Key result
Bursts of cardiac sympathetic nerve activity in conscious sheep caused significant increases in heart rate (Δ: +2.1 beats/min, P=0.002) and cardiac output, which were attenuated by propranolol.
Why the study?
Sympathetic transduction had been studied primarily in skeletal muscle, but whether directly recorded resting cardiac sympathetic nerve activity regulates cardiac variables remained unexamined.
In conscious sheep, bursts of cardiac sympathetic nerve activity dynamically increase heart rate and coronary blood flow via β-adrenergic signaling.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for sympathetic β-adrenergic effects on heart rate; does not inform clinical practice.
Sympathetic transduction is the study of how impulses of sympathetic nerve activity (SNA) affect end‐organ function. Recently, the transduction of resting bursts of muscle SNA (MSNA) has been investigated and shown to have a role in the maintenance of blood pressure through changes in vascular tone in humans. In the present study, we investigate whether directly recorded resting cardiac SNA (CSNA) regulates heart rate (HR), coronary blood flow (CoBF), coronary vascular conductance (CVC), cardiac output (CO) and mean arterial pressure. Instrumentation was undertaken to record CSNA and relevant vascular variables in conscious sheep. Recordings were performed at baseline, as well as after the infusion of a β‐adrenoceptor blocker (propranolol) to determine the role of β‐adrenergic signalling in sympathetic transduction in the heart. The results show that after every burst of CSNA, there was a significant effect of time on HR ( n = 10, ∆: +2.1 ± 1.4 beats min –1 , P = 0.002) and CO ( n = 8, ∆: +100 ± 150 mL min –1 , P = 0.002) was elevated, followed by an increase in CoBF ( n = 9, ∆: +0.76 mL min –1 , P = 0.001) and CVC ( n = 8, ∆: +0.0038 mL min –1 mmHg –1 , P = 0.0028). The changes in HR were graded depending on the size and pattern of CSNA bursts. The HR response was significantly attenuated after the infusion of propranolol. Our study is the first to explore resting sympathetic transduction in the heart, suggesting that CSNA can dynamically change HR mediated by an action on β‐adrenoceptors. image Key points Sympathetic transduction is the study of how impulses of sympathetic nerve activity (SNA) affect end‐organ function. Previous studies have examined sympathetic transduction primarily in the skeletal muscle and shown that bursts of muscle SNA alter blood flow to skeletal muscle and mean arterial pressure, although this has not been examined in the heart. We investigated sympathetic transduction in the heart and show that, in the conscious condition, the size of bursts of SNA to the heart can result in incremental increases in heart rate and coronary blood flow mediated by β‐adrenoceptors. The pattern of bursts of SNA to the heart also resulted in incremental increases in heart rate mediated by β‐adrenoceptors. This is the first study to explore the transduction of bursts of SNA to the heart.
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Gimhani et al. (2024) studied Healthy (n=10). Propranolol infusion vs. Baseline was evaluated on Change in heart rate after every burst of cardiac sympathetic nerve activity (Δ: +2.1 beats min-1, p=0.002). Bursts of cardiac sympathetic nerve activity in conscious sheep caused significant increases in heart rate (Δ: +2.1 beats/min, P=0.002) and cardiac output, which were attenuated by propranolol.
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