TY - JOUR
T1 - Sequential afferent and sympathetic renal denervation impact on cardiovascular and renal homeostasis in the male Sprague-Dawley rat
AU - Parvin, Irin
AU - Gauthier, Madeline M.
AU - Dennis, Melissa R.
AU - Encinas, Noah M.
AU - Nangia, Ellen L.
AU - Schwartz, Kyle L.
AU - Banek, Christopher T.
N1 - Publisher Copyright:
© 2023 Elsevier Inc.
PY - 2023/7/15
Y1 - 2023/7/15
N2 - Renal denervation (RDNx) is emerging as a promising treatment for cardiovascular disease, yet the underlying mechanisms and contributions of afferent (sensory) and efferent (sympathetic) renal nerves in healthy conditions remains limited. We hypothesize that sympathetic renal nerves contribute to long-term MAP and renal function, whereas afferent renal nerves do not contribute to the maintenance of cardiovascular and renal function. To test this hypothesis, we performed two experiments. In experiment one, we performed total renal denervation (T-RDNx), ablating afferent and sympathetic renal nerves, in normotensive adult SD rats to determine effects on MAP and renal function. Experiment 2 employed a sequential surgical ablation using: (1) afferent targeted renal denervation (A-RDNx), then (2) sympathetic (T-RDNx) denervation to determine the individual contributions to cardiovascular and renal homeostasis. In experiment 1, MAP decreased following T-RDNx and GFR increased. In experiment 2, A-RDNx led to an increase in MAP but did not change renal function. In contrast, T-RDNx decreased MAP and improved renal filtration. Together, these data partially support our hypothesis that renal sympathetic nerves contribute to the chronic regulation of arterial pressure and renal function. Contrary to the hypothesis, A-RDNx produced an increase in MAP without a detected change in renal function. We concluded that renal sympathetic nerves influence MAP and renal function regulation through a well-defined tonic contribution to renal vascular resistance and sodium reabsorption, whereas afferent renal nerves likely contribute to the maintenance of MAP through a tonic sympatho-inhibitory, negative feedback regulation in the normotensive, healthy rat.
AB - Renal denervation (RDNx) is emerging as a promising treatment for cardiovascular disease, yet the underlying mechanisms and contributions of afferent (sensory) and efferent (sympathetic) renal nerves in healthy conditions remains limited. We hypothesize that sympathetic renal nerves contribute to long-term MAP and renal function, whereas afferent renal nerves do not contribute to the maintenance of cardiovascular and renal function. To test this hypothesis, we performed two experiments. In experiment one, we performed total renal denervation (T-RDNx), ablating afferent and sympathetic renal nerves, in normotensive adult SD rats to determine effects on MAP and renal function. Experiment 2 employed a sequential surgical ablation using: (1) afferent targeted renal denervation (A-RDNx), then (2) sympathetic (T-RDNx) denervation to determine the individual contributions to cardiovascular and renal homeostasis. In experiment 1, MAP decreased following T-RDNx and GFR increased. In experiment 2, A-RDNx led to an increase in MAP but did not change renal function. In contrast, T-RDNx decreased MAP and improved renal filtration. Together, these data partially support our hypothesis that renal sympathetic nerves contribute to the chronic regulation of arterial pressure and renal function. Contrary to the hypothesis, A-RDNx produced an increase in MAP without a detected change in renal function. We concluded that renal sympathetic nerves influence MAP and renal function regulation through a well-defined tonic contribution to renal vascular resistance and sodium reabsorption, whereas afferent renal nerves likely contribute to the maintenance of MAP through a tonic sympatho-inhibitory, negative feedback regulation in the normotensive, healthy rat.
KW - Glomerular filtration rate
KW - Mean arterial pressure
KW - Renal denervation
KW - Renal nerves
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U2 - 10.1016/j.lfs.2023.121768
DO - 10.1016/j.lfs.2023.121768
M3 - Article
C2 - 37169146
AN - SCOPUS:85157984769
SN - 0024-3205
VL - 325
JO - Life Sciences
JF - Life Sciences
M1 - 121768
ER -