Endothelium-dependent vasodilation in essential hypertension
Sammanfattning: The vascular endothelium plays a crucial role in the regulation of several homeostatic parameters in the circulation. In this thesis, the influences of essential hypertension and antihypertensive agents on endothelium-dependent vasodilation (EDV) were evaluated in the human forearm circulation.Patients with essential hypertension were found to be characterized by a defect EDV, even if there was substantial variation within the hypertensive patient group. The occurrence of left ventricular hypertrophy (LVH) was related to an impaired EDV in essential hypertensive patients. Evidence was found for a disturbed vasodilator function in young normotensives with a familial history of hypertension (FHH). Young borderline-hypertensive subjects showed an attenuated EDV. An acute noradrenaline-induced increase in blood pressure to hypertensive levels in otherwise normotensive subjects attenuated EDV.Antihypertensive treatment was found to influence endothelial vasodilator function, but different antihypertensive agents showed divergent effects.During local infusion in the forearm of healthy volunteers in the absence of blood pressure changes, the ACE-inhibitor enalapril potentiated EDV, the non-selective beta-blocker propranolol impaired EDV, while the Ca-antagonist verapamil facilitated vasodilation in general. Despite a similar blood pressure reduction one hour after administration of the ACE-inhibitior captopril and the Ca-antagonist nifedipine, only captopril potentiated EDV in hypertensive patients. A positive long-term effect of captopril on endothelium-dependent vasodilation was seen in a pilot study.In conclusion, as a group, essential hypertensive patients were characterized by a defect EDV in the forearm circulation. This was mainly seen in patients with LVH.A FHH was associated with a disturbed vasodilator function. Borderline hypertensive subjects were characterized by an attenuated EDV. Acute hypertension impaired EDV. Antihypertensive treatment was found to influence EDV in divergent ways. ACE-inhibitors improved EDV.
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