Table 1.

In-vivo deletion of key regulatory molecules and their comparison with renin–angiotensin system knockouts

Mouse strains	Circulating renin	Kidney renin	Renal abnormalities		Blood pressure	Ref
			Parenchyma	Renal arterial tree
Ren1c knockoout	Absent	Absent	Severe hydronephrosis, medullary atrophy, interstitial fibrosis, perivascular lymphocytic infiltration	Thick wall	Decreased	[13,14]
Ren1c (s) knockout	NR	Absent	Severe hydronephrosis	NR	Decreased	[15••]
Angiotensinogen knockout	Increased	Increased	Hydronephrosis, papillary atrophy, lymphocytic infiltration	Thick wall	Decreased	[16]
ACE knockout	Increased	Increased	Hydronephrosis, medullary and papillary atrophy, interstitial fibrosis	Thick wall	Decreased	[17]
AT1aþAT1b knockout	Increased	Increased	Medullary atrophy	Thick wall	Decreased	[18]
Renin DTA	Reduced	Almost absent	Glomerular and tubular atrophy, areas of undifferentiated cells	Normal to thinner	Decreased	[19]
Dicer conditional knockout (renin cells)	Reduced	Almost absent	Characteristic striped renal fibrosis, glomerulosclerosis, glomerular and tubular dilatation, tubular atrophy	Distorted or absent vessels	Decreased	[20••]
Cbp/p300 conditional knockout (renin cells)	Reduced	Almost absent	Cystic glomeruli, abnormal vessels, extensive fibrosis	Thin wall	Decreased (unpublished)	[12••]
Gsα conditional knockout (renin cells)	Reduced	Almost absent	NR	Total number reduced and shorter	Decreased	[10,11•]
PPARγ conditional knockout (renin cells)	Increased	Increased	NR	Normal	Normal	[21••]
Connexin40 knockout	Increased	Increased	Displacement of renin cells to the extraglomerular mesangium	NR	Increased	[22–24]

ACE, angiotensin-converting enzyme; NR, not reported; PPARγ, peroxisome proliferator-activated receptor-gamma.