Serotonergic and Catecholaminergic Mechanisms for Baroreflex Regulation in the NTS

2019 ◽  
pp. 255-266
Author(s):  
Ruben D. Bunag ◽  
Hiroshi Itoh
1998 ◽  
Vol 78 (4) ◽  
pp. 501-504 ◽  
Author(s):  
Hsieh Ming-Tsuen ◽  
Chueh Fu-Yu ◽  
Lin Shui-Mu ◽  
Chueh Fu-Shin ◽  
Chen Chieh-Fu ◽  
...  

1977 ◽  
Vol 5 (6) ◽  
pp. 337-344 ◽  
Author(s):  
Gábor L. Kovács ◽  
Laszló Vécsei ◽  
Gyula Szabó ◽  
Gyula Telegdy

1988 ◽  
Vol 254 (2) ◽  
pp. R289-R295
Author(s):  
K. V. Thrivikraman ◽  
D. E. Carlson ◽  
D. S. Gann

Temporal changes in monoaminergic activity in the locus coeruleus (LC) in response to hemorrhage of 10 or 20% of blood volume were assessed using normal pulse voltammetry in alpha-chloralose-urethan-anesthetized cats. Oxidation current was measured with a carbon microelectrode, and changes at 230 and 450 mV were used as estimates of catecholaminergic and indolaminergic activity, respectively. Plasma adrenocorticotropin (ACTH) was measured by radioimmunoassay. Hemorrhage of 20% blood volume caused a transient increase in the catecholaminergic activity in a compact area in the ventral LC (vLC) that preceded increases in the plasma ACTH. The increase in oxidation current at 450 mV was similar to that at 230 mV, suggesting no significant contribution from indolamines. Dorsal rostral pontine sites outside this area exhibited either sustained decreases in oxidation current or no change in response to hemorrhage. The proportion of sites that exhibited transient increases in oxidation current in the vLC after the 10% blood loss was less than that after the 20% blood loss, suggesting that this response was dependent on the magnitude of hemorrhage. Since the LC was implicated previously in the control of ACTH release, we suggest that hemodynamic signals traversing the LC activate catecholaminergic mechanisms that, in turn, participate in the regulation of ACTH release after hemorrhage.


1974 ◽  
Vol 77 (2) ◽  
pp. 209-220 ◽  
Author(s):  
Alan Corbin ◽  
G. Virginia Upton ◽  
C. C. Mabry ◽  
Dorothy R. Hollingsworth

ABSTRACT Our results indicate that generalized lipodystrophy (GLD) possesses as one of its manifestations, diencephalic neuroendocrinopathy. It has been postulated that deranged hypothalamic catecholaminergic mechanisms lead to the hypersecretion of hypophysiotrophic hormones that are detectable in the peripheral circulation. Initial treatment of a pre-puberal GLD patient with chlorpromazine was unrewarding. Chronic treatment of the same patients with the selective dopaminergic blocking agent, pimozide, eliminated corticotrophin releasing factor and luteinizing hormone releasing factor activities from the general circulation. Pimozide treatment ameliorated most of the distorted blood chemistry profile, led to return of facial subcutaneous fat, and elimination of cutaneous hyperpigmentation, fever, abdominal pain, hypertrichosis, oilness of hair, scaliness of skin and to a state of general well-being. The results of these studies, structured within the framework of our present knowledge concerning hypothalamic neurotransmitter/releasing hormone physiology, support the concept of diencephalic involvement in GLD and may provide a guideline to effective therapy.


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