Table 1.

Cellular and tissue effects of Ang II, Ang 1–7, aldosterone, and (pro)renin in normal conditions.

	Ang II (via AT1R∗)	Ang 1–7 (via Mas1R∗)	Aldosterone (via MR∗)	(Pro)renin (via (P)RR∗)
Cardiomyocytes	Hypertrophy [44]	Hypertrophy inhibition [112, 113]	Hypertrophy [86] Apoptosis [87] Oxidative stress [87]	Hypertrophy [136, 137] Hyperplasia [138] Cell elongation [139]
Cardiac fibroblasts	Proliferation [44] Extracellular matrix production [45–48]	Antiproliferative effects [114, 115] Inhibition of collagen production [115]	Proliferation and migration [88] Extracellular matrix production (collagen/elastin) [48, 89, 90]
Endothelial cells	Oxidative stress [49] Inflammation [50, 51]	Nitric oxide production [116] Anti-inflammatory effects [117]	Oxidative stress [91] Inflammation [92]	Hyperplasia [140] Survival [140]
Smooth muscle cells	Oxidative stress [52] Hypertrophy [53, 54] Proliferation [55] Migration [56, 57] Extracellular matrix production [58]	Antiproliferative effects [118, 119]	Proliferation [93] Migration [94] Extracellular matrix production [95, 96]	Hyperplasia [141, 142] Survival [142] Oxidative stress [142]
Macrophages	Inflammation [51, 59]	Anti-inflammatory effects [120]	Inflammation [97] Oxidative stress [98]	Inflammation [143]
Heart	Hypertrophy [60] Fibrosis [61] Apoptosis [62, 63]	Antiarrhythmic effects [121] Antifibrotic effects [122] Antiremodeling effects [123–126]	Hypertrophy [99] Fibrosis [100] Proarrhythmogenic [101] Inflammation [102]	Cardiac function deterioration [144] Fibrosis [144] Angiogenesis [144]
Vessels	Impaired vascular relaxation to Ach [52] Atherosclerosis [41–43]	Vasodilation [127, 128] Antiatherosclerotic effects [128]	Impaired vascular relaxation to Ach [91] Atherosclerosis [103]	Angiogenesis [140, 145]

^∗Cellular and tissue effects are predominantly mediated by the indicated receptors.

Ang is for angiotensin; AT1R is for Ang II type 1 receptor; Mas1R is for Mas1 receptor; MR is for mineralocorticoid receptor; and (P)RR is for (pro)renin receptor.