Antagonism by the tetramine disulfide benextramine of the inhibitory effects mediated by prejunctional alpha2-adrenoceptors and by postjunctional histamine H2 receptors in the mouse vas deferens

1984 ◽  
Vol 62 (9) ◽  
pp. 1147-1151 ◽  
Author(s):  
M. M. Vohra ◽  
A. Chaudhry
Keyword(s):  
Vas Deferens ◽  
Inhibitory Effect ◽  
Inhibitory Effects ◽  
Mouse Vas Deferens ◽  
Alpha Adrenoceptors ◽  
Twitch Response ◽  
H2 Receptors ◽  
A Site ◽  
Non Equilibrium

The actions of benextramine, which blocks postjunctional alpha-adrenoceptors noncompetitively and irreversibly (non-equilibrium type) on prejunctional alpha-adrenoceptors (alpha2) and postjunctional histamine H2 receptors, were studied in the mouse vas deferens, using clonidine and histamine, respectively, as the agonists. Both agonists caused a dose-related inhibition of the electrically evoked twitch responses, an inhibition that their respective antagonists (yohimbine or phentolamine, and cimetidine) antagonized competitively. Benextramine, however, antagonized the agonists' inhibitory effect noncompetitively. At the concentrations used, while clonidine or yohimbine and phentolamine protected the prejunctional alpha-adrenoceptors (alpha2) against the benextramine noncompetitive blockade, histamine or cimetidine failed to protect the histamine H2 receptor against benextramine blockade. Therefore, although benextramine acts prejunctionally to block the alpha2-adrenoceptors in the mouse vas deferens either by interacting directly with the same site as clonidine or yohimbine and phentolamine, or allosterically with a site close to it, it does not appear to act irreversibly, either directly or allosterically, with the same site as histamine or cimetidine. The mechanism by which benextramine blocks the histamine-induced inhibition of the electrically evoked twitch response in the mouse vas deferens remains to be established.

TYRAMINE AND PRESYNAPTIC ALPHA ADRENOCEPTORS IN THE MOUSE VAS DEFERENS

Abstracts ◽  
1978 ◽  
pp. 551
Author(s):  
N. Shepperson ◽  
I. Marshall ◽  
P.A. Nasmyth
Keyword(s):  
Vas Deferens ◽  
Mouse Vas Deferens ◽  
Alpha Adrenoceptors

THE RELATIONSHIP BETWEEN 3H-NA OVERFLOW AND THE TWITCH RESPONSE OF THE MOUSE VAS DEFERENS

Abstracts ◽  
1978 ◽  
pp. 441
Author(s):  
N.B. Shepperson ◽  
I. Marshall ◽  
P.A. Nasmyth
Keyword(s):  
Vas Deferens ◽  
Mouse Vas Deferens ◽  
Twitch Response ◽  
The Relationship

Pre- and postjunctional effects of some prostanoids in human isolated vas deferens

1991 ◽  
Vol 260 (4) ◽  
pp. R792-R797 ◽  
Author(s):  
F. Holmquist ◽  
H. Hedlund ◽  
K. E. Andersson
Keyword(s):  
Vas Deferens ◽  
Thromboxane A2 ◽  
Electrical Field Stimulation ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Inhibitory Effects ◽  
Concentration Dependent Manner ◽  
Thromboxane A2 Receptor ◽  
Thromboxane Receptor ◽  
Thromboxane A2 Analogue

The effects of prostaglandin (PG) E1, PGE2, the thromboxane A2 analogue U-44069, and the prostacyclin derivative iloprost were studied on isometric contractions induced by norepinephrine (NE) and by electrical field stimulation of nerves in isolated preparations of the human vas deferens. The effects of these agents on the electrically induced release of 3H from preparations preincubated with [3H]NE were also investigated. PGE1 and PGE2 inhibited the electrically induced contractions concentration dependently. U-44069 augmented the contractions without affecting baseline tension, and in preparations where the contractions had been inhibited by PGE1 or PGE2, U-44069 restored the contractions almost to starting levels. The thromboxane A2-receptor antagonist BM 13505, having no effect or inhibitory effects on electrically induced contractions, abolished the stimulatory effect of U-44069. Contractions induced by exogenous NE were augmented by U-44069, whereas PGE1 and BM 13505 were without effects. The electrically induced release of 3H was inhibited by PGE1 and PGE2 in a concentration-dependent manner, whereas U-44069 and BM 13505 increased the release of 3H. Furthermore, the inhibitory effect of PGE1 on 3H release was partly counteracted by U-44069. Iloprost had no significant effect on electrically induced contractions or on 3H release. These results suggest that, in the human vas deferens, thromboxane A2 augments contractions predominantly through a postjunctional site of action, whereas PGs of the E type have a prejunctional inhibitory effect. In addition, the pre- and post-junctional effect profiles of U-44069 and BM 13505 suggest that there may be more than one thromboxane receptor.

scholarly journals Inhibitory effects of certain enantiomeric cannabinoids in the mouse vas deferens and the myenteric plexus preparation of guinea-pig small intestine

1992 ◽  
Vol 105 (4) ◽  
pp. 980-984 ◽  
Author(s):  
R.G. Pertwee ◽  
L.A. Stevenson ◽  
D.B. Elrick ◽  
R. Mechoulam ◽  
A.D. Corbett
Keyword(s):  
Small Intestine ◽  
Guinea Pig ◽  
Myenteric Plexus ◽  
Vas Deferens ◽  
Inhibitory Effects ◽  
Mouse Vas Deferens

Orphanin FQ has an inhibitory effect on the guinea pig ileum and the mouse vas deferens

1997 ◽  
Vol 772 (1-2) ◽  
pp. 102-106 ◽  
Author(s):  
Ge Zhang ◽  
Thomas F Murray ◽  
David K Grandy
Keyword(s):  
Guinea Pig ◽  
Vas Deferens ◽  
Inhibitory Effect ◽  
Orphanin Fq ◽  
Guinea Pig Ileum ◽  
Mouse Vas Deferens

Interactions between alpha-adrenoceptors and adenosine receptors on microvascular smooth muscle

1991 ◽  
Vol 260 (5) ◽  
pp. H1655-H1666 ◽  
Author(s):  
K. Nishigaki ◽  
J. E. Faber ◽  
M. Ohyanagi
Keyword(s):  
Adenosine Receptor ◽  
Adenosine Receptors ◽  
Inhibitory Effect ◽  
Inhibitory Effects ◽  
Receptor Stimulation ◽  
Alpha Adrenoceptors ◽  
Adenosine Receptor Antagonist ◽  
Adenosine Receptor Agonist ◽  
Muscle Concentration ◽  
Tissue Acidosis

alpha 2-Adrenoceptor but not alpha 1-adrenoceptor constriction of arterioles is selectively inhibited by tissue acidosis, ischemia, and increased metabolic rate. To further examine neural-local interactions, we studied the effect of adenosine receptor stimulation on alpha 1- or alpha 2-adrenoceptor constriction. Intravital microscopy was used to study large arterioles (133 +/- 3 microns diam; mean +/- SE), small arterioles (16 +/- 1 microns), and large venules (178 +/- 3 microns) of rat cremaster skeletal muscle. Concentration-response (diameter change) curves were obtained for bath-added norepinephrine in the presence of either rauwolscine or prazosin to provide selective alpha 1- and alpha 2-constriction, respectively. The adenosine receptor agonist 5'-N-ethylcarboxamidoadenosine (2.24 x 10(-8) M) significantly attenuated both alpha 1- and alpha 2-constriction by 5- to 20-fold; alpha 1-constriction was three- to fourfold more sensitive than alpha 2-constriction. Similar inhibitory effects were obtained with adenosine (2.24 x 10(-6) M). The adenosine receptor antagonist 8-[4-[N(2-aminoethyl)carbamoylmethoxy]phenyl]-1,3-dipropylxanthine (0.7 microM) reversed the inhibitory effect of adenosine, which implicates extracellular A2 adenosine receptors. Intrinsic tone in large vessels was unaffected by adenosine receptor stimulation but was completely inhibited in small arterioles. These findings suggest that both alpha 2- and especially alpha 1-adrenoceptor constriction and intrinsic tone (of small but not large arterioles) are inhibited by physiologically relevant concentrations of adenosine.

Angiotensin II mediates drinking elicited by eating in the rat

1990 ◽  
Vol 258 (2) ◽  
pp. R436-R442 ◽  
Author(s):  
F. S. Kraly ◽  
R. Corneilson
Keyword(s):  
Angiotensin Ii ◽  
Drinking Behavior ◽  
Inhibitory Effect ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Inhibitory Effects ◽  
Physiological Conditions ◽  
Sprague Dawley Rats ◽  
Subcutaneous Dose ◽  
H2 Receptors

Captopril (CA) was used to block synthesis of endogenous angiotensin II (ANG II) in periphery and/or brain of adult male Sprague-Dawley rats in tests for drinking elicited by eating pelleted chow. Blockade of ANG II-converting enzyme (ACE) in periphery alone (using 0.5 mg/kg CA) increased drinking elicited by eating, whereas simultaneous blockade of ACE in periphery and brain (using subcutaneous 100 mg/kg CA or subcutaneous 0.5 mg/kg plus third ventricular 25 micrograms CA) decreased such drinking. The inhibitory effect of 100 mg/kg CA on water-to-food ratio was prevented by a dipsogenically subthreshold subcutaneous dose (5 micrograms/kg) of ANG II. Blockade of ACE in brain alone (third ventricular 25 micrograms CA) had no effect on food-related drinking. Pharmacological antagonism of ANG II (100 mg/kg CA) together with antagonism of histamine H1 and H2 receptors (using intraperitoneal dexbrompheniramine and cimetidine) were not additive in their inhibitory effects on drinking elicited by eating. Blockade of ACE (100 mg/kg CA) inhibited drinking elicited by subcutaneous histamine, but blockade of histamine receptors failed to inhibit drinking elicited by subcutaneous ANG II. These results support a role for endogenous ANG II under what appear to be physiological conditions for drinking behavior, i.e., when drinking is elicited by eating, and they suggest the working hypothesis of ANG II mediation of a histaminergic mechanism for food-related drinking in the rat.

scholarly journals Genetic heterogeneity of histamine H2-receptors in the mouse vas deferens

1984 ◽  
Vol 83 (3) ◽  
pp. 723-731 ◽  
Author(s):  
J. A. Calvete ◽  
J.L.M. Donegan ◽  
R.J. Hayes ◽  
N.S. Oates ◽  
T.P. Sloan
Keyword(s):  
Genetic Heterogeneity ◽  
Vas Deferens ◽  
Mouse Vas Deferens ◽  
H2 Receptors
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