Tissue angiotensin generation and regulation of vascular tone

Effect of lisinopril on tissue levels of neuropeptide Y in normotensive and spontaneously hypertensive rats

“…12 Acutely, inhibition of AII formation may alter the release of sympathetic neurotransmitters or may have a direct action on effector cell-responsiveness. [3][4][5][6] With chronic ACE inhibition transmitter synthesis may be altered or other actions resulting in structural changes in the vasculature may occur. [3][4][5][6] NPY is located primarily in sympathetic nerve fibres surrounding small arteries where it probably plays a role in the regulation of vascular resistance.…”

“…[3][4][5][6] With chronic ACE inhibition transmitter synthesis may be altered or other actions resulting in structural changes in the vasculature may occur. [3][4][5][6] NPY is located primarily in sympathetic nerve fibres surrounding small arteries where it probably plays a role in the regulation of vascular resistance. Tissue levels of NPY were lower in extracts of atria and skeletal muscle from SHR, but treatment with lisinopril significantly increased NPY content of these tissues.…”

“…1 However, the presence of components of RAS in the vascular wall is widely accepted as evidence for a key local role for AII in modulating sympathetic function and vascular tone. [2][3][4] The success of chronic ACE inhibition as a treatment for hypertension is linked to the degree of inhibition of vascular ACE, resulting in reduced local effects of AII on vascular smooth muscle cells and inhibition of the facilitatory actions of AII on noradrenaline release and neurogenic vasoconstrictor responses. [3][4][5] Demonstrating this interplay between vascular ACE and the sympathetic nervous system has been difficult because of the lack of sensitive markers.…”

Dissociation between the circulating renin-angiotensin system and angiotensin II receptors in central losartan-induced hypertension

“…Thus, it is possible that the pathway that activates the a 1 -adrenergic receptors mediating the pressor effect of losartan starts in forebrain structures that converge to the intermediolateral column and from there proceed through efferent signals to blood vessels. The sympathetic system also provides efferents to ß-adrenergic receptors of the juxtaglomerular cells to release renin (16) and ß-adrenergic receptors activate the intrinsic vascular renin-angiotensin system (17,18). Moreover, ß-adrenergic activation in the heart increases cardiac output (16).…”

Immunological and Molecular Mechanisms Leading to Fibrosis: Origin of Renal Myofibroblasts

“…Recently the urinary angiotensinogen (Kim et al, 2011) and the intrarenal Ang II level (Del Prete et al, 2003) have been demonstrated to correlate with the severity of the chronic renal disease. As Ang II plays a key role in regulation of vascular tone (Cockcroft et al, 1995) and may induce proteinuria (Ren et al, 2011), oxidative stress, inflammation and renal fibrosis (Benigni et al, 2010) it is not surprising that ACE inhibitors or AT1 receptor antagonists have a renoprotective effect, which is independent from their antihypertensive effect (Mallamaci et al, 2011). Actually, the captopril trial on patients with type I diabetic nephropathy patients has shown a 50 % reduction in the end point of death by captopril administration (Lewis et al, 2003).…”