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2. Effects of pertussis toxin treatment of rats on estradiol-induced adenohypophyseal growth reaction and on adrenergic lipolysis
- Creator:
- Hynie, S. and Klenerová, V.
- Type:
- article, model:article, and TEXT
- Subject:
- adenohypophysis, adenylyl cyclase, estradiol, forskolin, isoprénaline, lipolysis, pertussis toxin, and rat
- Language:
- English
- Description:
- After long-lasting administration of estradiol (4—6 weeks) in the presence or absence of pertussis toxin treatment we followed up the changes in body weight and adenohypophyseal weight in rats subjected to this treatment. The most striking effect was the potentiating effect of pertussis toxin on the estradiol-induced adenohypophyseal growth reaction. Adenylyl cyclase activity in the adenohypophysis was significantly increased in the estradiol- treated group and the addition of pertussis toxin did not further increase this enzyme activity. The lipolytic activity in adipose tissue exhibited a similar response as adenohypophyseal growth. Adrenergic lipolysis stimulated by pertussis toxin was highly significantly increased in tissues of rats treated with pertussis toxin. Our results show that the estrogen-induced adenohypophyseal growth reaction is highly potentiated by the treatment of rats with pertussis toxin and that this effect is in many aspects similar to that observed in adrenergic lipolysis. It thus seems that both processes might be mediated via a pertussis toxin-sensitive G protein which is involved in inhibitory regulation of adenylyl cyclase.
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
3. Inactivation of Gi proteins by pertussis toxin diminishes the effectiveness of adrenergic stimuli in conduit arteries from spontaneously hypertensive rats
- Creator:
- Zemančíková, A., Török, J., Josef Zicha, and Jaroslav Kuneš
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie, hypertenze, tepny, physiology, hypertension, arteries, pertussis toxin, adrenergic contractions, conduit arteries, angiotensin II, Gi proteins, 14, and 612
- Language:
- English
- Description:
- Treatment with pertussis toxin (PTX) which eliminates the activity of Gi proteins effectively reduces blood pressure (BP) and vascular resistance in spontaneously hypertensive rats (SHR). In this study we have compared the functional characteristics of isolated arteries from SHR with and without PTX-treatment (10 μg/kg i.v., 48 h before the experiment). Rings of thoracic aorta, superior mesenteric artery and main pulmonary artery were studied under isometric conditions to measure the reactivity of these vessels to receptor agonists and to transmural electrical stimuli. We have found that the treatment of SHR with PTX had no effect on endothelium-dependent relaxation of thoracic aorta induced by acetylcholine. In PTX-treated SHR, the maximum contraction of mesenteric artery to exogenous noradrenaline was reduced and the dose-response curve to cumulative concentration of noradrenaline was shifted to the right. Similarly, a reduction in the magnitude of neurogenic contractions elicited by electrical stimulation of perivascular nerves was observed in the mesenteric artery from PTX-treated SHR. PTX treatment of SHR also abolished the potentiating effect of angiotensin II on neurogenic contractions of the main pulmonary artery. These results indicate that PTX treatment markedly diminishes the effectiveness of adrenergic stimuli in vasculature of SHR. This could importantly affect BP regulation in genetic hypertension., A. Zemančíková, J. Török, J. Zicha, J. Kuneš., and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
4. Nifedipine-sensitive vascular reactivity of femoral arteries in WKY: the effects of pertussis toxin pretreatment and endothelium removal
- Creator:
- Silvia Líšková, Jaroslav Kuneš, and Josef Zicha
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, farmakologie, toxiny, endotel, pharmacology, toxins, endothelium, pertussis toxin, inhibitory G proteins, nifedipine, voltage-dependent Ca2+ channels, norepinephrine, isolated femoral artery, 14, and 612
- Language:
- English
- Description:
- Maintenance of norepinephrine (NE)-induced contraction is dependent on Ca2+ influx through L-type voltage-dependent Ca2+ channels (VDCC), which is opposed by nitric oxide. Adrenergic receptors are coupled with different G proteins, including inhibitory G proteins (Gi) that can be inactivated by pertussis toxin (PTX). Our study was aimed to investigate the effects of endothelium removal, PTX pretreatment and acute VDCC blockade by nifedipine on the contractions of femoral arteries stimulated by norepinephrine. We used 12-week-old male WKY, half of the rats being injected with PTX (10 μg/kg i.v., 48 h before the experiment), which considerably reduced their blood pressure (BP). Contractions of isolated arteries were measured using Mulvany-Halpern myograph. NE dose-response curves determined in femoral arteries from PTX-treated WKY rats were shifted to the right compared to those from control WKY. On the contrary, removal of endothelium augmented NE dose-response curves shifting them to the left. Acute VDCC blockade by nifedipine (10-7 M) abolished all differences in NE dose-response curves which were dependent on the presence of either intact endothelium or functional Gi proteins because all NE dose-response curves were identical to the curve seen in vessels with intact endothelium from PTX-treated animals. We can conclude that BP reduction after PTX injection is accompanied by the attenuation of NE-induced contraction of femoral arteries irrespective of endothelium presence. Moreover, our data indicate that both vasodilator action of endothelium and Gi-dependent vasoconstrictor effect of norepinephrine operate via the control of Ca2+ influx through VDCC., S. Líšková, J. Kuneš, J. Zicha., and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
5. The effects of pertussis toxin-treatment on integrated vasoactive response of vascular system in spontaneously hypertensive rats
- Creator:
- Soňa Čačányiová, Kristek, F., Jaroslav Kuneš, and Josef Zicha
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie, krevní tlak, acetylcholin, physiology, blood pressure, acetylcholine, spontaneously hypertensive rats (SHR), pertussis toxin, noradrenaline, bradykinin, vasoactive responses, 14, and 612
- Language:
- English
- Description:
- We investigated the effect of pertussis toxin (PTX) on hypotensive response induced by acetylcholine (ACh) and bradykinin (BK) and on noradrenaline (NA)-induced pressor response in spontaneously hypertensive rats (SHR). Fifteen-week-old Wistar rats and age-matched SHR were used. Half of SHR received PTX (10 μg/kg/i.v.) and the experiments were performed 48 h later. After the anesthesia the right carotid artery was cannulated in order to record blood pressure (BP). The hypotensive response to ACh was enhanced in SHR compared to Wistar rats. After pretreatment of SHR with PTX the hypotensive response to ACh was reduced compared to untreated SHR and it was also diminished in comparison to Wistar rats. Similarly, the hypotensive response to BK was also decreased after PTX pretreatment. The pressor response to NA was increased in SHR compared to Wistar rats. NA-induced pressor response was considerably decreased after PTX pretreatment compared to untreated SHR. In conclusion, the enhancement of hypotensive and pressor responses in SHR was abolished after PTX pretreatment. Our results suggested that the activation of PTX-sensitive inhibitory Gi proteins is involved in the regulation of integrated vasoactive responses in SHR and PTX pretreatment could be effectively used for modification of BP regulation in this type of experimental hypertension., S. Čačányiová, F. Kristek, J. Kuneš, J. Zicha., and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public