Interaction of angiotensin with noradrenergic neuroeffector transmission

Review: Angiotensin-converting enzyme in skeletal muscle: sentinel of blood pressure control and glucose homeostasis

“…The facilitated release of local norepinephrine by prejunctional receptors could also modulate RAS activity. 34,35 How much of the Ang II can reach its receptor sites is determined by the activity of ACE and Ang II-degrading endo-and amino-peptidases. 36 As a result of the distribution of ACE and AT 1 -receptors, Ang II action is greatest in PV and CV.…”

“…141 At the conclusion of this section it must be emphasised once more that kinins, in the intact organism, diminish the influence of the neuroendocrine sympathetic nervous system (NESNS) on the vascular SMC and on glucose metabolism in the contracting high-oxidative red fibres. 34,35,142,143 Possible role for endothelial and skeletal muscle tissue ACE in the development of type 2 diabetes, hypertension, and atherosclerosis Risk factors for the development of atherosclerosis, including male gender, aging, ACE-D-allele, stress, central obesity, smoking, hypertension, type 2 diabetes, and dyslipidaemia, are associated with various degrees of endothelial dysfunction (summarised in table 1). 117,[144][145][146][147][148][149][150][151][152][153][154] This dysfunction appears to be linked to an accelerated rate of ACE activity in the endothelial tissue of the whole vascular system, leading to increased generation of Ang II and enhanced degradation of kinins, and these observations support the concept that ACE overactivity plays a major role in the development of the atherosclerotic process in the vessel wall.…”

Ability of angiotensin II to modulate striatal dopamine release via the AT1 receptor in vitro and in vivo

“…It has been appreciated for some time that angiotensin II modulates catecholamine neurotransmitter release in the peripheral nervous system (for reviews see Story & Ziogas, 1987;Reid, 1992) and it is therefore of interest that growing evidence implicates a similar ability of angiotensin II to facilitate the neurotransmission of catecholamines in the CNS (Huang et al, 1987;Finocchiaro et al, 1990;Barnes et al, 1991a;Qadri et al, 1991;Dwoskin et al, 1992;Stadler et al, 1992;Mendelsohn et al, 1993;. Given the established role of the nigro-striatal dopamine system in the control of movement, the demonstration that angiotensin II enhances the release of dopamine in the rat striatum may provide a neurochemical mechanisms underlying the modulation of locomotor activity and other dopaminemediate behaviours that have been shown to be susceptible to pharmacological manipulation following interaction with the angiotensin system (see above).…”

Effect of angiotensin-converting enzyme inhibitors on systemic inflammation and myocardial sympathetic innervation in normotensive patients with type 2 diabetes mellitus

“…Our 123 I-MIBG findings with ACE-i are consistent with those in cardiovascular diseases that involve cardiac sympathetic overactivity, such as heart failure and essential hypertension. Angiotensin II is known to facilitate norepinephrine release at presynaptic sites 22 and acts as a sympathetic nervous system activator. 23 In addition, ACE inhibition may lead to enhanced prostaglandin synthesis, which may inhibit norepinephrine release at presynaptic sites.…”