ANG II modulates both slow and rapid baroreflex responses of barosensitive bulbospinal neurons in the rabbit rostral ventrolateral medulla

Saigusa, Takeshi; Ai, Jun

doi:10.1152/ajpregu.00285.2013

Cited by 4 publications

(2 citation statements)

References 54 publications

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“…Есть данные о том, что изменение установочной точки барорефлекса напрямую связано с изменением уровня Ang II в тканях мозга, в частности в продолговатом моз-ге (Saigusa, Arita, 2014). Так, хроническое повышение экспрессии мРНК Agt и Ren с помощью искусственного встраивания дополнительных копий этих генов вело к хро-ническому увеличению частоты сердечных сокращений у мышей (Merrill et al, 1996).…”

Section: результаты и обсуждениеunclassified

Effects of brain renin- angiotensin system inhibition in ISIAH rats with inherited stress-induced arterial hypertension

Климов¹,

Рязанова²,

Fedoseeva³

et al. 2017

Vestn. VOGiS

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The renin-angiotensin system (RAS) is one of the main systems regulating arterial pressure and water-salt homeostasis of the body and is involved in the pathogenesis of cardiovascular diseases. Angiotensin peptides -products of enzymatic hydrolysis of angiotensinogen -can be synthesized not only in the blood stream, but also in tissues, including various regions of the brain. Studies of local tissue RAS in the context of arterial hypertension have been conducted for a long time. It has been shown that a steady arterial pressure increase is often associated with changes in the functioning of the central (brain) RAS in various animal models of hypertensive disease and in humans. Nevertheless, it is still not completely clear whether these changes alone are sufficient for the formation of hypertensive status, and whether the components of the central RAS can be used as targets for the treatment of hypertensive disease. Effects of prolonged inhibition of the brain RAS on blood pressure and expression of RAS genes in brain and kidney tissues in ISIAH (inherited stress-induced arterial hypertension) rats were studied. Inhibition was performed using widely used pharmacological agents, losartan and benazepril. Osmotic minipumps were used to deliver drugs to the lateral ventricle of the brain. It was shown that prolonged inhibition of the central RAS, AT1 receptors in particular, can lead to a decrease in blood pressure and significant changes in the level of expression of brain RAS genes in ISIAH rats. The mRNA level of RAS genes in the kidney does not significantly change due to this inhibition. Thus, the participation of the central RAS in the pathogenesis and maintenance of hypertensive status during stress induced form of hypertensive disease in ISIAH rats was confirmed.Key words: hypertension; ISIAH rats; central RAS; mRNA expression; blood pressure.Ренин-ангиотензиновая система (РАС) -одна из основных систем, регулирующих артериальное давление и водно-солевой гомео-стаз организма и участвующих в патогенезе сердечно-сосудистых заболеваний. Ангиотензиновые пептиды -продукты фермента-тивного гидролиза ангиотензиногена -могут синтезироваться как в кровяном русле, так и в тканях, в том числе в различных отделах головного мозга. Исследования локальных тканевых РАС в контексте артериальной гипертонии ведутся уже достаточно давно. Показано, что стойкое повышение уровня артериального давления (АД) часто ассоциировано с изменениями в работе цент-ральной (мозговой) РАС в различных моделях гипертонической болезни (ГБ) и у людей. Тем не менее до сих пор до конца не ясно, являются ли данные изменения сами по себе достаточными для формирования гипертензивного статуса и можно ли использовать звенья центральной РАС в качестве мишеней для терапии гипер-тонической болезни. В работе исследовано влияние длительного ингибирования РАС головного мозга на артериальное давление и экспрессию генов РАС в тканях головного мозга и почке у крыс с наследственной стресс-индуцированной артериальной гиперто-нией (линия НИСАГ). Ингибирование проводи...

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Section: результаты и обсуждениеunclassified

Effects of brain renin- angiotensin system inhibition in ISIAH rats with inherited stress-induced arterial hypertension

Климов¹,

Рязанова²,

Fedoseeva³

et al. 2017

Vestn. VOGiS

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“…While many aspects of baroreflex regulation have been studied extensively (Benarroch (2008)), numerous factors modulating baroreflex responses are not fully understood, e.g. the role of angiotensin in modulation of baroreflex sensitivity (Palma-Rigo et al (2012); Saigusa and Arita (2014)), and the mechanical properties facilitating coupling of the nerve endings to the arterial wall (Brown (1980)). Both of which may be of significance in understanding the role of the baroreflex in hypertension as suggested by the recent study by Pettersen et al (2014).…”

Section: Action Potential Generationmentioning

confidence: 99%

Modeling the differentiation of A- and C-type baroreceptor firing patterns

2016

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The baroreceptor neurons serve as the primary transducers of blood pressure for the autonomic nervous system and are thus critical in enabling the body to respond effectively to changes in blood pressure. These neurons can be separated into two types (A and C) based on the myelination of their axons and their distinct firing patterns elicited in response to specific pressure stimuli. This study has developed a comprehensive model of the afferent baroreceptor discharge built on physiological knowledge of arterial wall mechanics, firing rate responses to controlled pressure stimuli, and ion channel dynamics within the baroreceptor neurons. With this model, we were able to predict firing rates observed in previously published experiments in both A- and C-type neurons. These results were obtained by adjusting model parameters determining the maximal ion-channel conductances. The observed variation in the model parameters are hypothesized to correspond to physiological differences between A- and C-type neurons. In agreement with published experimental observations, our simulations suggest that a twofold lower potassium conductance in C-type neurons is responsible for the observed sustained basal firing, whereas a tenfold higher mechanosensitive conductance is responsible for the greater firing rate observed in A-type neurons. A better understanding of the difference between the two neuron types can potentially be used to gain more insight into the underlying pathophysiology facilitating development of targeted interventions improving baroreflex function in diseased individuals, e.g. in patients with autonomic failure, a syndrome that is difficult to diagnose in terms of its pathophysiology.

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Prolonged blood pressure elevation following continuous infusion of angiotensin II—a baroreflex study in healthy humans

Sayk

Wobbe

Twesten

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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ANG II interacts with the sympathetic nervous system at central nervous blood pressure-regulating structures, including the baroreflex. It is unknown whether prolonged BP elevation mediated by high ANG II plasma levels could induce a persistent shift of the central nervous baroreflex setpoint, lasting beyond the short ANG II plasmatic half time of a few seconds, thereby consolidating elevated BP and/or increased SNA in healthy humans. In a blinded crossover design, ANG II or placebo (saline) was infused for a 6-h period in 12 resting normotensive students (6 males, 6 females) raising BP to borderline hypertensive levels. Between 60 and 120 min after the infusion period, muscle sympathetic nerve activity (MSNA) was assessed microneurographically and correlated with oscillometric BP measurements and heart rate at supine rest (baseline) and during pharmacologic baroreceptor challenge. Infusion of ANG II increased BP to borderline-hypertensive levels, as intended, whereas heart rate remained unaltered. At baroreflex assessment (i.e., 60-120 min after end of infusion period), systolic BP was significantly higher compared with placebo (Δ8.4 ± 3.1 mmHg; P < 0.05), whereas diastolic values were nearly equal between conditions. Baseline MSNA was neither decreased nor increased, and baroreflex sensitivity to vasoactive drug challenge was not altered. Our results show that elevation of ANG II plasma levels over 6 h was able to increase systolic, but not diastolic, BP far beyond blood-mediated ANG II effects. MSNA or heart rate did not counter-regulate this BP elevation, indicating that ANG II had sustainably reset the central nervous BP threshold of sympathetic baroreflex function to accept elevated BP input signals without counter-regulatory response.

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ANG II modulates both slow and rapid baroreflex responses of barosensitive bulbospinal neurons in the rabbit rostral ventrolateral medulla

Cited by 4 publications

References 54 publications

Effects of brain renin- angiotensin system inhibition in ISIAH rats with inherited stress-induced arterial hypertension

Effects of brain renin- angiotensin system inhibition in ISIAH rats with inherited stress-induced arterial hypertension

Modeling the differentiation of A- and C-type baroreceptor firing patterns

Prolonged blood pressure elevation following continuous infusion of angiotensin II—a baroreflex study in healthy humans

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