Modulation of Cardiac Autonomic Control in Humans by Angiotensin II

Townend, Jonathan N.; Al-Ani, Muzahim; West, J. M.; Littler, W. A.; Coote, John H.

doi:10.1161/01.hyp.25.6.1270

Cited by 78 publications

(54 citation statements)

References 32 publications

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“…21,[27][28][29] Many studies have demonstrated that HT volunteers exhibit a reduction in HRV that is associated with a decrease in vagal autonomic modulation and an increase in sympathetic modulation. [30][31][32] Our study demonstrated that untreated HT volunteers presented an increase in HVR that was characterized by an increase in total variance in the RRi compared with NT and HT volunteers treated with Enalapril. Although this increase appears paradoxical, it was the result of an increase in sympathetic autonomic modulation because the LF oscillations in these volunteers were notably high.…”

Section: Discussionmentioning

confidence: 57%

“…Indeed, ACEis and AT1 receptor antagonists promote an improvement in autonomic function in different contexts, including baroreflex sensitivity evaluation and HRV analysis. 11,28,30,36,37 The mechanisms that underlie ACEi improvement of HRV modulation have not been elucidated, but ACEis and/or AT1-receptor antagonists primarily affect neural sites that are involved in the cardiovascular regulation, such as the solitary tract nucleus, rostral ventrolateral medulla, paraventricular nucleus and area postrema. However, the identification of the exact mechanism of action has been hindered by the complex interaction of the sites involved in cardiovascular control.…”

Section: Discussionmentioning

confidence: 99%

“…However, the identification of the exact mechanism of action has been hindered by the complex interaction of the sites involved in cardiovascular control. 30,[38][39][40] Similar to Enalapril, physical training also reduces arterial pressure. The combination of Enalapril and physical training enhanced the reduction of AP, which reached values that were similar to the NT volunteers.…”

Section: Discussionmentioning

confidence: 99%

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Physical exercise improves cardiac autonomic modulation in hypertensive patients independently of angiotensin-converting enzyme inhibitor treatment

et al. 2011

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We investigated the influence of angiotensin-converting enzyme inhibitor (ACEi) treatment and physical exercise on arterial pressure (AP) and heart rate variability (HRV) in volunteer patients with hypertension. A total of 54 sedentary volunteers were divided into three groups: normotensive (NT Group), hypertensive (HT Group) and HT volunteers treated with ACEi (ACEi Group). All volunteers underwent an aerobic physical-training protocol for 15 weeks. HRV was investigated using a spectral analysis of a time series of R-R interval (RRi) that was obtained in a supine position and during a tilt test. Physical training promoted a significant reduction in the mean arterial pressure of the HT group (113 ± 3 vs. 106 ± 1 mm Hg) and the ACEi group (104 ± 2 vs. Keywords: aerobic physical training; angiotensin; heart rate variability INTRODUCTION Hypertension is highly prevalent in the adult population and represents one of the leading causes of morbidity and mortality worldwide. 1,2 This condition is directly related to the development of cardiovascular diseases, encephalic vascular accident and renal insufficiency. 3 The risk factors for hypertension are associated with many other factors, including lifestyle. 4 The excessive ingestion of salt and alcohol, obesity, smoking and sedentariness represent the main behavioral factors that contribute to the occurrence and development of hypertension. 5 The treatment of hypertension consists mainly of a pharmacological approach, and the angiotensin-converting enzyme inhibitors (ACEis) are an important class of medications. 6 ACEis reduce arterial pressure (AP) by decreasing the peripheral vascular resistance, and they reduce cardiac hypertrophy and the proliferation of vascular smooth muscle cells. 7-9 Additionally, ACEis have an important role in cardiac autonomic control. Some studies have shown that ACEi treatment of hypertension in experimental animals and humans improves baroreflex

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Section: Discussionmentioning

confidence: 57%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Physical exercise improves cardiac autonomic modulation in hypertensive patients independently of angiotensin-converting enzyme inhibitor treatment

et al. 2011

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“…39 Both sympathetic tone and cardiac vagal activity are known to be favourably modified by the reduction of circulating angiotensin II. 43,44 In the ramipril-treated aortic banded rats, regression of compensatory hypertrophy was also paralleled by improved survival: 31% died in the placebo treated group during 12 weeks follow-up compared with 11% in the ramipril-treated group. 37 …”

Section: Increased Survivalmentioning

confidence: 91%

ACE inhibition in aortic stenosis: dangerous medicine or golden opportunity?

Routledge

Townend

2001

J Hum Hypertens

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Conventionally angiotensin-converting enzyme (ACE) inhibitors are contraindicated in patients with aortic stenosis. Abundant evidence is now available showing that angiotensin II has a central role in the development of left ventricular hypertrophy (LVH), myocardial contractile failure and diastolic dysfunction in response to pressure overload. In animal models, ACE inhibitors have been shown to attenuate these pathological responses. In humans there is no such evidence available, however uncontrolled studies have shown that

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“…HF is characterized by altered neural cardiovascular regulation, including increased resting sympathetic nerve activity to the heart and vasculature, depressed vagal outflow to the heart, and attenuated baroreflex control of HR (6,31,33,36,37). Recently, Iellamo et al (14) found that the spontaneous baroreflex control of HR in HF subjects was significantly depressed compared with normal subjects.…”

Section: Cardiac Baroreflex Responses In Hfmentioning

confidence: 99%

Spontaneous baroreflex control of heart rate versus cardiac output: altered coupling in heart failure

Sala‐Mercado

Ichinose

Hammond

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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Sala-Mercado JA, Ichinose M, Hammond RL, Coutsos M, Ichinose T, Pallante M, Iellamo F, O'Leary DS. Spontaneous baroreflex control of heart rate versus cardiac output: altered coupling in heart failure. Am J Physiol Heart Circ Physiol 294: H1304-H1309, 2008. First published January 11, 2008 doi:10.1152/ajpheart.01186.2007.-Dynamic cardiac baroreflex responses are frequently investigated by analyzing the spontaneous reciprocal changes in arterial pressure and heart rate (HR). However, whether the spontaneous baroreflex-induced changes in HR translate into changes in cardiac output (CO) is unknown. In addition, this linkage between changes in HR and changes in CO may be different in subjects with heart failure (HF). We examined these questions using conscious dogs before and after pacing-induced HF. Spontaneous baroreflex sensitivity in the control of HR and CO was evaluated as the slopes of the linear relationships between HR or CO and left ventricular systolic pressure (LVSP) during spontaneous sequences of greater or equal to three consecutive beats when HR or CO changed inversely versus pressure. Furthermore, the translation of baroreflex HR responses into CO responses (HR-CO translation) was examined by computing the overlap between HR and CO sequences. In normal resting conditions, 44.0 Ϯ 4.4% of HR sequences overlapped with CO sequences, suggesting that only around half of the baroreflex HR responses cause CO responses. In HF, HR-LVSP, CO-LVSP, and the HR-CO translation significantly decreased compared with the normal condition (Ϫ2.29 Ϯ 0.5 vs. Ϫ5.78 Ϯ 0.7 beats ⅐ min Ϫ1 ⅐ mmHg Ϫ1 ; Ϫ70.95 Ϯ 11.8 vs. Ϫ229.89 Ϯ 29.6 ml ⅐ min Ϫ1 ⅐ mmHg Ϫ1 ; and 19.66 Ϯ 4.9 vs. 44.0 Ϯ 4.4%, respectively). We conclude that spontaneous baroreflex HR responses do not always cause changes in CO. In addition, HF significantly decreases HR-LVSP, CO-LVSP, and HR-CO translation.arterial baroreflex sensitivity; parasympathetic activity; stroke volume THE ARTERIAL BAROREFLEX is the primary short-term regulator of systemic blood pressure via modulation of parasympathetic and sympathetic nerve activity (26). Changes in arterial blood pressure result in arterial baroreflex-mediated reciprocal changes in heart rate (HR) and total peripheral resistance. Arterial baroreflex sensitivity (cardiac component) has often been assessed via techniques that analyze normally occurring spontaneous changes in blood pressure and the reciprocal changes in HR (3,12,21,32). This technique has been used as an index of cardiac baroreflex function in a number of species, including humans, and in many experimental and pathological conditions (1,3,11,13,18,21,25,32). Sinoaortic baroreflex denervation virtually abolishes baroreflex sensitivity assessed via this method, indicating that the spontaneous reciprocal changes in HR that occur as a result of changes in arterial pressure are indeed mediated by the baroreflex (1, 19). However, changes in HR do not necessarily dictate changes in cardiac output (CO) because stroke volume (SV) may also vary, for example, with ...

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Modulation of Cardiac Autonomic Control in Humans by Angiotensin II

Cited by 78 publications

References 32 publications

Physical exercise improves cardiac autonomic modulation in hypertensive patients independently of angiotensin-converting enzyme inhibitor treatment

Physical exercise improves cardiac autonomic modulation in hypertensive patients independently of angiotensin-converting enzyme inhibitor treatment

ACE inhibition in aortic stenosis: dangerous medicine or golden opportunity?

Spontaneous baroreflex control of heart rate versus cardiac output: altered coupling in heart failure

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