The impact of volume loading-induced low pressure baroreflex activation on arterial baroreflex-controlled sympathetic arterial pressure regulation in normal rats.

Yasuhiro Oga,Takuya Nishikawa,Kenji Sunagawa,Takeshi Tohyama,Kazuya Hosokawa,Tomoyuki Tobushi,Hiroyuki Tsutsui,Takuya Kishi,Keita Saku,Takafumi Sakamoto

doi:10.14814/phy2.13887

Abstract

Although low pressure baroreflex (LPB) has been shown to elicit various cardiovascular responses, its impact on sympathetic nerve activity (SNA) and arterial baroreflex (ABR) function has not been fully elucidated. The aim of this study was to clarify how volume loading‐induced acute LPB activation impacts on SNA and ABR function in normal rats. In 20 anesthetized Sprague‐Dawley rats, we isolated bilateral carotid sinuses, controlled carotid sinus pressure (CSP), and measured central venous pressure (CVP), splanchnic SNA, and arterial pressure (AP). We infused blood stepwise (3 mL/kg/step) to activate volume loading‐induced LPB. Under the ABR open‐loop condition, stepwise volume loading markedly increased SNA by 76.8 ± 21.6% at CVP of 3.6 ± 0.2 mmHg. In contrast, further volume loading suppressed SNA toward the baseline condition. Bilateral vagotomy totally abolished the changes in SNA by volume loading. To assess the impact of LPB on ABR function, we changed CSP stepwise. Low volume loading (CVP = 3.6 ± 0.4 mmHg) significantly shifted the sigmoidal CSP–SNA relationship (central arc) upward from baseline, whereas high volume loading (CVP = 5.4 ± 0.4 mmHg) returned it to the baseline level. Volume loading shifted the linear SNA–AP relationship (peripheral arc) upward without significant changes in slope. In conclusions, volume loading‐induced acute LPB activation evoked two‐phase changes, an initial increase followed by decline from baseline value, in SNA via resetting of the ABR central arc. LPB may contribute greatly to stabilize AP in response to volume status.

Highlights

The sympathetic nervous system has been shown to play a pivotal role in circulatory homeostasis
carotid sinus pressure (CSP) was maintained at 90 mmHg to abolish arterial baroreflex (ABR)
Bilateral vagotomy totally abolished the changes in sympathetic nerve activity (SNA) in response to volume loading

Summary

Introduction

The sympathetic nervous system has been shown to play a pivotal role in circulatory homeostasis. Various receptors sense vital variables such as blood pressure, oxygen saturation, and pH and transmit to the brainstem through afferent nerves, and in turn modulate efferent sympathetic nerve activity (SNA) Since SNA strongly contributes to both dynamic and static arterial pressure (AP) regulation by changing heart rate (HR), cardiac contractility, arterial resistance and stressed blood volume (Sakamoto et al 2015), the failure of SNA regulation destabilizes AP and leads to poor outcome in various cardiovascular diseases (Barron and Viskin 1998; Shan et al 2001; Eguchi et al 2012). To clarify the mechanism and the extent by which each particular reflex modifies SNA is important to understand the physiological role of the reflexes and the mechanism of circulatory homeostasis

Objectives

Results

Conclusion