The effects of angiotensin II and norepinephrine on afferent arterioles in the rat

Abstract

Perfusion-fixation and vascular casting were used to determine if angiotensin II and norepinephrine cause constriction of afferent arterioles, and if so, whether or not the constriction is principally attributable to a secondary (autoregulatory) response to elevated pressure in the renal circulation. Rats were divided into six groups, and were given five minute infusions of angiotensin II, norepinephrine, or normal saline before perfusion-fixation. Angiotensin II infusions were given to animals in Groups 1 and 2; in Group 1 the renal circulation was exposed to elevated blood pressure, but in Group 2 intrarenal pressure was maintained at normal levels by partial ligation of the aorta above the renal arteries. Groups 3 and 4 were comparable to Groups 1 and 2 respectively, except that norepinephrine was infused instead of angiotensin II. Groups 5 and 6 received infusions of normal saline instead of vasopressor substances. In Group 5, renal vessels were perfusion-fixed at elevated pressures, while in Group 6 renal vessels were perfusion-fixed at normal pressures. Scanning electron microscopy was used to examine and measure vascular casts of 40 to 50 afferent arterioles from each rat. In Groups 1 through 4, casts of afferent arterioles showed severe, focal, and irregularly distributed constriction. In Groups 5 and 6 there was no qualitative evidence of afferent arteriolar constriction or irregularities in vessel caliber. Vessel diameter measurements were significantly smaller in Groups 1 to 4 when compared to Groups 5 and 6, and arteriolar constriction in the juxtamedullary and cortical regions was quantitatively comparable in Groups 1 to 4. Arteriolar diameters in Group 5 were somewhat, but not significantly smaller than those in Group 6, suggesting that perfusion-fixation at elevated pressure alone may have made a minor contribution to afferent vasoconstriction. However, this constriction was clearly not of the same pattern or magnitude as that produced by angiotensin II or norepinephrine infusions. The results indicate that both angiotensin II and norepinephrine cause severe focal constriction of afferent arterioles, and that this constriction cannot be attributed primarily to a pressure-induced autoregulatory response in the renal vasculature.