PubMed · 1988 · 11 citations · 0 references
MedicinePharmacologyPhysiologyGeneral PharmacologyNeuroendocrinologyPharmacodynamicsCardiovascular PharmacologyCardiovascular PhysiologyCirculatory PhysiologyEndothelial ActivationEndothelial DysfunctionSodium HomeostasisAntihypertensive PharmacologyEndothelial Cell PhysiologyEndothelial Function ModulationNitroprusside TherapySalt-sensitive HypertensionVasodilator Pharmacology
The responses to noradrenaline (NA) and acetylcholine (ACh) of aortae and microvessels were compared in control and DOCA-salt hypertensive rats. Macro- and microvessels from hypertensive rats showed an increased response to NA and a decreased response to ACh (an endothelium-dependent vasodilator). Unlike ACh, sodium nitroprusside (an endothelium-independent agent), was equally effective in evoking a vasodilator response from aortae and microvessels of hypertensive rats. These data suggest that the impaired response to ACh and the increased response to NA in DOCA-salt hypertension may result from an alteration of endothelial cell function.