The aim of this study was to investigate the effect of high fructose intake associated with moderate increase in adiposity on rat arterial adrenergic responses and their modulation by perivascular adipose tissue (PVAT). After eight-week-lasting substitution of drinking water with 10 % fructose solution in adult normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR), their systolic blood pressure, plasma triglycerides, and relative liver weight were elevated when compared to their respective control groups. Moreover, in SHR, body weight and relative heart weight were increased after treatment with fructose. In superior mesenteric arteries, PVAT exerted inhibitory influence on adrenergic contractile responses and this effect was markedly stronger in control WKY than in SHR. In fructose-administered WKY, arterial adrenergic contractions were substantially reduced in comparison with the control group; this was caused mainly by enhancement of anticontractile action of PVAT. The diminution of the mesenteric arterial contractions was not observed after fructose treatment in SHR. We conclude that the increase in body adiposity due to fructose overfeeding in rats might have prehypertensive effect. However, in WKY it might cause PVAT-dependent and independent reduction in arterial contractile responses to adrenergic stimuli, which could attenuate the pathological elevation in vascular tone.
- MeSH
- adrenergní látky farmakologie MeSH
- arteriae mesentericae účinky léků fyziologie MeSH
- fruktosa aplikace a dávkování toxicita MeSH
- hypertenze patofyziologie MeSH
- krevní tlak účinky léků fyziologie MeSH
- krysa rodu rattus MeSH
- náhodné rozdělení MeSH
- potkani inbrední SHR MeSH
- potkani inbrední WKY MeSH
- tuková tkáň krevní zásobení účinky léků fyziologie MeSH
- vazokonstrikce účinky léků fyziologie MeSH
- vztah mezi dávkou a účinkem léčiva MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
Peptide urotensin II was originally isolated from the urophysis of teleost fishes; later it was identified also in higher vertebrates in various organs and tissues, including cardiovascular structures. Since its discovery it has been consi- dered as a highly potent vasoconstrictor inducing contraction of smooth muscle in subnanomolar concentrations. Its wide distribution as well as its high interspecies homology indicates that this peptide is involved in regulation of many important physiological functions in vertebrates. An effort to discover other possible functions of urotensin II was intensified by the identification of its G-protein coupled receptor and its identification in humans. Furthermore, altered levels of expression of urotensin II and its receptor were found in various disease states including hypertensi- on, diabetes, heart and renal failure, in experimental animal models as well as in humans. Therefore, there is widely discussed question regarding the possible role of urotensin II in etiopathogeneses of these diseases, however the exact mechanisms are still unknown. The aim of this review is to summarize the current knowledge about urotensin II with emphasis to its direct and undirect effects in cardiovascular system.
- Klíčová slova
- urotenzín II, rozvodné artérie,
- MeSH
- aorta thoracica účinky léků MeSH
- biosyntéza peptidů * MeSH
- Haplorrhini MeSH
- kardiovaskulární fyziologické jevy MeSH
- klinické zkoušky jako téma MeSH
- krevní tlak fyziologie MeSH
- krysa rodu rattus MeSH
- lidé MeSH
- ovce MeSH
- průchodnost cév účinky léků MeSH
- receptory peptidů chemie terapeutické užití MeSH
- ryby MeSH
- srdeční frekvence MeSH
- sympatický nervový systém fyziologie MeSH
- vazokonstriktory analýza terapeutické užití MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- lidé MeSH
- zvířata MeSH
- Publikační typ
- práce podpořená grantem MeSH
- MeSH
- antihypertenziva terapeutické užití MeSH
- fenotyp MeSH
- financování organizované MeSH
- hypertenze farmakoterapie genetika prevence a kontrola MeSH
- lidé MeSH
- potkani inbrední SHR fyziologie růst a vývoj MeSH
- růst a vývoj účinky léků MeSH
- vývojová biologie trendy MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- přehledy MeSH
It is documented that in chronic hypertensive state there is an increased vasodepressor response to calcium channel antagonists such as the dihydropyridine derivate nifedipine. This effect is generally proportional to initial blood pressure as was demonstrated in several models of experimental hypertension. In the present study we investigated the effect of chronic nifedipine treatment on the development of cardiovascular system in young spontaneously hypertensive rats (SHR) in order to evaluate whether it could prevent the abnormalities leading to hypertensive state. Four- and eight-week-old rats were treated with nifedipine (50 mg/kg/day) for 4 weeks. Blood pressure of nifedipine-treated SHR remained at the initial level in contrast to their untreated controls where it continued to increase. In both age groups, chronic nifedipine administration reduced neurogenic contractions of isolated superior mesenteric artery, but did not significantly affect the dose-response curve to exogenous noradrenaline in 8-week-old rats. In contrast, maximum response to noradrenaline was significantly attenuated in mesenteric artery of 12-week-old nifedipine-treated SHR. We can presume that the antihypertensive effect of nifedipine is similar in both stages of spontaneous hypertension development, but the mechanisms involved might be different. It seems that chronic reduction of calcium influx during the rapid phase of pathological blood pressure increase in SHR may eliminate the effect of enhanced sympathetic tone, which may have unfavorable consequences on cardiovascular structure and function.
- MeSH
- antihypertenziva farmakologie MeSH
- arteriae mesentericae metabolismus patofyziologie účinky léků MeSH
- blokátory kalciových kanálů farmakologie MeSH
- elektrická stimulace MeSH
- financování organizované MeSH
- hypertenze farmakoterapie metabolismus patofyziologie MeSH
- krevní tlak účinky léků MeSH
- krysa rodu rattus MeSH
- modely nemocí na zvířatech MeSH
- nifedipin farmakologie MeSH
- noradrenalin farmakologie MeSH
- potkani inbrední SHR MeSH
- potkani Wistar MeSH
- progrese nemoci MeSH
- stárnutí MeSH
- sympatický nervový systém patofyziologie účinky léků MeSH
- vápník metabolismus MeSH
- vazokonstrikce účinky léků MeSH
- vazokonstriktory farmakologie MeSH
- věkové faktory MeSH
- vztah mezi dávkou a účinkem léčiva MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- zvířata MeSH
Treatment with pertussis toxin (PTX) which eliminates the activity of G(i) 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 microg/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.
- MeSH
- acetylcholin metabolismus MeSH
- adrenergní látky metabolismus MeSH
- angiotensin II metabolismus MeSH
- aorta thoracica metabolismus účinky léků MeSH
- arteria mesenterica superior metabolismus účinky léků MeSH
- arteria pulmonalis metabolismus účinky léků MeSH
- arterie metabolismus účinky léků MeSH
- cévní endotel metabolismus účinky léků MeSH
- elektrická stimulace MeSH
- hypertenze farmakoterapie metabolismus MeSH
- inhibitory enzymů farmakologie MeSH
- krevní tlak genetika účinky záření MeSH
- krysa rodu rattus MeSH
- noradrenalin metabolismus MeSH
- pertusový toxin farmakologie MeSH
- potkani inbrední SHR MeSH
- proteiny vázající GTP - alfa-podjednotky Gi-Go antagonisté a inhibitory metabolismus MeSH
- signální transdukce fyziologie účinky léků MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
