Increased renin immunostaining in preglomerular arterioles after myocardial infarction in the rat.

In previous studies we demonstrated that the intrarenal circulation is vasoconstricted in congestive heart failure (CHF) and that pharmacologic inhibition of the renin-angiotensin system reversed the renal hemodynamic abnormalities. In the current investigation we tested the hypothesis that renin expression is increased in renal arterioles in CHF. Male Sprague-Dawley rats were studied 4 to 6 weeks after left coronary artery ligation and compared with sham-operated and normal age-matched controls. Renal vascular trees were microdissected and immunostained with a polyclonal renin antiserum. Renin immunostaining was localized to the afferent arterioles, with a greater percentage of arterioles staining in rats with CHF (55.3% +/- 2.1%) than in sham-operated (43.9% +/- 1.9%) or normal age controls (37.6% +/- 2.2%). Rats with CHF more frequently exhibited multiple bands of renin staining within a single arteriole (24.9% +/- 1.8%) as compared with sham-operated (13.3% +/- 1.9%) and normal age controls (11.3% +/- 1.4%). Juxtaglomerular apparatus staining was similar in all groups. These data indicate that renin-containing cells are increased in the afferent arteriole in CHF. Increased renin in the preglomerular arterioles may activate local angiotensin production, leading to intrarenal vasoconstriction, reduced nephron blood flow, sodium and water retention, and worsening of congestive heart failure.