Central regulation of thyroidal status in a teleost fish: Nutrient stimulation of T4 secretion and negative feedback of T3

2003 ◽  
Vol 298A (1) ◽  
pp. 32-43 ◽  
Author(s):  
Kevin A. Leiner ◽  
Duncan S. Mackenzie
Keyword(s):  
Negative Feedback ◽  
Teleost Fish ◽  
Central Regulation ◽  
Thyroidal Status ◽  
Stimulation Of

Measurement and regulation of thyroidal status in teleost fish

1993 ◽  
Vol 3 (4) ◽  
pp. 299-347 ◽  
Author(s):  
J. G. Eales ◽  
S. B. Brown
Keyword(s):  
Teleost Fish ◽  
Thyroidal Status

Central regulation of food intake during aging in the teleost fish Nothobranchius furzeri

2016 ◽  
Vol 207 ◽  
pp. 123-124
Author(s):  
A. Montesano ◽  
N. Arcamone ◽  
T. Genade ◽  
P. de Girolamo
Keyword(s):  
Food Intake ◽  
Teleost Fish ◽  
Central Regulation ◽  
Nothobranchius Furzeri

Dose-dependent heterogenous actions of vasopressin in rabbit cortical collecting ducts

1989 ◽  
Vol 256 (4) ◽  
pp. F556-F562 ◽  
Author(s):  
Y. Ando ◽  
M. D. Breyer ◽  
H. R. Jacobson
Keyword(s):  
Protein Kinase C ◽  
Negative Feedback ◽  
Cyclooxygenase Inhibitor ◽  
Pkc Inhibitor ◽  
Kinase C ◽  
Collecting Ducts ◽  
High Concentrations ◽  
Pi Hydrolysis ◽  
Dose Dependent ◽  
Stimulation Of

In cortical collecting ducts (CCD), arginine vasopressin (AVP) has been proposed to autoinhibit its own hydrosmotic effect through stimulation of prostaglandin (PG) synthesis or binding to a receptor coupled to phosphatidylinositol (PI) hydrolysis, the so-called V1-receptor, with resultant elevation of intracellular Ca2+ concentration [( Ca2+]i) and activation of protein kinase C (PKC). Using isolated perfused rabbit CCD, we examined whether blocking the negative feedback by a PKC inhibitor, staurosporine (SSP), or a cyclooxygenase inhibitor, indomethacin (IND), enhances AVP-induced increase in hydraulic conductivity (Lp). The Lp induced by a pharmacological concentration (23 nM) of AVP was lower than that induced by 230 pM AVP. This blunted Lp response to 23 nM AVP was significantly restored by SSP or IND pretreatment. In contrast, both SSP and IND did not affect the Lp induced by 23 pM or 230 pM AVP. Fluorescence microscopy of isolated perfused CCD using fura-2 showed a spike-like increase in [Ca2+]i only by 23 nM but not by 23 or 230 pM AVP. We conclude that 1) AVP can increase [Ca2+]i, activate PKC, and stimulate PG synthesis in CCD with resultant autoregulation of its own hydrosmotic effect and 2) importantly, however, this negative feedback occurs only with pharmacologically high concentrations of AVP. Therefore it is unlikely that circulating AVP, via binding to receptors on CCD, autoregulates water transport through activating PG synthesis and/or PI breakdown.

Negative feedback in NO/cGMP signalling

2005 ◽  
Vol 33 (5) ◽  
pp. 1119-1122 ◽  
Author(s):  
D. Koesling ◽  
F. Mullershausen ◽  
A. Lange ◽  
A. Friebe ◽  
E. Mergia ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Negative Feedback ◽  
Subsequent Increase ◽  
Intact Cells ◽  
Cgmp Signalling ◽  
Signalling Molecule ◽  
Regulatory Properties ◽  
Phosphodiesterase 5 ◽  
Cgmp Formation ◽  
Stimulation Of

Most of the effects of the signalling molecule nitric oxide (NO) are mediated by the stimulation of the NO-sensitive GC (guanylate cyclase) and the subsequent increase in cGMP formation. The enzyme contains a prosthetic haem group, which mediates NO stimulation. In addition to the physiological activator NO, NO-sensitizers like the substance YC-1 sensitize the enzyme towards NO and may therefore have important pharmacological implications. Two isoforms of NO-sensitive GC have been identified to date that share regulatory properties, but differ in the subcellular localization. The more ubiquitously expressed α1β1 heterodimer and the α2β1 isoform are mainly expressed in brain. In intact cells, NO-induced cGMP signalling not only depends on cGMP formation, but is also critically determined by the activity of the enzymes responsible for cGMP degradation, e.g. PDE5 (phosphodiesterase 5). Recently, direct activation of PDE5 by cGMP was demonstrated, limiting the cGMP increase and thus functioning as a negative feedback. As the cGMP-induced PDE5 activation turned out to be sustained, in the range of hours, it is probably responsible for the NO-induced desensitization observed within NO/cGMP signalling.

Feminising Interstitial Cell Tumour of the Testis

1973 ◽  
Vol 59 (2) ◽  
pp. 71-76
Author(s):  
S. P. Gray ◽  
H. Chandler ◽  
K. C. Bouskill ◽  
N. J. Blacklock
Keyword(s):  
Negative Feedback ◽  
Normal Level ◽  
Interstitial Cell ◽  
Testicular Tissue ◽  
Feedback Mechanism ◽  
Cell Tumour ◽  
Negative Feedback Mechanism ◽  
Normal Limits ◽  
Androgenic Steroids ◽  
Stimulation Of

AbstractA case of an interstitial cell tumour of the testis associated with bilateral gynae-comastia is described. The patient excreted excessive amounts of oestrogen in the urine whilst the 17-oxosteroids were within normal limits. Analysis of the testicular tumour removed at operation showed that it contained much more oestrone, andros-terone, dehydroepiandrosterone (DHEA), and aetiocholanolone, than did the non neoplastic testicular tissue surrounding the tumour.It is suggested that these steroids produced by the tumour were the cause of the patient’s feminisation, and that there were two effects reinforcing each other, viz, the excess of oestrogen itself and the presence of sufficient amounts of weakly androgenic steroids to lower the normal level of testosterone production by the testis.These effects could have been mediated in two different ways; indirectly by stimulation of the negative feedback mechanism of the pituitary causing less ICSH to reach the testis, and directly by the inhibition of the enzymes concerned with the normal biosynthesis of testosterone in the testis.

scholarly journals Protein C activation on endothelial cells by prothrombin activation products generated in situ: meizothrombin is a better protein C activator than α-thrombin

1996 ◽  
Vol 319 (2) ◽  
pp. 399-405 ◽  
Author(s):  
Tilman M. HACKENG ◽  
Guido TANS ◽  
Stefan J KOPPELMAN ◽  
Philip G. de GROOT ◽  
Jan ROSING ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Negative Feedback ◽  
Protein C ◽  
Coagulation Factor ◽  
Protein S ◽  
Prothrombinase Complex ◽  
Activation Products ◽  
Prothrombin Activation ◽  
Stimulation Of

The conversion of protein C into activated protein C (APC) by the thrombin-thrombomodulin complex on the surface of endothelial cells initiates an essential negative feedback reaction on blood coagulation. APC, together with its non-enzymic cofactor protein S, inactivates factors Va and VIIIa, the non-enzymic protein cofactors of the prothrombinase and intrinsic tenase complex, by proteolytic degradation. In this study we report that prothrombin activation products, generated by the prothrombinase complex on the surface of quiescent endothelial cells, are able to activate protein C. Subsequent inactivation of factor Va by the APC that was formed decreased the rate of prothrombin activation, thus demonstrating in vitro the negative feedback loop on coagulation factor activation. The anticoagulant feedback reaction of APC on the prothrombinase complex was stimulated 3–4-fold by the addition of protein S but not by thrombin-cleaved protein S or by protein S complexed with C4b-binding protein. Stimulation of endothelial cells with 50 pM tumour necrosis factor (TNF) or 500 pM interleukin 1 (IL-1) resulted in a 70% decrease in activation of protein C by exogenously added α-thrombin, which seemed to be due to down-regulation of thrombomodulin activity on the surface of endothelial cells. However, when prothrombin activation products generated in situ were allowed to activate protein C, stimulation of endothelial cells with TNF and IL-1 resulted in only a 25% decrease in activation of protein C. Stimulation with TNF or IL-1 did not affect the ability of endothelial cells to support prothrombinase activity. We investigated whether the differences in extent of protein C activation by exogenously added α-thrombin and by prothrombin activation products generated in situ were due to meizothrombin formed during prothrombin activation. Previous reports from our groups revealed that meizothrombin is generated as a transient intermediate during prothrombin activation on phospholipid vesicles and endothelial cells. Here we show that meizothrombin is at least a 6-fold better activator of protein C on the surface of endothelial cells than is α-thrombin. These results demonstrate that meizothrombin, formed during the initial phase of prothrombin activation, efficiently down-regulates both its own formation and that of thrombin.

THE EFFECT OF OVARIAN STEROIDS ON HYPOTHALAMIC THRESHOLDS FOR OVULATION IN THE FEMALE RAT

1971 ◽  
Vol 49 (3) ◽  
pp. 421-429 ◽  
Author(s):  
P. G. McDONALD ◽  
D. P. GILMORE
Keyword(s):  
Negative Feedback ◽  
Median Eminence ◽  
Preoptic Area ◽  
Feedback Effect ◽  
Female Rats ◽  
Female Rat ◽  
Ovarian Hormone ◽  
Ovarian Steroids ◽  
Positive Feedback Effect ◽  
Stimulation Of

SUMMARY Electrochemical stimulation of the basal and preoptic hypothalamus, under sodium pentobarbitone anaesthesia, was carried out on the day of pro-oestrus in normal cycling and in ovarian hormone-treated female rats. Control rats ovulated in response to 25, 50 and 100 μA for 60 s in the median eminence and to 10 μA for 60 s in the preoptic area. Oestradiol (1 μg) given 24 h before median eminence stimulation significantly increased the number of rats ovulating. An injection of progesterone (1 mg) 24 h before median eminence stimulation did not affect the number of animals ovulating or the number of ova shed. In contrast, there was a significant reduction in the number of animals ovulating after preoptic stimulation. Stimulation of the median eminence 2–4 h after progesterone administration increased the number of animals ovulating. The results suggest that both oestradiol and progesterone exert a positive feedback effect at or below the level of the median eminence and that the negative feedback effect of progesterone is exerted on the preoptic area.

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