Baroreflex control of sympathetic activity in experimental hypertension

Irigoyen, Maria Cláudia; Krieger, Eduardo Moacyr

doi:10.1590/s0100-879x1998000900015

Cited by 36 publications

(24 citation statements)

References 37 publications

(41 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Similar basal SSNA (total discharge in mV/cardiac cycle) is a good index for the presence of baroreceptors resetting to hypertensive levels and permits the normalization of sympathetic inhibition in the chronic phase of CH, besides the maintenance of high pressure. 17,18,33 On the other hand, the predominance of LF component indicates that the sympathetic inhibition in the CH VEH was not exactly similar but smaller than that of other groups, besides the similar total neural efferent activity. Actually, it is well documented in hypertension that in the presence of baroreceptors resetting, both baroreceptor reflex control of HR and total peripheral resistance were significantly depressed (smaller gain 11,21,24,30 ).…”

Section: Discussionmentioning

confidence: 95%

“…The procedure used to record whole nerve SSNA was similar to that used in previous studies. 17,18 Upper left lateral laparotomy allowed for isolation of the left splanchnic nerve, which was placed on bipolar platinum electrodes; a third electrode, fixed in the muscle, served as reference. Whole SSNA was filtered (band pass of 100 to 3000 Hz), amplified (Differential Amplifier, 502A, Tektronix), full-wave rectified, and integrated (time constant of 3.9 milliseconds).…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Chronic AT ₁ Receptor Blockade Alters Autonomic Balance and Sympathetic Responses in Hypertension

et al. 2001

View full text Add to dashboard Cite

Abstract-In the coarctation hypertension model, we have shown that chronic treatment with losartan causes both normalization of impaired reflex control of heart rate and partial correction of the depressed aortic nerve activity/ pressure relationship, even with the persistence of hypertension. In the present study, we analyzed the effects of angiotensin II blockade on the efferent pathways of coarcted and sham-operated groups treated chronically with vehicle or losartan (10 mg/kg per day PO). Hypertension was induced by subdiaphragmatic aortic coarctation, and the treatments lasted 9 days (4 control and 5 experimental days). On day 5, autoregressive power spectral analysis was performed on heart rate recordings made in conscious rats. Other groups were used for sympathetic splanchnic nerve activity recordings made simultaneously with pressure (anesthetized rats) at basal condition and during loading/unloading of baroreceptors. Losartan treatment induced a significant reduction in basal pressure but did not interfere with the development of hypertension (similar pressure increases of 24% and 28% over control values in losartan and vehicle groups, respectively). In vehicle-treated rats, establishment of hypertension was accompanied by a marked change in power spectral density from high-(1.19Ϯ0.06 Hz, 33Ϯ6%) to low-frequency components (0,42Ϯ0.03 Hz, 54Ϯ6%), with increased low-frequency-to-high-frequency ratio. When compared with sham-operated vehicle-treated rats, there was also increase in the gain of sympathetic activity/pressure relationship, with displacement of lower plateau toward high levels of sympathetic activity. No changes in the power spectral density and sympathetic activity/pressure relationship were observed when hypertension developed in the presence of chronic angiotensin type 1 (AT 1 ) receptor blockade. The data suggest that angiotensin II, activated during the establishment of coarctation hypertension, acts via AT 1 receptors to alter sympathovagal balance, facilitating the sympathetic outflow to heart and peripheral circulation during baroreceptors unloading. Data also indicate that the observed effects are not conditioned by preexisting pressure levels. Key Words: receptors, angiotensin II Ⅲ losartan Ⅲ blood pressure Ⅲ heart rate Ⅲ hypertension, experimental Ⅲ rats I t is well known that the renin-angiotensin system (RAS) is involved in cardiovascular regulation and in the development/maintenance of hypertension. [1][2][3][4][5] The presence of an endogenous RAS in brain areas involved in cardiovascular regulation has been confirmed by several techniques. 3,6,7 Stimulation of high affinity angiotensin (Ang) II receptors 8 leads to a set of coordinated autonomic and endocrine responses yielding to blood pressure increase and hypertension. 1,2,5,8,9 Blockade of RAS usually reverses the angiotensin-induced effects simultaneously with a significant pressure reduction. It is not well established if the various autonomic/endocrine changes observed in hypertension were caused only by the direct effe...

show abstract

Section: Discussionmentioning

confidence: 95%

Section: Methodsmentioning

confidence: 99%

Chronic AT ₁ Receptor Blockade Alters Autonomic Balance and Sympathetic Responses in Hypertension

et al. 2001

View full text Add to dashboard Cite

show abstract

“…Indeed, chronic blockade of AT 1 receptors in coarcted hypertensive rats caused both a marked depression on Aogen expression within the NTS and area postrema and a significant blood pressure fall, 14 which occurred simultaneously with increased gain of arterial baroreceptors (high sensitivity and reduced variability of aortic nerve activity 17 ), reduced sympathovagal balance to the heart, 18 normalization of baroceptor reflex control of HR, and sympathetic nerve discharge, 16,18 thus correcting the deleterious changes induced by hypertension. 35,36 It is important to note that chronic treatment with losartan caused exactly the same effects of training on NTS Aogen expression: Aogen mRNA expression was markedly reduced in hypertensive rats pretreated with losartan without any significant change on AT 1A receptor density. 14 In addition, in the vehicle-treated groups (similar to the present observation in sedentary versus trained groups; Figure 3) there was a positive correlation between Aogen mRNA expression and basal MAP, which was significantly reduced in the presence of chronic AT 1 receptor blockade with losartan.…”

Section: Felix and Michelini Exercise Training And Brain Ras 783mentioning

confidence: 91%

Training-Induced Pressure Fall in Spontaneously Hypertensive Rats Is Associated With Reduced Angiotensinogen mRNA Expression Within the Nucleus Tractus Solitarii

Félix

Michelini

2007

Hypertension

View full text Add to dashboard Cite

Abstract-Knowing that exercise training reduces arterial pressure in hypertensive individuals and that pressure fall is accompanied by blockade of brain renin-angiotensin system, we sought to investigate whether training (T) affects central renin-angiotensin system. Spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto controls (WKY) were submitted to training or kept sedentary (S) for 3 months. After functional recordings, brain was removed and processed for autoradiography (brain stem sequential slices hybridized with 35 S-oligodeoxynucleotide probes for angiotensinogen [Aogen] and angiotensin II type 1 [AT 1A ] receptors). Resting arterial pressure and heart rate were higher in SHR S (177Ϯ2 mm Hg, 357Ϯ12 bpm versus 121Ϯ1 mm Hg, 320Ϯ9 bpm in WKY S ; PϽ0.05). Training was equally effective to enhance treadmill performance and to cause resting bradycardia (Ϫ10%) in both groups. Training-induced blood pressure fall (Ϫ6.3%) was observed only in SHR T . In SHR S (versus WKY S ) AT 1A and Aogen mRNA expression were significantly increased within the NTS and area postrema (average of ϩ67% and ϩ41% for AT 1A and Aogen, respectively; PϽ0.05) but unchanged in the gracilis nucleus. Training did not change AT 1A expression but reduced NTS and area postrema Aogen mRNA densities specifically in SHR T (PϽ0.05 versus SHR S , with values within the range of WKY groups). In SHRs, NTS Aogen mRNA expression was correlated with resting pressure (yϭ5.95x ϩ41; rϭ0.55; PϽ0.05), with no significant correlation in the WKY group. Concurrent training-induced reductions of both Aogen mRNA expression in brain stem cardiovascular-controlling areas and mean arterial pressure only in SHRs suggest that training is as efficient as the renin-angiotensin blockers to reduce brain renin-angiotensin system overactivity and to decrease arterial pressure. Key Words: angiotensin II Ⅲ angiotensin receptors Ⅲ blood pressure Ⅲ heart rate Ⅲ hypertension Ⅲ experimental Ⅲ rats T he renin-angiotensin system (RAS) is a widely distributed regulatory system with hormonal, paracrine, and intracrine functions in many tissues. 1-4 Brain RAS has been implicated in the pathogenesis (development/maintenance) of several forms of hypertension. 2,4 -6 All of the components of the RAS (precursor, enzymes, peptides, and receptors) are present in brain areas involved in cardiovascular control as the hypothalamic paraventricular nucleus and dorsal brain stem areas including the nucleus tractus solitarii (NTS), the dorsal motor nucleus of the vagus nerve, and the area postrema. 4,[7][8][9][10][11] It is important to notice that angiotensinogen (Aogen), angiotensin II (Ang II), and Ang II type 1 (AT 1A ) receptors are densely expressed within the NTS, indicating the importance of local RAS on cardiovascular control. 4,8,10 -14 In previous studies we showed both the close relationship between increased Aogen and Ang II AT 1A receptor mRNA expression in brain stem areas and elevated blood pressure 14 and the permissive role of Ang II to orchestrate, via AT 1 rec...

show abstract

“…This autonomic dysfunction seems to correlate with an increase in sympathetic outflow and in BP levels. 10 On the other hand, previous studies have demonstrated that regular exercise causes significant changes in baroreflex control of HR in experimental hypertension. Exercise training improves baroreflex control of HR during the increase and decrease of BP in spontaneously hypertensive rats.…”

mentioning

confidence: 98%

Exercise Training Restores Baroreflex Sensitivity in Never-Treated Hypertensive Patients

Laterza

Matos²,

Trombetta³

et al. 2007

Hypertension

232

165

View full text Add to dashboard Cite

Abstract-The effects of exercise training on baroreflex control of sympathetic nerve activity in human hypertension are unknown. We hypothesized that exercise training would improve baroreflex control of muscle sympathetic nerve activity (MSNA) and heart rate (HR) in patients with hypertension and that exercise training would reduce MSNA and blood pressure (BP) in hypertensive patients. Twenty never-treated hypertensive patients were randomly divided into 2 groups: exercise-trained (nϭ11; age: 46Ϯ2 years) and untrained (nϭ9; age: 42Ϯ2 years) patients. An age-matched normotensive exercise-trained group (nϭ12; age: 42Ϯ2 years) was also studied. Key Words: hypertension Ⅲ baroreflex sensitivity Ⅲ sympathetic nerve activity Ⅲ exercise Ⅲ blood pressure T here is accumulated evidence that arterial baroreflex plays an important role in the regulation of the cardiovascular system. During spontaneous variation of blood pressure (BP), stimulation or deactivation of the arterial baroreceptors located in the carotid sinus and aortic arch causes reflex bradycardia and tachycardia, respectively. At the vascular level, stimulation of the arterial baroreceptors results in sympathetic inhibition and, in consequence, reflex vasodilation. In contrast, the deactivation of the arterial baroreceptors elicits sympathetic-mediated vasoconstriction. 1 All of these responses work in concert to maintain the BP levels in the reference range. 1It has been described that arterial baroreflex sensitivity can be profoundly altered in some cardiovascular diseases. 2,3 In hypertension, some investigators, 4 -6 but not all, 7-9 observed that baroreflex control of heart rate (HR) and sympathetic nerve activity is significantly reduced. This autonomic dysfunction seems to correlate with an increase in sympathetic outflow and in BP levels. 10 On the other hand, previous studies have demonstrated that regular exercise causes significant changes in baroreflex control of HR in experimental hypertension. Exercise training improves baroreflex control of HR during the increase and decrease of BP in spontaneously hypertensive rats. 11,12 Furthermore, these studies indicate that the improvement in baroreflex sensitivity is, in part, mediated by the enhancement of the aortic depressor nerve sensitivity. In humans with hypertension, little information exists regarding the effects of exercise training on the baroreflex sensitivity. One of the few studies showed that exercise training caused a modest improvement in baroreflex bradycardia. 13 Thus, the effects of regular exercise on the baroreflex control of sympathetic nerve activity in humans with hypertension are unknown.It has been consistently shown that exercise training is a powerful nonpharmacological strategy to reduce BP levels in humans with hypertension. 14 -16 However, the mechanisms involved in the BP reduction after exercise training are still a matter of discussion. In the present study, we investigated the

show abstract

Baroreflex control of sympathetic activity in experimental hypertension

Cited by 36 publications

References 37 publications

Chronic AT ₁ Receptor Blockade Alters Autonomic Balance and Sympathetic Responses in Hypertension

Chronic AT ₁ Receptor Blockade Alters Autonomic Balance and Sympathetic Responses in Hypertension

Training-Induced Pressure Fall in Spontaneously Hypertensive Rats Is Associated With Reduced Angiotensinogen mRNA Expression Within the Nucleus Tractus Solitarii

Exercise Training Restores Baroreflex Sensitivity in Never-Treated Hypertensive Patients

Contact Info

Product

Resources

About

Baroreflex control of sympathetic activity in experimental hypertension

Cited by 36 publications

References 37 publications

Chronic AT 1 Receptor Blockade Alters Autonomic Balance and Sympathetic Responses in Hypertension

Chronic AT 1 Receptor Blockade Alters Autonomic Balance and Sympathetic Responses in Hypertension

Training-Induced Pressure Fall in Spontaneously Hypertensive Rats Is Associated With Reduced Angiotensinogen mRNA Expression Within the Nucleus Tractus Solitarii

Exercise Training Restores Baroreflex Sensitivity in Never-Treated Hypertensive Patients

Contact Info

Product

Resources

About

Chronic AT ₁ Receptor Blockade Alters Autonomic Balance and Sympathetic Responses in Hypertension

Chronic AT ₁ Receptor Blockade Alters Autonomic Balance and Sympathetic Responses in Hypertension