Answers are grounded in this paper and cite their sources.
In 2K1C hypertensive rats, enhanced vascular reactivity to noradrenaline and endothelin suggests endothelial dysfunction may contribute to the maintenance of high blood pressure.
The response to noradrenaline and endothelin in isolated aortae in vitro and mesenteric microvessels in vivo - in situ was studied in 4-week 2K1C hypertensive rats. Enhanced reactivity to noradrenaline was observed in aortae with endothelium isolated from hypertensive rats, whereas in aortae without endothelium, noradrenaline induced similar responses in sham-operated control and hypertensive preparations. Endothelin responses were not altered in aortae with or without endothelium isolated from hypertensive rats. In mesenteric microvessels, both noradrenaline and endothelin evoked higher responses in 2K1C than in control animals. It is suggested that the enhanced reactivity observed could be involved in the maintainance of high blood pressure levels in 2K1C hypertension. The altered reactivity could be due to a dysfunction of the endothelial cells.
No takes yet. Share an insight, caveat, or question.
Fortes et al. (1990) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: