scholarly journals Potentiation by Higenamine of the Aconitine-Induced Positive Chronotropic Effect in Isolated Right Atria of Mice: The Effects of Cholera Toxin, Forskolin and Pertussis Toxin.

1996 ◽  
Vol 19 (8) ◽  
pp. 1032-1037 ◽  
Author(s):  
Ikuko KIMURA ◽  
Md. Amirul ISLAM ◽  
Masayasu KIMURA
Keyword(s):  
Cholera Toxin ◽  
Pertussis Toxin ◽  
Chronotropic Effect ◽  
Right Atria ◽  
Positive Chronotropic Effect

α1a-Adrenergic receptor mediated positive chronotropic effect in right atria isolated from rats

1994 ◽  
Vol 72 (12) ◽  
pp. 1574-1579 ◽  
Author(s):  
Anthony P. Williamson ◽  
Ernst Seifen ◽  
Jon P. Lindemann ◽  
Richard H. Kennedy
Keyword(s):  
Adrenergic Receptor ◽  
Response Curve ◽  
Male Rats ◽  
Chronotropic Effect ◽  
Rightward Shift ◽  
Spontaneous Rate ◽  
Negative Chronotropic Effect ◽  
Right Atria ◽  
Concentration Response Curve ◽  
Positive Chronotropic Effect

Experiments in right atria isolated from adult male rats were designed to determine which of the α1-adrenergic receptor (α1-AR) subtypes are involved in the positive chronotropic effect of phenylephrine, an α1-AR agonist. Chloroethylclonidine (CEC), an irreversible α1b-, α1c-, and α1d-AR antagonist, did not alter the efficacy or potency of phenylephrine; however, CEC did elicit a concentration-dependent negative chronotropic effect and reduce the absolute maximum spontaneous rate observed in the presence of phenylephrine. WB4101, a competitive α1a- and α1c-AR-selective antagonist, did not alter basal spontaneous rate or the efficacy of phenylephrine, but it did produce a significant rightward shift of the phenylephrine concentration–response curve. Phenoxybenzamine, an irreversible nonselective α-AR antagonist, elicited a concentration-dependent negative chronotropic effect, a significant rightward shift of the phenylephrine concentration–response curve, and a reduction in the efficacy of phenylephrine. The chronotropic action of the β-adrenergic agonist isoproterenol was not affected by CEC, WB4101, or phenoxybenzamine. These data suggest that the positive chronotropic effect of α1-adrenergic agonists in rat right atria is mediated via stimulation of α1a-ARs.Key words: α1-adrenergic receptor subtypes, chloroethylclonidine, WB4101, phenylephrine, right atria (rat).

scholarly journals Increased intracellular cyclic adenosine monophosphate inhibits T lymphocyte-mediated cytolysis by two distinct mechanisms.

1988 ◽  
Vol 167 (6) ◽  
pp. 1963-1968 ◽  
Author(s):  
L S Gray ◽  
J Gnarra ◽  
E L Hewlett ◽  
V H Engelhard
Keyword(s):  
Cholera Toxin ◽  
T Lymphocyte ◽  
Pertussis Toxin ◽  
Target Cell ◽  
Cyclic Adenosine Monophosphate ◽  
Second Messenger ◽  
Adenosine Monophosphate ◽  
Dose Dependent Fashion ◽  
Dose Dependent ◽  
Stimulation Of

Cholera toxin (CT), but not pertussis toxin (PT), treatment of cloned murine CTL inhibited target cell lysis in a dose-dependent fashion. The effects of CT were mimicked by forskolin and cyclic adenosine monophosphate (cAMP) analogues. Inhibition of cytotoxicity by CT and cAMP analogs was mediated in part by attenuation of conjugate formation. Additionally, both CT and cAMP analogs blocked the increase in intracellular Ca2+ induced by stimulation of the TCR complex by mAbs. These findings indicate that cAMP inhibits the activity of CTL by two distinct mechanisms and suggests a role for this second messenger in CTL-mediated cytolysis.

Pregnancy enhances G protein activation and nitric oxide release from uterine arteries

2001 ◽  
Vol 280 (5) ◽  
pp. H2069-H2075 ◽  
Author(s):  
L. P. Thompson ◽  
C. P. Weiner
Keyword(s):  
Nitric Oxide ◽  
Cholera Toxin ◽  
G Protein ◽  
Pertussis Toxin ◽  
Nitric Oxide Synthase Inhibitor ◽  
Protein Activation ◽  
Nitric Oxide Release ◽  
G Protein Activation ◽  
Hormonal Modulation ◽  
Synthase Inhibitor

We hypothesized that pregnancy modulates receptor-mediated responses of the uterine artery (UA) by altering G protein activation or coupling. Relaxation and contraction to NaF (0.5–11.5 mM), acetylcholine (10−9–10−5 M), and bradykinin (10−12–3 × 10−5 M) were measured in isolated UA of pregnant and nonpregnant guinea pigs. Responses were measured in the presence and absence of either cholera toxin (2 μg/ml) or pertussis toxin (Gαs and Gαiinhibitors, respectively). NaF relaxation was endothelium dependent and nitro-l-arginine sensitive (a nitric oxide synthase inhibitor). Relaxation to NaF, acetylcholine, and bradykinin were potentiated by pregnancy. Cholera but not pertussis toxin increased relaxation to acetylcholine and bradykinin in UA from nonpregnant animals, had no effect in UA from pregnant animals, and abolished the pregnancy-induced differences in acetylcholine relaxation. Cholera toxin potentiated the bradykinin-induced contraction of UA of both pregnant and nonpregnant animals, whereas pertussis toxin inhibited contraction of UA from pregnant animals only. Therefore, pregnancy may enhance agonist-stimulated endothelium-dependent relaxation and bradykinin-induced contraction of UA by inhibiting GTPase activity or enhancing Gαs but not Gαi activation in pregnant animals. Thus the diverse effects of pregnancy on UA responsiveness may result from hormonal modulation of G proteins coupled to their specific receptors.

Adjuvant action of cholera toxin and pertussis toxin in the induction of IgA antibody response to orally administered antigen

Vaccine ◽  
1993 ◽  
Vol 11 (2) ◽  
pp. 113-118 ◽  
Author(s):  
A.D. Wilson ◽  
A. Robinson ◽  
L. Irons ◽  
C.R. Stokes
Keyword(s):  
Antibody Response ◽  
Cholera Toxin ◽  
Pertussis Toxin ◽  
Iga Antibody

Effects of pertussis and cholera toxins on α-adrenoceptor function in rat tail artery: differences in hypertension

1993 ◽  
Vol 71 (10-11) ◽  
pp. 791-799 ◽  
Author(s):  
Xiao-Fang Li ◽  
Christopher R. Triggle
Keyword(s):  
Cholera Toxin ◽  
Pertussis Toxin ◽  
Rat Tail Artery ◽  
Response Curves ◽  
Contractile Responses ◽  
Tail Artery ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
The Right ◽  
Rat Tail

The α1- and α2-adrenoceptor-stimulated contractile responses of rat tail artery rings were compared in Sprague–Dawley (SD), spontaneously hypertensive (SHR), and Wistar–Kyoto (WKY) rats that were untreated, treated with pertussis toxin, or treated with cholera toxin. The maximal responses, expressed as milligrams of tension, induced by clonidine (an α2-adrenoceptor agonist) and cirazoline (a selective (α1-adrenoceptor agonist) were significantly greater in SHR than in SD or WKY, and the tissues were more sensitive to the agonists in SHR or SD than in WKY. Yohimbine (0.1 μM), a selective α2-adrenoceptor antagonist, shifted the dose–response curves for clonidine to the right. The effects of yohimbine were greater in SD than in WKY or SHR, but not different between WKY and SHR. Prazosin (0.05 μM), a selective α1-adrenoceptor antagonist, shifted the dose–response curves of cirazoline to the right, but the effects of prazosin were not different among these three strains of rats. Nifedipine (0.05 μM) completely blocked the response to clonidine in SD and WKY; however, in SHR, approximately one-third of the response to clonidine was resistant to nifedipine. Nifedipine, at 0.05 μM, only partially inhibited responses to cirazoline in SD, SHR, and WKY, and no differences were noted between the strains. Pertussis toxin pretreatment (50 μg/kg, 3 days before experiment) almost completely blocked the responses to clonidine, but only partially inhibited those to cirazoline. After pertussis toxin pretreatment, the responses (maximal effects and EC50s) to clonidine and cirazoline were not significantly different in arteries from the three strains of rats. A combination of pertussis toxin and nifedipine resulted in an additive inhibition of the responses induced by cirazoline. cholera toxin pretreatment (0.3 mg/kg, 3 days before experiment), however, had no effects on the contractile responses induced by either clonidine or cirazoline, or on the inhibitory effects of nifedipine in SHR, SD, and WKY. These results indicate that (i) the maximal responses to α1- and α2-adrenoceptor agonists are enhanced in rat tail artery rings from SHR; (ii) tissues from SH and SD rats are also more sensitive to cirazoline and clonidine than are tissues from WKY; (iii) responses to clonidine, but not cirazoline, in tissues from the SHR are less sensitive to nifedipine than tissues from SD and WKY; (iv) a G-protein sensitive to pertussis but not cholera toxin is involved in the regulation of both α1 and α2-adrenoceptor signal transduction processes in rat tail artery smooth muscle; and (v) pretreatment with pertussis toxin reduces the enhanced response levels of SHR tissues so that the maximal contractile responses to both α1- and α2-adrenoceptor agonists are equivalent in arteries from the three strains of rats.Key words: pertussis toxin, cholera toxin, α1-adrenoceptor, α2-adrenoceptor, rat tail artery ring.

Nitric oxide has no chronotropic effect in right atria isolated from rat heart

1994 ◽  
Vol 255 (1-3) ◽  
pp. 149-156 ◽  
Author(s):  
Richard H. Kennedy ◽  
Kristine K. Hicks ◽  
Johnny E. Brian ◽  
Ernst Seifen
Keyword(s):  
Nitric Oxide ◽  
Rat Heart ◽  
Chronotropic Effect ◽  
Right Atria
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