Cardiac hypertrophy and telemetered blood pressure 6 wk after baroreceptor denervation in normotensive rats

Vliet, Bruce N. Van; Hu, Ling Qun; Scott, T. M.; Chafe, L.; Montani, Jean‐Pierre

doi:10.1152/ajpregu.1996.271.6.r1759

Cited by 34 publications

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“…9,10 However, in normal rats with intact baroreceptors, BP varies within a relatively narrow range 10 -12 ; therefore, it is not known whether the kidney is able to cope with transient large fluctuations of BP, such as those occurring spontaneously in the sinoaortic baroreceptor-denervated (SAD) rat. [11][12][13][14] In the present study, RBF and BP were simultaneously recorded during long periods of spontaneous activity in conscious SAD rats. Rats were studied 2 weeks after surgery, ie, in the early chronic phase of denervation, when mean levels of BP are nearly normal and BP variability is markedly increased.…”

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confidence: 87%

Renal Blood Flow Dynamics and Arterial Pressure Lability in the Conscious Rat

et al. 2001

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Abstract-It is not known whether renal blood flow (RBF) is still autoregulated when the kidney is exposed to large transient blood pressure (BP) fluctuations such as those occurring spontaneously in conscious sinoaortic baroreceptordenervated (SAD) rats. In this study, BP and RBF were simultaneously recorded in 8 SAD rats (2 weeks before study) and 8 baroreceptor-intact rats during Ϸ3 hours of spontaneous activity. The kidney used for RBF recordings was denervated to prevent the interference of changes in renal sympathetic tone with autoregulatory mechanisms. In intact rats, RBF variability (coefficient of variation 9.1Ϯ0.8%) was larger (PϽ0.02) than BP variability (5.9Ϯ0.2%). This was mainly because of slow changes in RBF that were unrelated to BP and also to a prominent oscillation of RBF of Ϸ0.25-Hz frequency. Autoregulatory patterns were identified at frequencies Ͻ0. Key Words: autoregulation Ⅲ blood pressure Ⅲ rats Ⅲ denervation A lthough hemodynamic factors are likely to play a role in the progression of renal failure, 1,2 the possible deleterious effects of an exaggerated blood pressure (BP) variability on the kidney have not yet been established. It is often proposed that autoregulatory mechanisms prevent acute changes in systemic BP from being transmitted to the glomerular capillary circulation. 3 Most studies on renal blood flow (RBF) autoregulation have been performed in anesthetized rats, with the use of either induced 4 or spontaneous 5 changes in BP. In the conscious rat, RBF autoregulation has been described by measuring RBF responses to steady-state changes in renal perfusion pressure induced by reversible constrictions of the abdominal aorta above or below the renal arteries. 6,7 This technique suffers from 2 major limitations. First, it is difficult to determine the higher limit of autoregulation because it is impossible to raise renal perfusion pressure by Ͼ20% to 25% with the use of an aortic cuff. Second, the technique overlooks the essentially dynamic nature of autoregulation. 8 Spontaneous autoregulatory patterns have been reported in the renal circulation of conscious rats. 9,10 However, in normal rats with intact baroreceptors, BP varies within a relatively narrow range 10 -12 ; therefore, it is not known whether the kidney is able to cope with transient large fluctuations of BP, such as those occurring spontaneously in the sinoaortic baroreceptor-denervated (SAD) rat. [11][12][13][14] In the present study, RBF and BP were simultaneously recorded during long periods of spontaneous activity in conscious SAD rats. Rats were studied 2 weeks after surgery, ie, in the early chronic phase of denervation, when mean levels of BP are nearly normal and BP variability is markedly increased. 11,14 Sympathetic nerves play a major role in promoting behaviorally coupled changes in RBF 15 and are probably also involved in generating BP fluctuations in SAD rats, at least the acute pressor episodes. 16 To avoid the interference of sympathetically mediated vasoconstriction with autoregulatory responses, t...

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confidence: 87%

Renal Blood Flow Dynamics and Arterial Pressure Lability in the Conscious Rat

et al. 2001

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“…At 12 weeks, rats underwent the bilateral SAD according to the procedure described previously by Krieger 22 and van Vliet et al 23,24 At 18 weeks (6 weeks after the SAD operation), rats underwent the implantation of a BP radiotelemeter (model TA 11 PA-C 40, Data Sciences International). Seven days after the telemeter implantation (19 weeks), 24-hour BP and heart rate were monitored in unrestricted, conscious rats.…”

Section: Bilateral Sad Telemetric Hemodynamic Monitoringmentioning

confidence: 99%

“…Accordingly, in the present study, we investigated whether the angII system-mediated inflammation would be involved in the mechanism underlying the large BPV-induced aggravation of hypertensive remodeling. For this purpose, we created a rat model representing chronic hypertension with exaggerated BPV by performing bilateral sinoaortic denervation (SAD) [22][23][24] in spontaneously hypertensive rats (SHRs). …”

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Exaggerated Blood Pressure Variability Superimposed on Hypertension Aggravates Cardiac Remodeling in Rats via Angiotensin II System-Mediated Chronic Inflammation

et al. 2009

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Abstract-Hypertensive patients with large blood pressure variability (BPV) have aggravated end-organ damage.However, the pathogenesis remains unknown. We investigated whether exaggerated BPV aggravates hypertensive cardiac remodeling and function by activating inflammation and angiotensin II-mediated mechanisms. A model of exaggerated BPV superimposed on chronic hypertension was created by performing bilateral sinoaortic denervation (SAD) in spontaneously hypertensive rats (SHRs). SAD increased BPV to a similar extent in Wistar Kyoto rats and SHRs without significant changes in mean blood pressure. SAD aggravated left ventricular and myocyte hypertrophy and myocardial fibrosis to a greater extent and impaired left ventricular systolic function in SHRs. SAD induced monocyte chemoattractant protein-1, transforming growth factor-␤, and angiotensinogen mRNA upregulations and macrophage infiltration of the heart in SHRs. The effects of SAD on cardiac remodeling and inflammation were much smaller in Wistar Kyoto rats compared with SHRs. Circulating levels of norepinephrine, the active form of renin, and inflammatory cytokines were not affected by SAD in Wistar Kyoto rats and SHRs. A subdepressor dose of candesartan abolished the SAD-induced left ventricular/myocyte hypertrophy, myocardial fibrosis, macrophage infiltration, and inductions of monocyte chemoattractant protein-1, transforming growth factor-␤, and angiotensinogen and subsequently prevented systolic dysfunction in SHRs with SAD. These findings suggest that exaggerated BPV induces chronic myocardial inflammation and thereby aggravates cardiac remodeling and systolic function in hypertensive hearts. The cardiac angiotensin II system may play a role in the pathogenesis of cardiac remodeling and dysfunction induced by a combination of hypertension and exaggerated BPV. Key Words: blood pressure variability Ⅲ hypertension Ⅲ inflammation Ⅲ angiotensin II Ⅲ cardiac hypertrophy T he goal of hypertension treatment is not only to reduce blood pressure (BP) levels but also to prevent cardiovascular events. Among hypertensive patients, patients with large BP variability (BPV) have more advanced end-organ damage, such as left ventricular (LV) hypertrophy and carotid atherosclerosis. [1][2][3][4][5][6][7] Recent studies have shown that exaggerated BPV is a risk factor for cardiovascular events in hypertensive patients, 8 -10 independent of diurnal BP changes. 11 An exaggerated BPV is a characteristic feature of hypertension, especially in the elderly and in patients with carotid atherosclerosis. 12-14 However, little is known about the mechanism underlying the aggravation of end-organ damage induced by a combination of hypertension and large BPV aggravates.Our recent studies have shown that perivascular inflammation plays a pivotal role in hypertensive cardiac remodeling, especially in myocardial fibrosis (for review see References 15 and 16): in Wistar Kyoto rats (WKYs) with suprarenal aortic constriction, BP elevation induces perivascular inflammation characterized by ...

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“…Modified from Eto et al 16 Circulation Journal Vol.73, December 2009 includes ablation of the aortic depressor nerve and superior laryngeal nerve, resection of the superior cervical ganglia and cervical sympathetic trunks, and denervation of the aortic and carotid sinus baroreceptors. [20][21][22] Sympathetic nerve activity is transiently increased soon after SAD and activation wanes within a couple of weeks. Seven weeks after the SAD operation, the circulating and myocardial norepinephrine levels were similar in WKY with sham operation (WKY+ sham), WKY with SAD (WKY+ SAD), SHR with sham operation (SHR + sham) and SHR with SAD (SHR + SAD).…”

Section: A Rat Model Of a Combination Of Hypertension And Large Bp Vamentioning

confidence: 99%

Large Blood Pressure Variability and Hypertensive Cardiac Remodeling Role of Cardiac Inflammation

Kai

Kudo

Takayama

et al. 2009

Circ J

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iurnal blood pressure (BP) change, such as nocturnal BP fall, is an established risk for target organ damage and cardiovascular events. [1][2][3][4] Along with diurnal BP change, an increase in short-term BP variability is a characteristic feature of hypertension, especially in the elderly and in patients with carotid atherosclerosis. [5][6][7][8] Among hypertensive patients with similar BP levels, the degree of hypertensive target organ damage is more advanced in patients with larger BP variability. 9-11 However, little is known about the mechanism whereby a combination of hypertension and large BP variability aggravates target organ damage. In this article, we review the clinical relevance of BP variability in hypertensive patients, and introduce our recent studies showing that chronic cardiac inflammation plays a role in aggravating hypertensive cardiac remodeling in a novel rat model of hypertension and large BP variability. Short-Term BP Variability and Hypertensive Target Organ DamageTwenty-four-hour BP varies not only because of a reduction during night sleep (diurnal BP change), but also because of sudden, fast and short-lasting changes (short-term BP variability) that may occur both during the day and, to a lesser extent, during the night. 12 It has been shown that short-term BP variability increases in hypertensive patients as their BP levels increase, when quantified as the standard deviations (SDs) of the BP values recorded intra-arterially in 30-min intervals. 5 Parati et al investigated the incidence and the severity of target organ damage in 108 hypertensive patients. 9 The patients were divided into 5 groups according to the increasing value of their 24-h average mean BP, and the subjects in each group were further subdivided into 2 classes according to whether their intra-half-hour SD of mean BP, ie, short-term BP variability, was below or above the average of SDs of all the study patients. Within each group, although the 2 classes had a similar 24-h mean BP, the incidence and the severity of target organ damage were greater in the class in which short-term BP variability was higher (Figure 1). 9 Palatini et al studied 67 normotensive patients and 171 borderline, 309 mild, 140 moderate and 41 severe hypertensive patients with noninvasive ambulatory BP monitoring. 10 Each patient was assigned a target organ damage score of 0 to 5 on the basis of funduscopic changes and degree of left ventricular (LV) hypertrophy calculated from ECG and chest roentgenogram. An increased daytime BP variability was associated with a higher degree of hypertensive cardiovascular complications. 10 Moreover, a longitudinal study revealed that the degree of target organ damage and echocardiographic LV hypertrophy at a followup examination (4-13 years later, mean 7.4 years) depended on the extent of 24-h BP variability at the time of the initial evaluation, independently of the 24-h mean BP, in 73 Large Blood Pressure Variability andHypertensive Cardiac Remodeling Role of Cardiac InflammationHisashi Kai, MD; Hiroshi Kudo...

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Cardiac hypertrophy and telemetered blood pressure 6 wk after baroreceptor denervation in normotensive rats

Cited by 34 publications

References 0 publications

Renal Blood Flow Dynamics and Arterial Pressure Lability in the Conscious Rat

Renal Blood Flow Dynamics and Arterial Pressure Lability in the Conscious Rat

Exaggerated Blood Pressure Variability Superimposed on Hypertension Aggravates Cardiac Remodeling in Rats via Angiotensin II System-Mediated Chronic Inflammation

Large Blood Pressure Variability and Hypertensive Cardiac Remodeling Role of Cardiac Inflammation

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