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22. 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
23. The interaction of calcium entry and calcium sensitization in the control of vascular tone and blood pressure of normotensive and hypertensive rats
- Creator:
- Josef Zicha, Behuliak, M., Mária Pintérová, Bencze, M., Jaroslav Kuneš, and Ivana Vaněčková
- Format:
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, vápník, cévy, krevní tlak, calcium, vessels, blood pressure, calcium sensitization, RhoA/Rho kinase, fasudil, Ca2+ entry, nifedipine, BAY K8644, 14, and 612
- Language:
- English
- Description:
- ncreased systemic vascular resistance is responsible for blood pressure (BP) elevation in most forms of human or experimental hypertension. The enhanced contractility of structurally remodeled resistance arterioles is mediated by enhanced calcium entry (through L type voltagedependent calcium channels - L-VDCC) and/or augmented calcium sensitization (mediated by RhoA/Rho kinase pathway). It is rather difficult to evaluate separately the role of these two pathways in BP control because BP response to the blockade of either pathway is always dependent on the concomitant activity of the complementary pathway. Moreover, vasoconstrictor systems enhance the activity of both pathways, while vasodilators attenuate them. The basal fasudil-sensitive calcium sensitization determined in rats deprived of endogenous renin-angiotensi n system (RAS) and sympathetic nervous system (SNS) in wh ich calcium entry was dose- dependently increased by L-VDCC opener BAY K8644, is smaller in spontaneously hypertensive rats (SHR) than in normotensive Wistar-Kyoto (WKY) rats. In co ntrast, if endogenous RAS and SNS were present in intact rats, fasudil caused a greater BP fall in SHR than WKY rats. Our in vivo experiments indicated that the endogenous pressor systems (RAS and SNS) augment calcium sensitization mediated by RhoA/Rho kinase pathway, whereas the endogenous vasodilator systems (such as nitric oxide) attenuate this pathway. However, the modulation of calcium entry and calcium sensitization by nitric oxide is strain-dependent because NO deficiency significan tly augments low calcium entry in WKY and low calcium sensitization in SHR. Further in vivo and in vitro experiments should clarify the interrelationships between endogenous vasoactive systems an d the contribution of calcium entry and/or calcium sensitization to BP maintenance in various forms of experimental hypertension., J. Zicha ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
24. The interaction of genetic and environmental factors in the etiology of hypertension
- Creator:
- Jaroslav Kuneš and Josef Zicha
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie, syndrom inzulinové rezistence, hypertenze, geny, životní prostředí, ekologická genetika, physiology, insulin resistance syndrome, hypertension, genes, environment, ecological genetics, 14, and 612
- Language:
- English
- Description:
- Essential hypertension is a major risk factor for several cardiovascular diseases. It is a complex trait resulting from the interactions of multiple genetic and environmental factors. Moreover, not only genetic but also epigenetic inheritance plays a significant role. One can speculate that hypertension develops as a consequence of “errors” in well-coordinated regulatory systems of blood pressure. Errors in the cascade of molecular, biochemical and genetic processes, which regulate blood pressure, have finally enough potential to result in hypertension. Numerous environmental factors surrounding the organism during its development should influence the expression of genetic information. However, despite the considerable research effort, it is still difficult to identify all genes and/or other genetic determinants leading to essential hypertension and other cardiovascular diseases. This is mainly because these diseases usually become a medical problem in adulthood, although their roots might be traced back to earlier stages of ontogeny. The link between distinct developmental periods (e.g. birth and adulthood) should involve changes in gene expression involving epigenetic phenomena. The purpose of the present paper is to bring a piece of light on gene-environmental interactions potentially implicated in the pathogenesis of hypertension., J. Kuneš, J. Zicha., and Obsahuje seznam literatury
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
25. Tolerance to acute ischemia in adult male and female spontaneously hypertensive rats
- Creator:
- Josef Bešík, Ondrej Szárszoi, Jaroslav Kuneš, Ivan Netuka, Jan Malý, František Kolář, Jan Pirk, and Bohuslav Ošťádal
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie, hypertenze, pohlavní rozdíly, physiology, hypertension, sex differences, srdeční tolerance, ischemické / reperfuzní poškození, spontánně hypertenzivní krysy, genderové rozdíly, cardiac tolerance, ischemia / reperfusion injury, spontaneously hypertensive rats, gender differences, 14, and 612
- Language:
- English
- Description:
- Clinical and experimental studies have repeatedly indicated that overloaded hearts have a higher vulnerability to ischemia/reperfusion injury. The aim of the present study was to answer the question whether the degree of tolerance to oxygen deprivation in hearts of spontaneously hypertensive rats (SHR) may be sex-dependent. For this purpose, adult SHR and their normotensive control Wistar Kyoto (WKY) rats were used. The isolated hearts were perfused according to Langendorff at constant pressure (proportionally adjusted to the blood pressure in vivo). Recovery of contractile parameters (left ventricular systolic, diastolic and developed pressure as well as the peak rate of developed pressure) was measured during reperfusion after 20 min of global no-flow ischemia in 5 min intervals. Mean arterial blood pressure was measured by direct puncture of carotid artery under light ether anesthesia in a separate group of animals. The degree of hypertension was comparable in both sexes of SHR. The recovery of contractile functions in SHR males and females was significantly lower than in WKY rats during the whole investigated period. There was no sex difference in the recovery of WKY animals; on the other hand, the recovery was significantly better in SHR females than in SHR males. It may be concluded that the hearts of female SHR are more resistant to ischemia/reperfusion injury as compared with male SHR. This fact could have important clinical implications for the treatment of cardiovascular disease in women., J. Bešík, O. Szárszoi, J. Kuneš, I. Netuka, J. Malý, F. Kolář, J. Pirk, B. Ošťádal., and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
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