomethacin abolished sham feeding-induced duodenal alkaline secretion. We conclude that duodenal alkaline secretion fluctuates cyclically in phase with duodenal motility, vagal excitation results in a potent stimulation of duodenal motor and secretory activity, and the mechanism of vagally induced duodenal alkaline secretion is only partly cholinergic and does not involve endogenous generation of prostaglandins.

Atriopeptin stimulation of rectal gland function in Squalus acanthias

1985 ◽  
Vol 249 (3) ◽  
pp. R348-R354 ◽  
Author(s):  
R. Solomon ◽  
M. Taylor ◽  
D. Dorsey ◽  
P. Silva ◽  
F. H. Epstein
Keyword(s):  
Volume Expansion ◽  
Epithelial Transport ◽  
Extracellular Volume ◽  
Chloride Secretion ◽  
Hormonal Control ◽  
Rectal Gland ◽  
Gland Function ◽  
Stimulation Of

The rectal gland of the shark plays a significant role in the homeostasis of extracellular volume. Regulation of rectal gland function is under hormonal control, but the precise identity of the humoral mediator is unknown. Atriopeptin stimulates rectal gland chloride secretion in vivo. This stimulation of epithelial transport is accompanied by systemic and local hemodynamic effects. Atriopeptin also stimulates chloride secretion by the in vitro perfused rectal gland, an effect that is not accompanied by hemodynamic changes. Extracts of shark heart, but not muscle, brain, kidney, or intestine, contain a heat-stable trypsin-sensitive substance capable of in vitro stimulation of rectal gland chloride secretion. Electron micrographic analysis reveals multiple neurosecretory-like granules in atrial cardiocytes that are only rarely seen in ventricular cardiocytes. By using the in vitro perfused gland as a biologic assay, serum obtained after extracellular volume expansion reveals the presence of a rectal gland stimulatory factor that is not present in serum before expansion. These results are consistent with the hypothesis that atriopeptin is present in shark cardiocytes and is released during volume expansion. The atriopeptin stimulates rectal gland chloride secretion, providing a negative feedback mechanism for the regulation of extracellular volume.

VARIOUS EFFECTS OF THYROXINE ANALOGUES ON THE HEART AND SERUM CHOLESTEROL IN THE RAT

1960 ◽  
Vol 21 (1) ◽  
pp. 25-32 ◽  
Author(s):  
G. S. BOYD ◽  
M. F. OLIVER
Keyword(s):  
Heart Rate ◽  
Oxygen Consumption ◽  
Serum Cholesterol ◽  
Rate Ratio ◽  
Heart Weight ◽  
Liver Cholesterol ◽  
Response Curves ◽  
Experimental Conditions ◽  
Cholesterol Levels ◽  
Stimulation Of

SUMMARY A series of twelve iodinated thyroxine analogues was studied for thyro-activity in the rat. Each analogue produced antigoitrogenic activity, increased oxygen consumption, heart rate and heart weight, and decreased serum and liver cholesterol levels. A 'serum cholesterol/heart rate ratio' may be computed for these analogues under fixed experimental conditions. While the dose-response curves for different analogues in any of these assays are rarely parallel, it is, nevertheless, clear that under certain experimental conditions some iodothyronines cause a relatively greater depression of cholesterol levels and less stimulation of heart rate than others. Some of the most active in this respect are DT4, DT3, DT2 and T4F.

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