Depressor effect of closed-loop chip system in spontaneously hypertensive rats

Gao, Xing-Ya; Huang, Xiaoxu; Wang, Han Jun; Zhou, Li; Xu, Yao; Wang, Wei; Zhu, Guo‐Qing

doi:10.1016/j.autneu.2007.09.001

Cited by 4 publications

(3 citation statements)

References 26 publications

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“…Duran et al and Gao et al showed that ADN stimulation decreases blood pressure also in spontaneously hypertensive rats (SHR) in the same manner as in normotensive rats, implying that the mechanisms of the baroreflex remain intact even in chronically elevated blood pressure [43,44]. We will test our approach of baroreflex activation with a cuff electrode in spontaneous hypertensive rats by using a fully implantable, feedback-driven stimulator.…”

Section: Discussionmentioning

confidence: 98%

Blood pressure control with selective vagal nerve stimulation and minimal side effects

et al. 2014

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Section: Discussionmentioning

confidence: 98%

Blood pressure control with selective vagal nerve stimulation and minimal side effects

et al. 2014

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“…Nevertheless, in the present study, it was observed that ADN stimulation evoked greater hypotensive response and similar bradycardia in L-NAME-induced hypertensive rats compared with normotensive control rats. Studies carried out in conscious or anesthetized rats with different types of arterial hypertension (i.e., SHR and 2K1C) not involving the inhibition of NO production have also shown a greater hypotensive response to electrical stimulation of baroreceptors afferents (8,35,52). On the other hand, it has been demonstrated that systemic inhibition of NOS can have an effect on the reflex control of HR, but the results are inconsistent.…”

Section: Discussionmentioning

confidence: 99%

Hemodynamic responses to aortic depressor nerve stimulation in conscious l-NAME-induced hypertensive rats

Durand¹,

Castania²,

Fazan³

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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The present study investigated whether baroreflex control of autonomic function is impaired when there is a deficiency in NO production and the role of adrenergic and cholinergic mechanisms in mediating reflex responses. Electrical stimulation of the aortic depressor nerve in conscious normotensive and nitro-l-arginine methyl ester (L-NAME)-induced hypertensive rats was applied before and after administration of methylatropine, atenolol, and prazosin alone or in combination. The hypotensive response to progressive electrical stimulation (5 to 90 Hz) was greater in hypertensive (-27 ± 2 to -64 ± 3 mmHg) than in normotensive rats (-17 ± 1 to -46 ± 2 mmHg), whereas the bradycardic response was similar in both groups (-34 ± 5 to -92 ± 9 and -21 ± 2 to -79 ± 7 beats/min, respectively). Methylatropine and atenolol showed no effect in the hypotensive response in either group. Methylatropine blunted the bradycardic response in both groups, whereas atenolol attenuated only in hypertensive rats. Prazosin blunted the hypotensive response in both normotensive (43%) and hypertensive rats (53%) but did not affect the bradycardic response in either group. Prazosin plus angiotensin II, used to restore basal arterial pressure, provided hemodynamic responses similar to those of prazosin alone. The triple pharmacological blockade abolished the bradycardic response in both groups but displayed similar residual hypotensive response in hypertensive (-13 ± 2 to -27 ± 2 mmHg) and normotensive rats (-10 ± 1 to -25 ± 3 mmHg). In conclusion, electrical stimulation produced a well-preserved baroreflex-mediated decrease in arterial pressure and heart rate in conscious l-NAME-induced hypertensive rats. Moreover, withdrawal of the sympathetic drive played a role in the reflex bradycardia only in hypertensive rats. The residual fall in pressure after the triple pharmacological blockade suggests the involvement of a vasodilatory mechanism unrelated to NO or deactivation of α(1)-adrenergic receptor.

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“…Studies evaluating the hemodynamic responses caused by electrical stimulation of the baroreceptors in anesthetized rats demonstrated that the hemodynamic responses were reduced in SHR, suggesting an alteration of the baroreflex circuitry (15,16). Nevertheless, in a recent study, Salgado et al (17) demonstrated that electrical stimulation of the aortic depressor nerve (ADN) in conscious SHR produced equivalent or even greater depressor responses compared to normotensive rats, indicating that conscious SHR exhibited a well-preserved baroreflex response to the electrical stimulation of the ADN, probably because this maneuver bypasses the mechanical transduction of the baroreceptors.…”

Section: Introductionmentioning

confidence: 99%

Time course of the hemodynamic responses to aortic depressor nerve stimulation in conscious spontaneously hypertensive rats

Durand

Mota

Barale

et al. 2012

Braz J Med Biol Res

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The time to reach the maximum response of arterial pressure, heart rate and vascular resistance (hindquarter and mesenteric) was measured in conscious male spontaneously hypertensive (SHR) and normotensive control rats (NCR; Wistar; 18-22 weeks) subjected to electrical stimulation of the aortic depressor nerve (ADN). The parameters of stimulation were 1 mA intensity and 2 ms pulse length applied for 5 s, using frequencies of 10, 30, and 90 Hz. The time to reach the hemodynamic responses at different frequencies of ADN stimulation was similar for SHR (N = 15) and NCR (N = 14); hypotension = NCR (4194 ± 336 to 3695 ± 463 ms) vs SHR (3475 ± 354 to 4494 ± 300 ms); bradycardia = NCR (1618 ± 152 to 1358 ± 185 ms) vs SHR (1911 ± 323 to 1852 ± 431 ms), and the fall in hindquarter vascular resistance = NCR (6054 ± 486 to 6550 ± 847 ms) vs SHR (4849 ± 918 to 4926 ± 646 ms); mesenteric = NCR (5574 ± 790 to 5752 ± 539 ms) vs SHR (5638 ± 648 to 6777 ± 624 ms). In addition, ADN stimulation produced baroreflex responses characterized by a faster cardiac effect followed by a vascular effect, which together contributed to the decrease in arterial pressure. Therefore, the results indicate that there is no alteration in the conduction of the electrical impulse after the site of baroreceptor mechanical transduction in the baroreflex pathway (central and/or efferent) in conscious SHR compared to NCR.

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Depressor effect of closed-loop chip system in spontaneously hypertensive rats

Cited by 4 publications

References 26 publications

Blood pressure control with selective vagal nerve stimulation and minimal side effects

Blood pressure control with selective vagal nerve stimulation and minimal side effects

Hemodynamic responses to aortic depressor nerve stimulation in conscious l-NAME-induced hypertensive rats

Time course of the hemodynamic responses to aortic depressor nerve stimulation in conscious spontaneously hypertensive rats

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