Differential modulation of baroreflex control of heart rate by neuron- vs. glia-derived angiotensin II

Sakai, Koji; Chapleau, Mark W.; Morimoto, Satoshi; Cassell, Martin D.

doi:10.1152/physiolgenomics.00168.2004

Cited by 35 publications

(42 citation statements)

References 37 publications

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“…Besides the experimental considerations, it has to be pointed out that the estimates of BRS presently obtained using the recent methods were close to the maximal gain derived from the full baroreflex curves (roughly between 2 and 5 ms/mmHg) (22)(23)(24)29). The sequence technique (2,7,10,21,34) or the spectral method (gain of the transfer function or alpha coefficient) (2, 7, 9 -12, 16, 18, 32) also indicated values of BRS in the same order of magnitude as the present values, between 1 and 4 ms/mmHg.…”

Section: Discussionsupporting

confidence: 57%

Applicability of recent methods used to estimate spontaneous baroreflex sensitivity to resting mice

Laude

Baudrie²,

Elghozi³

2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Laude D, Baudrie V, Elghozi J-L. Applicability of recent methods used to estimate spontaneous baroreflex sensitivity to resting mice. Am J Physiol Regul Integr Comp Physiol 294: R142-R150, 2008. First published November 7, 2007 doi:10.1152/ajpregu.00319.2007.-Shortterm blood pressure (BP) variability is limited by the arterial baroreflex. Methods for measuring the spontaneous baroreflex sensitivity (BRS) aim to quantify the gain of the transfer function between BP and pulse interval (PI) or the slope of the linear relationship between parallel BP and PI changes. These frequency-domain (spectral) and time-domain (sequence) techniques were tested in conscious mice equipped with telemetric devices. The autonomic relevance of these indexes was evaluated using pharmacological blockades. The significant changes of the spectral bandwidths resulting from the autonomic blockades were used to identify the low-frequency (LF) and highfrequency (HF) zones of interest. The LF gain was 1.45 Ϯ 0.14 ms/mmHg, with a PI delay of 0.5 s. For the HF gain, the average values were 2.0 Ϯ 0.19 ms/mmHg, with a null phase. LF and HF bands were markedly affected by atropine. On the same 51.2-s segments used for cross-spectral analysis, an average number of 26.4 Ϯ 2.2 slopes were detected, and the average slope in resting mice was 4.4 Ϯ 0.5 ms/mmHg. Atropine significantly reduced the slopes of the sequence method. BRS measurements obtained using the sequence technique were highly correlated to the spectral estimates. This study demonstrates the applicability of the recent methods used to estimate spontaneous BRS in mice. There was a vagal predominance in the baroreflex control of heart rate in conscious mice in the present conditions. baroreceptors; heart rate; sympathetic; vagus nerve THE IMPORTANCE OF THE BAROREFLEX in blood pressure (BP) regulation in mice can be appreciated by the marked increase in BP variability that occurs after sinoaortic deafferentation of baroreceptors that are located in the carotid sinuses and aortic arch (9, 21). The ability of the baroreflex to buffer BP fluctuations varies depending on the frequency of the BP fluctuations (19). BP and heart rate (HR) fluctuate at regular frequencies, the magnitude of which can be accurately quantified using power spectral analysis (25, 30). The absolute frequency bands at which these oscillations occur in mice were analyzed in a previous report (3). One recent approach to estimating the spontaneous baroreflex sensitivity (BRS) over a stationary period is the calculation of the gain of the transfer function between BP and R-R interval in the low-frequency (LF) and high-frequency (HF) bands (20,28). This spectral analysis approach has been recently applied to conscious mice (2, 7, 9 -12, 16, 18, 32). Another recent approach is the dynamic evaluation of the spontaneous BRS called the sequence technique (4). This method is based on the computerized scanning of beat-to-beat series of systolic BP and R-R interval values in search of spontaneous sequences of consecutive increases o...

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Section: Discussionsupporting

confidence: 57%

Applicability of recent methods used to estimate spontaneous baroreflex sensitivity to resting mice

Laude

Baudrie²,

Elghozi³

2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…26,28 Indeed, in the NTS, NADPH oxidase subunits are also present in astrocytes 27 ; therefore, we cannot exclude the possibility that inhibition of Rac1/NAD(P)H oxidase in glia also decreased blood pressure in the present study. The precise role of glia in cardiovascular regulation is unknown.…”

Section: Discussionmentioning

confidence: 65%

Inhibition of Rac1-Derived Reactive Oxygen Species in Nucleus Tractus Solitarius Decreases Blood Pressure and Heart Rate in Stroke-Prone Spontaneously Hypertensive Rats

et al. 2007

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Abstract-Reactive oxygen species (ROS) in the brain are thought to contribute to the neuropathogenesis of hypertension by enhancing sympathetic nervous system activity. The nucleus tractus solitarius (NTS), which receives afferent input from baroreceptors, has an important role in cardiovascular regulation. reduced nicotinamide-adenine dinucleotide phosphate oxidase is thought to be a major source of ROS in the NTS. Rac1 is a small G protein and a key component of reduced nicotinamide-adenine dinucleotide phosphate oxidase. The role of Rac1-derived ROS in the NTS in cardiovascular regulation of hypertension is unknown. Therefore, we examined whether inhibition of Rac1 in the NTS decreases ROS generation, thereby reducing blood pressure in stroke-prone spontaneously hypertensive rats (SHRSPs).The basal Rac1 activity level in the NTS was greater in SHRSPs than in Wistar-Kyoto rats. Inhibition of Rac1, induced by transfecting adenovirus vectors encoding dominant-negative Rac1 into the NTS, decreased blood pressure, heart rate, and urinary norepinephrine excretion in SHRSPs but not in Wistar-Kyoto rats. Inhibition of Rac1 also reduced nicotinamide-adenine dinucleotide phosphate oxidase activity and ROS generation. In addition, Cu/Zn-superoxide dismutase activity in the NTS of SHRSPs was decreased compared with that of Wistar-Kyoto rats, despite the increased ROS generation. Overexpression of Cu/Zn-superoxide dismutase in the NTS decreased blood pressure and heart rate in SHRSPs. These results indicate that the activation of Rac1 in the NTS generates ROS via reduced nicotinamide-adenine dinucleotide phosphate oxidase in SHRSPs, and this mechanism might be important for the neuropathogenesis of hypertension in SHRSPs. Key Words: blood pressure Ⅲ heart rate Ⅲ sympathetic nervous system Ⅲ hypertension Ⅲ brain T here is accumulating evidence that reactive oxygen species (ROS) in the cardiovascular regulatory nuclei in the brain have a crucial role in blood pressure regulation in hypertension via modulating the sympathetic nervous system. 1-5 Reduced nicotinamide-adenine dinucleotide phosphate [NAD(P)H] oxidase is a major source of ROS in hypertension 6 and has a critical role in generating ROS in the brain. 2,5,7 Rac1 is a small G protein that is an important signaling molecule involved in integrating intracellular transduction pathways toward NAD(P)H oxidase activation. 2,8,9 Rac1 requires lipid modifications to migrate from the cytosol to the plasma membrane, which is a necessary step for activating the ROSgenerating NAD(P)H oxidase enzyme system. 8,9 The nucleus tractus solitarius (NTS) in the brain stem has an important role in cardiovascular regulation. 10 -16 The NTS receives afferent input from baroreceptors and chemoreceptors 12 and has reciprocal interconnections with other nuclei involved in central autonomic regulation. 17 In addition, the essential NAD(P)H oxidase subunit gp91 phox is present in somatodendritic and axonal profiles that contain angiotensin II (Ang II) subtype 1 receptors in the NTS, and Ang I...

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“…Increased expression of both the human renin and AGT genes in the brain results in increased blood pressure and water intake (96,97) and depending on the cellular sites of production (glia vs. neurons) can differentially modulate baroreflex function (118). Moreover, increased fluid intake and blood pressure caused by increased production of ANG II in the brain is attenuated when the source of the ANG II substrate, AGT, is selectively deleted from the SFO (117,126), and mice selectively expressing ANG II only in the SFO exhibit increased fluid intake (20).…”

Section: Localization Of Ras Components Required For Ang II Productionmentioning

confidence: 99%

Mechanisms of brain renin angiotensin system-induced drinking and blood pressure: importance of the subfornical organ

Coble¹,

Grobe

Johnson³

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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Coble JP, Grobe JL, Johnson AK, Sigmund CD. Mechanisms of brain renin angiotensin system-induced drinking and blood pressure: importance of the subfornical organ. Am J Physiol Regul Integr Comp Physiol 308: R238 -R249, 2015. First published December 17, 2014 doi:10.1152/ajpregu.00486.2014.-It is critical for cells to maintain a homeostatic balance of water and electrolytes because disturbances can disrupt cellular function, which can lead to profound effects on the physiology of an organism. Dehydration can be classified as either intra-or extracellular, and different mechanisms have developed to restore homeostasis in response to each. Whereas the renin-angiotensin system (RAS) is important for restoring homeostasis after dehydration, the pathways mediating the responses to intra-and extracellular dehydration may differ. Thirst responses mediated through the angiotensin type 1 receptor (AT 1R) and angiotensin type 2 receptors (AT 2R) respond to extracellular dehydration and intracellular dehydration, respectively. Intracellular signaling factors, such as protein kinase C (PKC), reactive oxygen species (ROS), and the mitogen-activated protein (MAP) kinase pathway, mediate the effects of central angiotensin II (ANG II). Experimental evidence also demonstrates the importance of the subfornical organ (SFO) in mediating some of the fluid intake effects of central ANG II. The purpose of this review is to highlight the importance of the SFO in mediating fluid intake responses to dehydration and ANG II.angiotensin; blood pressure; barin; fluid; renin FLUID BALANCE is crucial for the homeostasis and survival of organisms because they have to properly maintain fluid and electrolyte concentrations for the normal function of all cells. Fluid balance can go awry in pathological states such as in chronic kidney disease and diabetes. Among its many roles in maintaining homeostasis, the renin-angiotensin system (RAS) is an important regulator of fluid balance. The RAS achieves this through the actions of its main effector peptide, angiotensin II (ANG II) through the ANG II type 1 (AT 1 R) and type 2 (AT 2 R) receptors. Activation of AT 1 R by blood-borne ANG II in target tissues causes increases in sodium and water retention, arginine vasopressin (AVP), and aldosterone release, vasoconstriction, increased sympathetic nervous system activity, and increased fluid intake. ANG II is produced by the consecutive enzymatic action of renin on its substrate angiotensinogen (AGT) and by angiotensin-converting enzyme (ACE) on its substrate angiotensin I (ANG I). The renin-AGT cleavage step is generally the rate-limiting step in the production of ANG II, and this is certainly true in the brain where the amount of renin is limiting. The RAS exists in two forms: a circulatory form where ANG II acts as an endocrine factor, and a tissue-specific form, where local production of ANG II acts in an autocrine or paracrine manner to induce AT 1 R signaling on ANG II producing or nearby cells (75). Intracrine, or intracellular forms of the RAS, hav...

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Differential modulation of baroreflex control of heart rate by neuron- vs. glia-derived angiotensin II

Cited by 35 publications

References 37 publications

Applicability of recent methods used to estimate spontaneous baroreflex sensitivity to resting mice

Applicability of recent methods used to estimate spontaneous baroreflex sensitivity to resting mice

Inhibition of Rac1-Derived Reactive Oxygen Species in Nucleus Tractus Solitarius Decreases Blood Pressure and Heart Rate in Stroke-Prone Spontaneously Hypertensive Rats

Mechanisms of brain renin angiotensin system-induced drinking and blood pressure: importance of the subfornical organ

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