Reduced spontaneous baroreceptor sensitivity in patients with renovascular hypertension

Gao, Sinsia A.; Johansson, Mats; Rundqvist, Bengt; Lambert, Gavin W.; Jensen, Gert; Friberg, Peter

doi:10.1097/00004872-200201000-00016

Cited by 35 publications

(27 citation statements)

References 20 publications

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“…9 -11 Importantly, examining the same patient with or without renal hypertension did not show any difference in total noradrenaline spillover. 9,11 Reports of noradrenaline turnover in 2K1C rabbits have found no change in turnover from a range of tissues suggesting that there is not a generalized change in sympathetic activity in this model. 12 Thus there is a paradox.…”

mentioning

confidence: 70%

“…Results from a "within-patient" study, before and 12 months after reversal of renovascular hypertension, showed no change in total noradrenaline spillover, suggesting that the hypertension did not elevate global sympathetic activity. 11 Thus our assumption that RSNA reflects sympathetic activity in other beds is reasonable, but we cannot be certain about this without direct recordings. Nevertheless, our studies and others do not support the view that the activity of the sympathetic nervous system in general is enhanced in renovascular hypertension.…”

Section: Head and Burke Sympathetic Responses In Hypertensive Rabbitsmentioning

confidence: 93%

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Sympathetic Responses to Stress and Rilmenidine in 2K1C Rabbits

Head

Burke

2004

Hypertension

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Abstract-We determined whether the sympathetic excitatory responses to environmental stressors and the sympathoinhibitory responses to rilmenidine are altered by renovascular hypertension. Rabbits were made hypertensive with a clip on the right renal artery, and a left renal nerve recording electrode was implanted. After 3 or 6 weeks, the animals were given air-jet stress and loud noise stress before and after intravenous rilmenidine. Three and 6 weeks after renal clipping, mean arterial pressure was 28% and 36% greater than preclip values. Air-jet stress elicited a marked increase in renal sympathetic nerve activity, mean arterial pressure, and heart rate. Renal sympathetic nerve activity responses were much greater in hypertensive rabbits, but the pressor responses were similar to those observed in normotensive animals. Acute administration of rilmenidine decreased blood pressure more in hypertensive animals but with a much lesser inhibition of sympathetic activity. Rilmenidine markedly reduced increased sympathetic activity during air-jet stress in 3-week clipped rabbits but to a lesser extent in the other groups. These studies show that while sympathetic responses to stress were markedly enhanced in renal clip hypertensive rabbits, they did not result in greater pressor responses, thus suggesting that vascular neuroeffector mechanisms were not altered. By contrast, the increased effects of rilmenidine suggest a much greater contribution to the hypertension by the sympathetic nervous system, but one that is caused by an enhanced "nonvascular" neuroeffector mechanism. As such, sympathoinhibitory agents such as rilmenidine are very suitable and very effective agents for the treatment of renovascular hypertension. Key Words: renal nerves Ⅲ hypertension Ⅲ stress Ⅲ sympathetic nervous system Ⅲ rabbits Ⅲ blood pressure Ⅲ heart rate T here has been a long-standing interest in the role of the sympathetic nervous system in hypertension, but more so in view of increasing evidence that it can contribute to the long-term setting of blood pressure. 1 In renovascular hypertension, there is much evidence for a greater dependence of the hypertension on the sympathetic nervous system. 2 A greater depressor response to ganglion blockade has been observed in renal wrap hypertensive rats. 3 Studies in the rabbit by Cox and Bishop showed that during angiotensin (Ang) infusion, the hypertension was initially caused by Ang-mediated vasoconstriction that subsided and was replaced by a greater neurogenic component. 4 One of the major difficulties in determining the contribution of the sympathetic nervous system in hypertension has been in making direct comparisons of microvolt values between different groups. Recently, we developed a novel method for comparing sympathetic activity between groups of animals 5 and found that renal sympathetic nerve activity (RSNA) is not increased but initially decreased or unchanged in 2-kidney 1-clip (2K1C) hypertensive rabbits. 6 Studies in renal wrap 7 and chronic Ang-induced hypertension 8 support...

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confidence: 70%

Section: Head and Burke Sympathetic Responses In Hypertensive Rabbitsmentioning

confidence: 93%

Sympathetic Responses to Stress and Rilmenidine in 2K1C Rabbits

Head

Burke

2004

Hypertension

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“…97 The secondary pathophysiological effects process includes elevation of renin levels, diminished peripheral and renal angiotensin II receptor response, 102 increased sympathetic tone, 103 and reduced baroreceptor sensitivity. 104 Elevation of renal vein renin is characteristic of renovascular hypertension, but the negative predictive value is low because phase III renovascular hypertension is associated with low renin levels. 97 Embolization from the aorta may also play a role in the pathophysiology of end-stage renal disease and hypertension, although evidence is scarce.…”

Section: Regional Disease Statesmentioning

confidence: 99%

Atherosclerotic Vascular Disease Conference

Faxon¹,

Fuster²,

Libby³

et al. 2004

Circulation

309

144

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“…Oxidative stress in the brain was suggested to contribute to SNS activation in other hypertensive models, [37][38][39][40] and BRS was impaired in other hypertensive models. 41,42) Thus, it is possible that the results obtained in the present study might be common in hypertensive models. Further studies are needed to determine these issues.…”

Section: Discussionmentioning

confidence: 78%

Inhibition of Oxidative Stress in Rostral Ventrolateral Medulla Improves Impaired Baroreflex Sensitivity in Stroke-Prone Spontaneously Hypertensive Rats

et al. 2012

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SummaryReactive oxygen species (ROS) in rostral ventrolateral medulla (RVLM) of brainstem contribute to sympathoexcitation and are critically involved in the pathogenesis of hypertension. Baroreflex sensitivity (BRS) is a valuable prognostic parameter of the autonomic nervous system, and is impaired in hypertension. The aim of the present study was to determine whether or not a chronic reduction of ROS in the RVLM improves impaired BRS in hypertensive rats. We transfected adenovirus vectors encoding either manganese superoxide dismutase (AdMnSOD) or β-galactosidase (AdLacZ) into the RVLM of stroke-prone spontaneously hypertensive rats (SHRSP). We measured BRS using the spontaneous sequence method. BRS was significantly lower in SHRSPs than in Wistar-Kyoto rats. In the AdMnSOD-transfected SHRSP, blood pressure, heart rate, and sympathetic nervous system activation were significantly decreased from day 5 after the gene transfer. BRS in the AdMnSOD-transfected SHRSP was significantly increased from day 4 after the gene transfer with the reduction of ROS in the RVLM. Furthermore, in the AdMnSOD-transfected SHRSP, intravenous infusion of atropine dramatically decreased BRS. In contrast, in the AdLacZ-transfected SHRSP, atropine did not decrease BRS. These results suggest that chronic reduction of ROS in the local RVLM improves the impaired BRS in SHRSP through inhibition of the sympathetic component. (Int Heart J 2012; 53: 193-198) Key words: Baroreflex sensitivity, Reactive oxygen species, Brain, Sympathetic nervous system, Hypertension A change in arterial blood pressure (BP), such as that resulting from postural change, is detected by baroreceptors, and the afferent nerves provide the information to the central nervous system. 1,2) The arterial baroreflex regulated by the central nervous system acts to oppose the increase in BP by inhibiting sympathetic activity, causing vasodilation and slowing heart rate (HR) in the short-term. 1,2)Previous reports have suggested that baroreflex sensitivity (BRS) is impaired in cardiovascular diseases such as hypertension, [3][4][5][6] heart failure, 7,8) and myocardial infarction. 9) It has been suggested that BP variability, which is a cardiovascular risk factor, contributes to end-organ damage. [10][11][12] The assessment of BRS has been considered to be the established tool for the evaluation of autonomic control of the cardiovascular system.9,13) Classically, BRS has been evaluated by the drug-induced Oxford method.14) However, pharmacological assessment of BRS is difficult to determine repeatedly in humans, but can be done in acute experiments with anesthetized animals. Recently, the spontaneous sequence method has proved to be a reliable and noninvasive method for assessing BRS, and the assessment of BRS can now be performed repeatedly in humans and animals in a conscious state. 4,15) The rostral ventrolateral medulla (RVLM) is the vasomotor center that determines basal sympathetic nervous system (SNS) activation, and is responsible for maintaining sympathetic out flow...

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Reduced spontaneous baroreceptor sensitivity in patients with renovascular hypertension

Abstract: Patients with renovascular hypertension showed reduced cardiac baroreceptor reflex sensitivity and increased noradrenergic activity, which to some extent was reversed 1 year following successful renal angioplasty.

Cited by 35 publications

References 20 publications

Sympathetic Responses to Stress and Rilmenidine in 2K1C Rabbits

Sympathetic Responses to Stress and Rilmenidine in 2K1C Rabbits

Atherosclerotic Vascular Disease Conference

Inhibition of Oxidative Stress in Rostral Ventrolateral Medulla Improves Impaired Baroreflex Sensitivity in Stroke-Prone Spontaneously Hypertensive Rats

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