Impaired vascular β-adrenergic relaxation in spontaneously hypertensive rats: The differences between conduit and resistance arteries
Jazyk angličtina Země Nizozemsko Médium print-electronic
Typ dokumentu časopisecké články
PubMed
37708986
DOI
10.1016/j.ejphar.2023.176045
PII: S0014-2999(23)00557-5
Knihovny.cz E-zdroje
- Klíčová slova
- Blood pressure, Femoral artery, Isoprenaline, Resistance mesenteric artery, β(1)-agonist dobutamine, β(2)-agonist salmeterol,
- MeSH
- adrenergní látky * MeSH
- agonisté adrenergních beta-receptorů farmakologie MeSH
- arteriae mesentericae MeSH
- cévní endotel MeSH
- cévní rezistence MeSH
- cyklooxygenasy MeSH
- hypertenze * MeSH
- isoprenalin farmakologie MeSH
- krysa rodu Rattus MeSH
- potkani inbrední SHR MeSH
- potkani inbrední WKY MeSH
- salmeterol xinafoát MeSH
- synthasa oxidu dusnatého MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- adrenergní látky * MeSH
- agonisté adrenergních beta-receptorů MeSH
- cyklooxygenasy MeSH
- isoprenalin MeSH
- salmeterol xinafoát MeSH
- synthasa oxidu dusnatého MeSH
It was suggested that impaired β-adrenergic relaxation in spontaneously hypertensive rats (SHR) might contribute to their high blood pressure (BP). Our study was focused on isoprenaline-induced dilatation of conduit femoral or resistance mesenteric arteries and on isoprenaline-induced BP reduction in SHR and Wistar-Kyoto rats (WKY). We confirmed decreased β-adrenergic relaxation of SHR femoral arteries due to the absence of its endothelium-independent component, whereas endothelium-dependent component of β-adrenergic smooth muscle relaxation was similar in both strains. Conversely, isoprenaline-induced relaxation of resistance mesenteric arteries was similar in both strains and this was true for endothelium-dependent and endothelium-independent components. We observed moderately reduced sensitivity of SHR mesenteric arteries to salmeterol (β2-adrenergic agonist) and this strain difference disappeared after endothelium removal. However, there was no difference in mesenteric arteries relaxation by dobutamine (β1-adrenergic agonist) which was independent of endothelium. The increasing isoprenaline doses elicited similar BP decrease in both rat strains, although BP sensitivity to isoprenaline was slightly decreased in SHR. The blockade of cyclooxygenase (indomethacin) and NO synthase (L-NAME) further reduced BP sensitivity to isoprenaline in SHR. On the other hand, salmeterol elicited similar BP decrease in both strains and the blockade of cyclooxygenase and NO synthase increased BP sensitivity to salmeterol in SHR as compared to WKY. In conclusion, attenuated β-adrenergic vasodilatation of conduit arteries of SHR but similar β-adrenergic relaxation of resistance mesenteric arteries from WKY and SHR and their similar BP response to β-adrenergic agonists do not support major role of altered β-adrenergic vasodilatation for high BP in genetic hypertension.
Citace poskytuje Crossref.org
Altered Balance between Vasoconstrictor and Vasodilator Systems in Experimental Hypertension