Acute effects of intravenous nifedipine or azelnidipine on open-loop baroreflex static characteristics in rats

Yamamoto, Hiromi; Kawada, Toru; Shimizu, Shuji; Kamiya, Atsunori; Turner, Michael J.; Miyazaki, Shunichi; Sugimachi, Masaru

doi:10.1016/j.lfs.2015.01.024

Cited by 9 publications

(8 citation statements)

References 31 publications

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“…3), which is also in line with our previous study (18). The relative insensitivity of the peripheral arc transfer function to changes in mean SNA and AP may be explained by a nearly linear static input-output relationship between SNA and AP (23,25,31). When the operating point is within the linear input-output range of the peripheral arc, Fig.…”

Section: Table 1 Parameters Of Aortic Baroreflex Dynamic Characterissupporting

confidence: 90%

Tonic aortic depressor nerve stimulation does not impede baroreflex dynamic characteristics concomitantly mediated by the stimulated nerve

Kawada

Turner

Shimizu

et al. 2018

American Journal of Physiology-Regulatory, Integrative and Comp

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Although electrical activation of the carotid sinus baroreflex (baroreflex activation therapy) is being explored as a device therapy for resistant hypertension, possible effects on baroreflex dynamic characteristics of interaction between electrical stimulation and pressure inputs are not fully elucidated. To examine whether the electrical stimulation of the baroreceptor afferent nerve impedes normal short-term arterial pressure (AP) regulation mediated by the stimulated nerve, we electrically stimulated the right aortic depressor nerve (ADN) while estimating the baroreflex dynamic characteristics by imposing pressure inputs to the isolated baroreceptor region of the right ADN in nine anesthetized rats. A Gaussian white noise signal with a mean of 120 mmHg and standard deviation of 20 mmHg was used for the pressure perturbation. A tonic ADN stimulation (2 or 5 Hz, 10 V, 0.1-ms pulse width) decreased mean sympathetic nerve activity (367.0 ± 70.9 vs. 247.3 ± 47.2 arbitrary units, P < 0.01) and mean AP (98.4 ± 7.8 vs. 89.2 ± 4.5 mmHg, P < 0.01) during dynamic pressure perturbation. The ADN stimulation did not affect the slope of dynamic gain in the neural arc transfer function from pressure perturbation to sympathetic nerve activity (16.9 ± 1.0 vs. 14.7 ± 1.6 dB/decade, not significant). These results indicate that electrical stimulation of the baroreceptor afferent nerve does not significantly impede the dynamic characteristics of the arterial baroreflex concomitantly mediated by the stimulated nerve. Short-term AP regulation by the arterial baroreflex may be preserved during the baroreflex activation therapy.

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Section: Table 1 Parameters Of Aortic Baroreflex Dynamic Characterissupporting

confidence: 90%

Tonic aortic depressor nerve stimulation does not impede baroreflex dynamic characteristics concomitantly mediated by the stimulated nerve

Kawada

Turner

Shimizu

et al. 2018

American Journal of Physiology-Regulatory, Integrative and Comp

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“…There is a reduction in baroreflex sensitivity in the anesthetized state (45–48). Presumably, this reduction contributed to the loss of susceptibility of the generation of vasovagal responses.…”

Section: Resultsmentioning

confidence: 99%

Vestibular Activation Habituates the Vasovagal Response in the Rat

et al. 2017

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Vasovagal syncope is a significant medical problem without effective therapy, postulated to be related to a collapse of baroreflex function. While some studies have shown that repeated static tilts can block vasovagal syncope, this was not found in other studies. Using anesthetized, male Long–Evans rats that were highly susceptible to generation of vasovagal responses, we found that repeated activation of the vestibulosympathetic reflex (VSR) with ±2 and ±3 mA, 0.025 Hz sinusoidal galvanic vestibular stimulation (sGVS) caused incremental changes in blood pressure (BP) and heart rate (HR) that blocked further generation of vasovagal responses. Initially, BP and HR fell ≈20–50 mmHg and ≈20–50 beats/min (bpm) into a vasovagal response when stimulated with Sgv\S in susceptible rats. As the rats were continually stimulated, HR initially rose to counteract the fall in BP; then the increase in HR became more substantial and long lasting, effectively opposing the fall in BP. Finally, the vestibular stimuli simply caused an increase in BP, the normal sequence following activation of the VSR. Concurrently, habituation caused disappearance of the low-frequency (0.025 and 0.05 Hz) oscillations in BP and HR that must be present when vasovagal responses are induced. Habituation also produced significant increases in baroreflex sensitivity (p < 0.001). Thus, repeated low-frequency activation of the VSR resulted in a reduction and loss of susceptibility to development of vasovagal responses in rats that were previously highly susceptible. We posit that reactivation of the baroreflex, which is depressed by anesthesia and the disappearance of low-frequency oscillations in BP and HR are likely to be critically involved in producing resistance to the development of vasovagal responses. SGVS has been widely used to activate muscle sympathetic nerve activity in humans and is safe and well tolerated. Potentially, it could be used to produce similar habituation of vasovagal syncope in humans.

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“…CSP was first decreased to 60 mmHg for 5 min, then increased in a staircase manner from 60 to 180 mmHg in increment of 20 mmHg. Each step was maintained for 60 s. Carotid sinus baroreceptors were exposed to non-pulsatile pressure [10][11][12][13][14].…”

Section: Surgical Preparationmentioning

confidence: 99%

“…In order to more systematically understand the total picture of the effects of guanfacine on SNA and AP, this study employed a framework of open-loop analysis of the carotid sinus baroreflex where the carotid sinus baroreceptor regions were isolated from systemic circulation [10][11][12][13][14]. In this method, the baroreceptor input pressure is controlled externally independent of changes in AP, which enables the examination of the effect of intravenous guanfacine at different levels of SNA.…”

Section: Introductionmentioning

confidence: 99%

Systematic understanding of acute effects of intravenous guanfacine on rat carotid sinus baroreflex-mediated sympathetic arterial pressure regulation

et al. 2016

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Acute effects of intravenous nifedipine or azelnidipine on open-loop baroreflex static characteristics in rats

Cited by 9 publications

References 31 publications

Tonic aortic depressor nerve stimulation does not impede baroreflex dynamic characteristics concomitantly mediated by the stimulated nerve

Tonic aortic depressor nerve stimulation does not impede baroreflex dynamic characteristics concomitantly mediated by the stimulated nerve

Vestibular Activation Habituates the Vasovagal Response in the Rat

Systematic understanding of acute effects of intravenous guanfacine on rat carotid sinus baroreflex-mediated sympathetic arterial pressure regulation

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