Predominant postglomerular vascular resistance response to reflex renal sympathetic nerve activation during ANG II clamp in rabbits

Abstract

. Predominant postglomerular vascular resistance response to reflex renal sympathetic nerve activation during ANG II clamp in rabbits. Am J Physiol Regul Integr Comp Physiol 287: R780 -R786, 2004. First published June 10, 2004 10.1152/ ajpregu.00202.2004.-We have shown previously that a moderate reflex increase in renal sympathetic nerve activity (RSNA) elevated glomerular capillary pressure, whereas a more severe increase in RSNA decreased glomerular capillary pressure. This suggested that the nerves innervating the glomerular afferent and efferent arterioles could be selectively activated, allowing differential control of glomerular capillary pressure. A caveat to this conclusion was that intrarenal actions of neurally stimulated ANG II might have contributed to the increase in postglomerular resistance. This has now been investigated. Anesthetized rabbits were prepared for renal micropuncture and RSNA recording. One group (ANG II clamp) received an infusion of an angiotensin-converting enzyme inhibitor (enalaprilat, 2 mg/kg bolus plus 2 mg ⅐ kg, the other vehicle. Measurements were made before (room air) and during 14% O2. Renal blood flow decreased less during ANG II clamp compared with vehicle [9 Ϯ 1% vs. 20 Ϯ 4%, interaction term (PGT) Ͻ 0.05], despite a similar increase in RSNA in response to 14% O2 in the two groups. Arterial pressure and glomerular filtration rate were unaffected by 14% O2 in both groups. Glomerular capillary pressure increased from 33 Ϯ 1 to 37 Ϯ 1 mmHg during ANG II clamp and from 33 Ϯ 2 to 35 Ϯ 1 mmHg in the vehicle group before and during 14% O 2, respectively (PGT Ͻ 0.05). During ANG II clamp, postglomerular vascular resistance was still increased in response to RSNA during 14% O 2, demonstrating that the action of the renal nerves on the postglomerular vasculature was independent of the renin-angiotensin system. This further supports our hypothesis that increases in RSNA can selectively control pre-and postglomerular vascular resistance and therefore glomerular ultrafiltration. kidney; renal innervation; glomerular capillary pressure; renal micropuncture; hypoxia ALTERATIONS in renal sympathetic nerve activity (RSNA) produce several effects on renal function that contribute to the kidneys main task of homeostatic regulation of body fluid balance. Previously, we have identified ultrastructurally two distinct nerve types that are differentially distributed to afferent and efferent arterioles (24,25). Type I axons almost exclusively innervate the afferent arteriole, whereas type II axons are evenly distributed on both arterioles (25). Recently, we have shown that neuropeptide Y (NPY) is located in type II axon terminals but not type I axon terminals (23). Our findings are in accord with the study of Reinecke and Forssmann (38), who reported that the density of NPY-positive terminals was similar on the afferent and efferent arterioles (i.e., similar to type II axon distribution). Taken together, these findings implied that type I and II axons originated from different populations of...

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