Describing the Mechanosensitive Role of Afferent Renal Nerve Activity Related to Arterial Pressure
Author
Leung, ChristianIssue Date
2023Advisor
Banek, Christopher T.Fellous, Jean-Marc
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The University of Arizona.Rights
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction, presentation (such as public display or performance) of protected items is prohibited except with permission of the author.Embargo
Release after 06/05/2024Abstract
Afferent renal nerves reportedly have an influential role in cardiovascular homeostasis – in health and disease. While the effects of afferent renal nerve manipulation have been studied, particularly in the scope of renal nerve ablation, the underlying neural mechanism contributing to cardiovascular regulation remains unclear. The goal of this study is to identify the relationship between afferent renal nerve activity and arterial pressure changes in the kidney, in both healthy and deoxycorticosterone acetate (DOCA) salt rat model of hypertension (high blood pressure). Male Sprague-Dawley Rats (275–300 g) were divided into normotensive (healthy) (n=5) and hypertensive DOCA groups (n=3). The DOCA group were administered 100mg DOCA subcutaneously and 0.9% saline drinking water for 21 days. Multiunit, extracellular afferent renal nerve activity (ARNA) recordings were conducted under urethane anesthesia (1800 mg/kg/h, IV) at protocol end. Afferent renal spikes were extracted on Spike2 and correlated with systolic and diastolic pressure peaks from the arterial pressure trace. For healthy animals, we detected a significant increase in afferent renal nerve spiking at diastole (0.28 spikes per 10ms/total heartbeats ± 0.13 in the time bin 10-0 milliseconds before diastole, Dunnett’s Multiple Comparisons) when compared to each individual animal’s baseline spike rate. In the hypertensive group, we failed to detect elevated rate at systole or diastole but saw significant activity around each stimulus (0.53 spikes per 10ms/total heartbeats ± 0.24 at 40-30 milliseconds before diastole and 0.49 s spikes per 10ms/total heartbeats ± 0.34 at 20-30 milliseconds after diastole, Dunnett’s Multiple Comparisons). These results suggest that renal afferent spike train temporal structure in healthy animals relies on arterial pressure change while hypertensive DOCA animals have a peak spiking activity temporal shift, as well as a lower relative activation compared to healthy animals, possibly explaining the destruction of ARNA modulation of cardiac control in DOCA salt hypertension at the site of the kidney.Type
Electronic Thesistext
Degree Name
M.S.Degree Level
mastersDegree Program
Graduate CollegeBiomedical Engineering