Numerous studies concerning the cardiovascular system in SHR often yield controversial data. The background of this diversity has various roots, ranging from different vascular segments or areas studied up to the different age of experimental animals. Our study aimed to follow the BP as an integrated response of vascular system. This approach was justified since stabilized cardiac output in SHR was proved till 1 year of age. The groups of male SHR (aged 3, 5, 9, 17 and 52 weeks) and age-matched Wistar rats were used. Significant basal BP difference between SHR and Wistar rats was found at 9 weeks of age and continued till the age of 52 weeks, reaching 189.6±11.9 mm Hg in SHR and 117.3±6.9 mm Hg in Wistar rats (P<0.01). The significant difference in BP increase to two doses of noradrenaline (0.1 µg and 1 µg) between SHR and control rats was also found at the age of 9 weeks. At 52 weeks the BP increment to two doses of noradrenaline was in SHR 19.7±2.0 mm Hg and 60.5±3.9 mm Hg and in Wistar rats 7.4±1.9 mm Hg and 40.5±3.2 mm Hg (P<0.01). The hypotensive response to acetylcholine (0.1 µg, 1 µg and 10 µg) in SHR was enhanced at 17 weeks of age only and this amplification persisted till the age of 52 weeks. In 52- week-old SHR the hypotensive response to three doses was 69.9±10.2 mm Hg, 87.5±11.8 mm Hg and 103.4±10.6 mm Hg, while in Wistar rats it was 37.4±4.2 mm Hg (P<0.01), 62.3±3.5 mm Hg (P<0.01) and 73.5±2.8 mm Hg (P<0.05). In conclusion, the efficiency of cardiovascular system of SHR to respond to noradrenaline was already enhanced from 9 weeks of age, whereas the response to acetylcholine was not augmented before the age of 17 weeks.
- Klíčová slova
- SHR, Ontogenesis, Noradrenaline, Acetylcholine, Vascular system,
- MeSH
- acetylcholin farmakologie MeSH
- financování organizované MeSH
- hypertenze patofyziologie MeSH
- krevní tlak účinky léků MeSH
- krysa rodu rattus MeSH
- modely nemocí na zvířatech MeSH
- noradrenalin farmakologie MeSH
- potkani inbrední SHR MeSH
- potkani Wistar MeSH
- stárnutí MeSH
- vazodilatancia farmakologie MeSH
- vazokonstriktory farmakologie MeSH
- vazomotorický systém patofyziologie růst a vývoj účinky léků MeSH
- věkové faktory MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
The impact on blood pressure of two vasodilating mechanisms, underlied by vascular smooth muscle hyperpolarization, was studied and compared to that induced by nitric oxide (NO) mechanism. Systemic blood pressure, after inhibitory intervention in arachidonic acid metabolism (cytochrome P-450 inhibition by miconazole 0.5 mg/100 g b.w.), one of the hyperpolarizing pathways, did not change. After the inhibition of the action voltage-dependent K+ channels operator (by 4-aminopyridine 0.1 mg/100 g b.w.), the other hyperpolarizing pathway, blood pressure declined slightly (from 132.3±3.2 mm Hg to 116.5±5.0 mm Hg, P<0.05). Inhibition of nitric oxide production (L-NAME 5 mg/100 g b.w.) increased blood pressure considerably (123.5±2.7 mm Hg to 155.4±3.1 mm Hg, P<0.001). After inhibition of the hyperpolarizing pathway by miconazole, hypotension induced by acetylcholine (Ach, 10 µg) represented 63.0±1.9 mm Hg vs control value 78.6±5.2 mm Hg (P<0.001), by bradykinin (BK) (100 µg) 59.4±3.9 mm Hg vs control value 71.2±6.1 mm Hg (P<0.05). After inhibition of the hyperpolarizing pathway by 4-aminopyridine, hypotension induced by ACh (10 µg) achieved 64.6±2.5 mm Hg vs control value 78.4±2.8 mm Hg (P<0.001) and that induced by BK (100 µg) 56.6±5.3 mm Hg vs control value 72.3±2.5 mm Hg (P<0.001). ACh or BK hypotension after the inhibition of the above hyperpolarizing pathways was significantly attenuated. On the contrary, after NO-synthase inhibition the hypotension to ACh was significantly enhanced. Blood pressure decrease after ACh (10 µg) hypotension was 91.8±4.1 mm Hg vs control value 79.3±3.3 mm Hg (P<0.01), and after BK (100 µg) it was 78.4±7.1 mm Hg vs control value 68.3±5.2 mm Hg. A different basal BP response, but equally attenuated hypotension to Ach and BK, was detected after the inhibition of two selected hyperpolarizing pathways. In cotrast, the inhibition of NO production elicited an increase in systemic BP and augmentation of ACh and BK hypotension. The effectiveness of further hyperpolarizing mechanisms in relation to systemic BP regulation and nitric oxide level remains open.
- MeSH
- acetylcholin farmakokinetika fyziologie MeSH
- bradykinin farmakokinetika fyziologie MeSH
- financování vládou MeSH
- hypertenze enzymologie etiologie MeSH
- interpretace statistických dat MeSH
- krevní tlak genetika účinky záření MeSH
- oxid dusnatý farmakokinetika fyziologie MeSH
- potkani Wistar MeSH
- vazodilatace fyziologie účinky léků MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
- Publikační typ
- srovnávací studie MeSH
- MeSH
- koronární cévy MeSH
- myokard metabolismus MeSH
- oxid dusnatý nedostatek MeSH
- psi MeSH
- srdce MeSH
- zvířata MeSH
- Check Tag
- psi MeSH
- zvířata MeSH
- MeSH
- kardiovaskulární fyziologické jevy MeSH
- nervová zakončení MeSH
- Publikační typ
- biografie MeSH
- O autorovi
- Doležel, Svatopluk, 1921-1996 Autorita
- MeSH
- DNA metabolismus MeSH
- hypertenze metabolismus MeSH
- koronární cévy metabolismus MeSH
- myokard metabolismus MeSH
- perikard MeSH
- psi MeSH
- RNA metabolismus MeSH
- svalové proteiny biosyntéza MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- psi MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- srovnávací studie MeSH
