Contribution of baroreceptors and chemoreceptors to ventricular hypertrophy produced by sino‐aortic denervation in rats

Vliet, Bruce N. Van; Chafe, L.; Montani, Jean‐Pierre

doi:10.1111/j.1469-7793.1999.0885u.x

Cited by 38 publications

(52 citation statements)

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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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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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“…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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confidence: 99%

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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“…A midline incision was made in the anterior neck and the area of the carotid bifurcation was exposed. The internal, external, and common carotid arteries were stripped of connective tissues, and the region was painted with 10% phenol in ethanol, as reported previously in rats (12,24). The recovery period from the carotid denervation was at least 4 days before the measurements of HR and MAP.…”

Section: Surgical Proceduresmentioning

confidence: 99%

Enhanced baroreflex sensitivity in free-moving calponin knockout mice

Masuki¹,

Takeoka

Taniguchi

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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Masuki, Shizue, Michiko Takeoka, Shun'ichiro Taniguchi, and Hiroshi Nose. Enhanced baroreflex sensitivity in free-moving calponin knockout mice. Am J Physiol Heart Circ Physiol 284: H939-H946, 2003. First published November 14, 2002 10.1152/ajpheart.00610.2002Calponin is an actin binding protein in vascular smooth muscle that modifies contractile responses. However, its role in mean arterial pressure (MAP) regulation has not been clarified. To assess this, MAP and heart rate (HR) were measured in calponin knockout (KO) mice, and the results were compared with those in wild-type (WT) mice. The measurements were performed every 100 ms during a 60-min free-moving state each day for 3 days. Mice in both groups rested during ϳ70% of the total measuring period. The mean HR during rest was significantly lower in KO mice than in WT mice but with no significant difference in MAP between the groups. The change in HR response (⌬HR) to spontaneous change in MAP (⌬MAP) varied in a wider range in KO mice with an 80% increase in the coefficient of variation for HR (P Ͻ 0.05), whereas MAP in KO mice was controlled in a narrow range similar to that in WT mice. The baroreflex sensitivity (⌬HR/ ⌬MAP), determined from the change in HR to the spontaneous change in MAP, was twofold higher in KO mice than that in WT mice (P Ͻ 0.01), whereas there were no significant differences in the baroreflex sensitivity determined by intravascular administration of phenylephrine and sodium nitroprusside between the two groups (P Ͼ 0.1). The MAP response to the administrated doses of phenylephrine in KO mice was reduced to one-half of that in WT mice (P Ͻ 0.01) but with no significant difference in the response to sodium nitroprusside between the groups. The differences in HR variability and the spontaneous baroreflex sensitivity between the two groups completely disappeared after carotid sinus denervation. These results suggest that the higher variability in HR for KO mice was caused by the increased spontaneous arterial baroreflex sensitivity, though not detected by the intra-arterial administration of the drug, and that the higher variability of HR may be a compensatory adaptation to the blunted ␣-adrenergic response of peripheral vessels to sympathetic nervous activity.carotid sinus denervation; heart rate variability CALPONIN, also called basic calponin or calponin H1, was first isolated from the chicken gizzard as an actinbinding protein, which was reported to be involved in the regulation of smooth muscle contraction (22). Calponin was reported to reduce unloaded isometric forces and shortening velocity (8,14,19,23) by the inhibition of actomyosin ATPase activity in a reconstituted isolated filament system (26). On the other hand, there have been several studies suggesting that calponin increases the contractile response to norepinephrine (NE) (18) or phenylephrine (PE) (9,16,20) by facilitating agonist-induced signal transduction.With the exception of these in vitro studies, however, there have been few studies investigating the role of cal...

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Contribution of baroreceptors and chemoreceptors to ventricular hypertrophy produced by sino‐aortic denervation in rats

Cited by 38 publications

References 36 publications

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

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

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

Enhanced baroreflex sensitivity in free-moving calponin knockout mice

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