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Endothelial function in mesenteric resistance arteries from the genetically hypertensive rat
Hanzhong Liu1, Janet M Ledingham, Ian Mullaney
1Department of Pharmacology, School of Medical Sciences, University of Otago, Dunedin, New Zealand.
Clinical and Experimental Pharmacology & Physiology
|May 16, 2002
Summary
Genetically hypertensive rats showed normal endothelial function, unlike spontaneously hypertensive rats. Nitric oxide synthase inhibition in hypertensive rats impaired endothelial function and reduced cGMP levels.
Area of Science:
- Cardiovascular Physiology
- Endothelial Biology
- Hypertension Research
Background:
- Endothelial dysfunction is a hallmark of hypertension.
- Investigating endothelial function in different hypertensive rat models is crucial for understanding disease mechanisms.
Purpose of the Study:
- To compare endothelial function in mesenteric resistance arteries of genetically hypertensive (GH) rats and spontaneously hypertensive (SHR) rats.
- To determine the effect of nitric oxide synthase (NOS) inhibition on endothelial function in GH rats.
Main Methods:
- Wire myography was used to assess contractile and relaxant responses in mesenteric resistance arteries.
- Intracellular cyclic guanosine monophosphate (cGMP) production was measured.
- NOS was inhibited using Nomega-nitro-L-arginine methyl ester (L-NAME) in GH rats.
Main Results:
- GH rats exhibited normal endothelium-dependent relaxation, similar to normotensive controls.
- SHR rats showed enhanced contractile responses and attenuated relaxation to acetylcholine (ACh).
- L-NAME treatment in GH rats led to impaired endothelium-dependent relaxation and reduced cGMP levels.
Conclusions:
- Endothelial function is preserved in GH rats, contrasting with SHR rats.
- Chronic NOS inhibition in GH rats mimics endothelial dysfunction observed in SHR.
- These findings highlight the role of nitric oxide in maintaining endothelial function in hypertension.