In vivo evaluation of serotonergic agents and alpha-adrenergic blockers on premature ejaculation by inhibiting the seminal vesicle pressure response to electrical nerve stimulation

1998 ◽  
Vol 82 (2) ◽  
pp. 237-240 ◽  
Author(s):  
Hsieh ◽  
Chang ◽  
Law ◽  
Hsieh ◽  
Cheng
2008 ◽  
Vol 179 (4S) ◽  
pp. 235-235
Author(s):  
Ahmet Cihan ◽  
Nergis Murat ◽  
Omer Demir ◽  
Guven Aslan ◽  
Sedef Gidener ◽  
...  

1989 ◽  
Vol 256 (4) ◽  
pp. G698-G703 ◽  
Author(s):  
W. S. Putnam ◽  
R. A. Liddle ◽  
J. A. Williams

Peptide YY (PYY) and pancreatic polypeptide (PP) have been shown to inhibit exocrine pancreatic secretion in vivo in a variety of species. This study evaluates the type of stimulation inhibited by PYY and PP by examining, in urethan-anesthetized rats, the inhibition of pancreatic secretion when stimulated to a comparable extent by cholecystokinin (CCK), 2-deoxy-D-glucose (2DG), bethanecol, and electrical vagal nerve stimulation. PYY at maximal infusion rates inhibited stimulation by CCK by 83%, bethanecol by 55%, and electrical nerve stimulation by 40%. The inhibition of CCK stimulation was half maximal at 250 pmol.kg-1.h-1. By contrast, PYY totally inhibited 2DG-stimulated secretion with half-maximal inhibition at 10 pmol. kg-1.h-1. PP acted similarly to PYY in inhibiting CCK and 2DG-stimulated pancreatic protein secretion but was fivefold weaker in each case. These findings indicate that PYY and PP have multiple actions but preferentially inhibit neurally mediated pancreatic secretion at a preacinar cell locus, possibly at a central site of action.


2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Jongcheon Lim ◽  
Matthew Ward ◽  
Amanda Maples ◽  
Anina Sun ◽  
Hyunsu Park ◽  
...  

1983 ◽  
Vol 245 (4) ◽  
pp. G597-G600
Author(s):  
P. F. Schmalz ◽  
K. G. Morgan ◽  
J. H. Szurszewski

Mechanical and intracellular electrical activities were recorded separately from circular muscle of the orad corpus of the canine stomach. In normal Krebs solution, transmural electrical nerve stimulation produced excitatory and inhibitory responses. The excitatory response was blocked by atropine; the inhibitory response was unaffected by phentolamine or propranolol alone or in combination. Both responses were blocked by tetrodotoxin. In the presence of pentagastrin, the inhibitory response to electrical nerve stimulation was potentiated in a dose-dependent manner. The threshold concentration for this potentiating effect was 3 X 10(-11) M. Intracellular recordings showed that hyperpolarization of the resting membrane potential in response to inhibitory nerve stimulation was greater in the presence of pentagastrin than in its absence. These data suggest that, in addition to a direct stimulatory effect on the muscle, pentagastrin also potentiates the effect of ongoing activity of intramural inhibitory nerves. This latter effect is only apparent when the inhibitory neural network is active. Thus, the in vivo effect of pentagastrin on motor activity of the corpus will depend on the degree of ongoing activity of intramural inhibitory nerves.


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