<p>The endothelium plays an important part in blood flow regulation by producing the vasodilatory substance nitric oxide (NO). Various studies have shown that commonly accepted risk factors for coronary heart disease, such as hypertension, diabetes, hypercholesterolemia, smoking and mental stress impair endothelium-derived vasodilation by the NO-pathway. This thesis focuses on the effects of mental stress on the endothelium. Furthermore, the effects of epinephrine (E) and norepinephrine (NE) and blockades of adrenergic receptors were studied in the forearm in young healthy subjects.</p><p>Different blockades were given locally in the forearm, not affecting general hemodynamics. β-adrenoceptor blockade impaired endothelium-dependent vasodilation (EDV), while α-adrenoceptor blockade and neurogenic blockade caused a general vasodilation which was not endothelium dependent. Neuropeptide Y did not seem to influence blood flow in the resting forearm.</p><p>A short period of mental stress induced by an arithmetic task, impaired EDV in the forearm. This negative effect could be blocked by β-adrenergic, but not α-adrenergic receptor blockade.</p><p>Local infusions of E and NE in the human forearm induced vasodilation and vasoconstriction, respectively. As both EDV and endothelium-independent vasodilation were affected by both E and NE, the two catecholamines did not seem to affect vascular tone by an endothelium-specific mechanism.</p><p>Both cold pressure stress and mental stress induced impairments in flow-mediated vasodilation (FMD) when normalised for the degree of hyperemic blood flow.</p><p>These findings give us new insights in how mental stress and sympathetic activation affects the endothelium and how the negative effects can be prevented.</p>

The endothelium plays an important part in blood flow regulation by producing the vasodilatory substance nitric oxide (NO). Various studies have shown that commonly accepted risk factors for coronary heart disease, such as hypertension, diabetes, hypercholesterolemia, smoking and mental stress impair endothelium-derived vasodilation by the NO-pathway. This thesis focuses on the effects of mental stress on the endothelium. Furthermore, the effects of epinephrine (E) and norepinephrine (NE) and blockades of adrenergic receptors were studied in the forearm in young healthy subjects. Different blockades were given locally in the forearm, not affecting general hemodynamics. β-adrenoceptor blockade impaired endothelium-dependent vasodilation (EDV), while α-adrenoceptor blockade and neurogenic blockade caused a general vasodilation which was not endothelium dependent. Neuropeptide Y did not seem to influence blood flow in the resting forearm. A short period of mental stress induced by an arithmetic task, impaired EDV in the forearm. This negative effect could be blocked by β-adrenergic, but not α-adrenergic receptor blockade. Local infusions of E and NE in the human forearm induced vasodilation and vasoconstriction, respectively. As both EDV and endothelium-independent vasodilation were affected by both E and NE, the two catecholamines did not seem to affect vascular tone by an endothelium-specific mechanism. Both cold pressure stress and mental stress induced impairments in flow-mediated vasodilation (FMD) when normalised for the degree of hyperemic blood flow. These findings give us new insights in how mental stress and sympathetic activation affects the endothelium and how the negative effects can be prevented.