Calcium-dependent stimulation of estrogen secretion by FSH from theca cells of the domestic hen (Gallus domesticus)

1989 ◽  
Vol 75 (2) ◽  
pp. 177-186 ◽  
Author(s):  
O.M. Onagbesan ◽  
M.J. Peddie
2009 ◽  
Vol 297 (5) ◽  
pp. R1469-R1476 ◽  
Author(s):  
M. Cecilia Ortiz-Capisano ◽  
Tang-Dong Liao ◽  
Pablo A. Ortiz ◽  
William H. Beierwaltes

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.


1983 ◽  
Vol 245 (6) ◽  
pp. R894-R900
Author(s):  
T. J. Shuttleworth

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.


1979 ◽  
Vol 237 (2) ◽  
pp. H112-H117
Author(s):  
D. D. McGregor

Vasomotor responses to nerve stimulation were studied in the feet of Pekin ducks (Anas platyrhynchos) and domestic chickens (Gallus domesticus). The birds were killed and the feet isolated and perfused with a Krebs solution. Electrical stimulation of pedal nerves gave vasoconstrictor responses that were abolished by injecting guanethidine and by treating birds with reserpine. After guanethidine or reserpine, nerve stimulation resulted only in vasodilatation, which was unaffected by hexamethonium. Vasodilator responses to nerve stimulation were not blocked by hyoscine or atropine, which blocked responses to acetylcholine, nor by metiamide, which blocked vasodilatation in response to histamine. Responses to nerve stimulation were blocked by tetrodotoxin. Isoprenaline produced vasoconstriction that was blocked by phentolamine and also weak vasodilator responses that were antagonized by propranolol. It is concluded that the vasoconstrictor innervation is adrenergic. The identy of the vasodilator neurotransmitter is unknown; it is apparently not acetylcholine, a catecholamine, or histamine.


1994 ◽  
Vol 266 (4) ◽  
pp. C904-C910 ◽  
Author(s):  
Z. Zhu ◽  
M. Lutz ◽  
L. K. Gates ◽  
L. J. Miller

The phosphorylation of one receptor that occurs as a result of the stimulation of a different receptor on a cell is a common mechanism for heterologous regulation or “cross-talk,” which has been implicated in desensitization. In this work, we focus on the mechanisms of phosphorylation of the rat pancreatic acinar cell cholecystokinin (CCK) receptor that occur upon stimulation of this cell by various agonists. Phosphorylation was allowed to occur in dispersed intact acinar cells in response to the experimental manipulation, and the phosphoreceptor was subsequently purified and quantified as an indication of response. Agonists such as vasoactive intestinal polypeptide and secretin, which act via activation of adenylate cyclase, had no effect on CCK receptor phosphorylation, whereas carbamylcholine and bombesin stimulated increased phosphorylation of the CCK receptor. Because these agents would be expected to activate protein kinase C (PKC) as well as a number of calcium-sensitive kinases and phosphatases, these activities were further dissociated by using more direct activators and inhibitors acting intracellularly. Manipulation of calcium independent of PKC by using a calcium ionophore, inhibition of calcium/calmodulin-dependent kinase II, and inhibition of calcium-dependent protein phosphatase type 2B had no effect on the state of CCK receptor phosphorylation.(ABSTRACT TRUNCATED AT 250 WORDS)


1983 ◽  
Vol 244 (5) ◽  
pp. E487-E493 ◽  
Author(s):  
B. L. Marrone ◽  
F. Hertelendy

The production of progesterone (P) and estrogen (E) by enzymatically dispersed granulosa and theca cells from chicken preovulatory follicles was examined in 3-h incubations. Accumulation of the P produced by granulosa cells was significantly reduced by the addition of theca cells, whereas E production was increased. The decrease in P accumulation was shown to be due to extensive metabolism of P by theca cells. There were no synergistic effects of luteinizing hormone (LH) and any substrate tested on E production by theca cells. Maturation of granulosa cells was characterized by an increased sensitivity to LH stimulation of P production, but there was no change in pregnenolone conversion to P. Conversely, maturation of theca cells was accompanied by decreased in both sensitivity to LH and the ability to convert substrates to E. The results are discussed in terms of the contribution of each cell type in the production of steroids by chicken follicles during maturation.


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