Sympathetic transduction to blood pressure in patients with chronic kidney disease
Claire E Kissell1, Benjamin E Young2, Jasdeep Kaur3
1Department of Kinesiology, University of Texas at Arlington, Arlington, TX, USA.
Insights
Patients with chronic kidney disease (CKD) do not show increased sympathetic nervous system response to blood pressure changes. This study found no augmented sympathetic transduction in CKD patients compared to controls.
Area of Science:
- Cardiovascular Physiology
- Nephrology
- Autonomic Nervous System
Background:
- Patients with chronic kidney disease (CKD) face a doubled risk of cardiovascular events compared to those with healthy kidneys.
- CKD may elevate resting sympathetic activity, but the link between sympathetic outflow and blood pressure changes (sympathetic transduction) is not fully understood.
- Elevated alpha-adrenergic receptor sensitivity in CKD patients might enhance sympathetic transduction.
Purpose of the Study:
- To investigate whether patients with CKD exhibit augmented sympathetic transduction to blood pressure.
- To compare sympathetic responses in CKD patients versus bodyweight-matched and lean controls.
Main Methods:
- Continuous recording of muscle sympathetic nerve activity (MSNA) and beat-to-beat blood pressure (BP) in 16 CKD patients, 17 bodyweight-matched (BWM) controls, and 11 lean controls.
- Signal averaging to quantify mean arterial pressure (MAP) and total vascular conductance (TVC) changes following MSNA bursts.
- Analysis of graded BP and vascular conductance responses relative to MSNA burst size.
Main Results:
- No significant differences were observed in peak MAP increases following MSNA bursts among CKD patients and control groups (P=0.28).
- Reductions in TVC following MSNA bursts were also comparable across all groups (P=0.69).
- Both CKD patients and controls demonstrated similar graded increases in MAP and decreases in TVC with increasing MSNA burst size (all P>0.05).
Conclusions:
- The study concludes that patients with CKD do not have augmented sympathetic transduction to blood pressure.
- Findings suggest that altered sympathetic transduction is not a primary mechanism driving cardiovascular risk in CKD.
Purpose:
Patients with chronic kidney disease (CKD) are more than twice as likely to die from a cardiovascular event than those with normal kidney function. Although CKD may increase resting sympathetic activity, quantification of resting sympathetic outflow alone does not account for the ensuing vasoconstriction, and blood pressure (BP) change (i.e., sympathetic transduction). Patients with CKD have been reported to exhibit elevated α-adrenergic receptor sensitivity, which may predispose this population to greater sympathetic transduction. We tested the hypothesis that patients with CKD have augmented sympathetic transduction to BP.
Methods:
In 16 patients with CKD, 17 bodyweight-matched (BWM) controls, and 11 lean controls of a similar age muscle sympathetic nerve activity (MSNA) and beat-to-beat BP were continuously recorded during quiet supine rest. Signal averaging was used to quantify changes in mean arterial pressure (MAP) and total vascular conductance (TVC) following spontaneous bursts of MSNA.
Results:
Peak increases in MAP following MSNA bursts were not different among patients with CKD and the control groups (CKD: 2.3 ± 1.1 mmHg; BWM controls: 2.1 ± 1.0 mmHg; lean controls: 1.7 ± 0.9 mmHg; P = 0.28). Likewise, nadir reductions in TVC following all bursts of MSNA were not different among patients with CKD and either control group (P = 0.69). Both patients with CKD and controls had graded increases in MAP and decreases in TVC with increasing burst size, which were not different among groups (all P > 0.05).
Conclusion:
In summary, these data indicate that patients with CKD do not have augmented sympathetic transduction to BP.
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