Biomedical subjects

He-Hui Xie

Publications and source records attributed to He-Hui Xie.

At least 19 recordsLinked to original sources

PubMed2006

Blood pressure variability, baroreflex sensitivity and organ damage in spontaneously hypertensive rats treated with various antihypertensive drugs.

Besides blood pressure, blood pressure variability and baroreflex sensitivity maybe important factors determining organ damage in hypertension. This study was designed to investigate the effects of various antihypertensive drugs on blood pressure and blood pressure variability reductions, baroreflex sensitivity, and target organ damage in spontaneously hypertensive rats (SHR). The dose is 20 mg/kg/day for atenolol, and 10 mg/kg/day for nifedipine, irbesartan and hydrochlorothiazide. We used relatively low doses of drugs to avoid a very remarkable normalization of blood pressure in the treatment, which would make it much difficult to distinguish the contribution of blood pressure variability and baroreflex sensitivity to organ protection from that of blood pressure. Drugs at the aforementioned doses were mixed into rat chow. SHR were treated for 4 months. Blood pressure was then continuously recorded for 24 h. After the determination of baroreflex sensitivity, rats were killed for organ-damage evaluation. It was found that long-term treatment with atenolol, nifedipine, irbesartan or hydrochlorothiazide all markedly reduced blood pressure variability, enhanced baroreflex sensitivity, and produced significant organ protection. Compared with blood pressure level, blood pressure variability and baroreflex sensitivity values showed a much closer or similar relationship with organ-damage parameters in every treatment group of rats. Multiple-regression analysis showed that the decrease in left ventricular hypertrophy, the decrease in aortic hypertrophy and the amelioration in renal lesion were all most closely correlated with the increase in baroreflex sensitivity and the decrease in systolic blood pressure variability. In conclusion, long-term treatment with atenolol, nifedipine, irbesartan or hydrochlorothiazide produced organ protection in SHR. Besides the blood pressure reduction, the decrease in blood pressure variability and the restoration of baroreflex sensitivity may contribute to this organ protection.

Animals↗

PubMed2006

Blood pressure variability is more important than blood pressure level in determination of end-organ damage in rats.

OBJECTIVE: This study was designed to determine how important a novel risk factor of elevated blood pressure variability (BPV) is in the determination of end-organ damage by comparison with the classic risk factor of a high blood pressure (BP) level. METHODS AND RESULTS: The effects of haemodynamics on cardiovascular morphology were evaluated by univariate and multivariate regression analysis in two different rat models with an enlarged distribution of haemodynamics. In male sham-operated and sinoaortic-denervated Wistar-Kyoto rats and spontaneously hypertensive rats (n = 34), BPV was more important than BP in cardiac and renal damage and aortic hypertrophy. BPV and BP had independent effects, explaining 59.4% of the variation in damage to these organs. In male (n = 44) and female (n = 46) F1 hybrids of Sprague-Dawley rats and spontaneously hypertensive rats, the greater importance of BPV than BP was further demonstrated in left ventricular hypertrophy, glomerular damage and aortic hypertrophy. The phenomenon was more evident in females than males for cardiovascular hypertrophy. BPV and BP or BPV alone had independent effects, explaining 46.9% (male) or 37.5% (female) of the variation in damage to these organs. CONCLUSION: BPV is a more critical determinant than BP level for cardiac damage, renal lesions and aortic hypertrophy in rats, strongly suggesting the significance of BPV control for the protection of these organs.

Animals↗

PubMed2006

Early structural changes of aortic wall in sinoaortic-denervated rats.

1. The present work was designed to observe the early structural changes in the aortic wall in Sprague-Dawley rats 1, 2 and 4 weeks after sinoaortic denervation (SAD). 2. Rats were examined 1, 2 and 4 weeks after SAD. Blood pressure (BP) was recorded in the conscious state. The thoracic aortas were taken for investigations, including: light microscopy, electron microscopy, immunohistochemistry and terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labelling (TUNEL). 3. Blood pressure variability (BPV) was significantly increased in the SAD groups 1, 2 and 4 after the operation when compared with the sham-operated ones. 4. Two weeks after SAD the percentage proportion of smooth muscle cell density (SMC%) was obviously increased. 5. Four weeks after SAD: the SMC%, percentage proportion of collagen density (CD%) and aortic wall thickness (WT) were obviously increased with vascular smooth muscle cells blebbing concomitantly. Endothelial cells showed degenerative changes and swelling with blebbing of the cell membrane and increased condensation of peripheral nuclear chromatin and cytoplasmic vacuolization. It was also found that the number of apoptotic endothelial cells was increased and expression of eNOS was reduced. 6. This is the first study that shows the time-course of aortic wall and endothelial cell changes induced by SAD. Increased BPV might be the priming factor in the development of organ damage induced by SAD.

Animals↗

PubMed2006

Arterial baroreflex is not involved in salt preference in rats.

1. One unusual and interesting feature of spontaneously hypertensive rats (SHR) is their salt preference. This behaviour is known to be independent of blood pressure. 2. Arterial baroreflex (ABR) function is impaired in SHR. Therefore, the present study was designed to explore the relationship between ABR function and salt preference in rats. 3. Twenty-seven SHR, aged 11 months, were used. Blood pressure and baroreflex sensitivity (BRS) were determined in conscious, freely moving SHR after the measurement of salt preference. It was found that BRS did not relate to the salt preference in these rats. 4. Another group of normotensive Sprague-Dawley rats, aged 10 weeks, underwent either sinoaortic denervation (SAD) or sham operation. Salt preference was determined before and 4 weeks after SAD. Sinoaortic denervation did not alter salt preference in normotensive rats. 5. It is concluded that ABR function does not influence the salt preference in rats.

Animals↗

PubMed2005

Effects of long-term treatment with candesartan on hemodynamics and organ damage in spontaneously hypertensive rats.

UNLABELLED: This study was designed to investigate the effects of candesartan on blood pressure (BP) and blood pressure variability (BPV) reductions, baroreflex sensitivity (BRS) amelioration, and organ protection in spontaneously hypertensive rats (SHR). METHODS: Studies were performed in two groups of SHR (n = 13 for control rats; and n = 20 for candesartan-treated rats) and one group of WKY rats (n = 13). Candesartan (3 mg /kg/d) was given in rat chow for 4 months. BP was then continuously recorded for 24 hours in conscious state. After the determination of BRS, rats were killed for organ-damage evaluation. RESULTS: Long-term treatment with candesartan significantly reduced BP and BPV expressed by both standard deviation and variation coefficient of BP, enhanced BRS and produced obvious organ protection. Compared with BP level, BPV and BRS values showed a closer or similar relationship with organ-damage parameters in SHR. Multiple regression analysis showed that the decrease in left ventricular hypertrophy was most closely associated with the increase in BRS, whereas the decrease in aortic hypertrophy was most closely associated with the decrease in 24-hour systolic BPV, and the amelioration in renal lesions, with the increase in BRS and the decrease in 24-hour systolic BPV. CONCLUSION: long-term treatment with candesartan results in organ protection in SHR. Besides BP reduction, the decrease in BPV and the restoration of BRS are significantly related to this organ protection.

Administration, Oral↗

PubMed2005

Arterial baroreflex dysfunction promotes atherosclerosis in rats.

The present study was designed to test the hypothesis that arterial baroreflex dysfunction promotes the development of atherosclerosis. Experiment 1: the baroreflex sensitivity (BRS) was measured in 30 Sprague-Dawley (SD) rats in conscious state with a computerized blood pressure monitoring system. Four weeks later, the rats were administered with Vitamin D3, and fed with the high-cholesterol diet for 8 weeks to induce atherosclerosis. The hearts and aortae were removed for pathological examination. A negative correlation was found between BRS and the scores of coronary (r=-0.464, P<0.01) or aortic atherosclerosis (r=-0.524, P<0.01) in SD rats. Experiment 2: sinoaortic denervation (SAD) was performed in SD rats. Then atherosclerosis was also induced. The atherosclerosis scores in SAD rats were significantly higher than those in sham-operated rats (aortic score: 1.50+/-0.41 versus 1.10+/-0.39, P<0.05; coronary score: 1.70+/-0.35 versus 1.25+/-0.54, P<0.05). Using immunohistochemistry and Western blotting methods, it was found that the expressions of C-reactive protein, intercellular adhesion molecule-1 and vascular-cell adhesion molecule-1 in coronary artery and aorta were increased in SAD rats compared with sham-operated rats. These results indicate that arterial baroreflex dysfunction promotes the development of atherosclerosis in rats, and that inflammation may be involved in this process.

Animals↗

PubMed2005

Effects of low-dose ketanserin on blood pressure variability, baroreflex sensitivity and end-organ damage in spontaneously hypertensive rats.

The present study was designed to investigate the effects of low-dose ketanserin on BPV (blood pressure variability), BRS (baroreflex sensitivity) and organ damage in SHR (spontaneously hypertensive rats). Ketanserin was mixed in rat chow at an estimated dose of 0.1 mg.kg(-1) of body weight.day(-1). SHR were treated for 4 months. BP (blood pressure) was then recorded continuously for 24 h in a conscious state. After determination of BRS, rats were killed for organ damage evaluation. It was found that long-term treatment with low-dose ketanserin did not lower BP levels, but significantly decreased BPV, enhanced BRS and reduced organ damage in SHR. Multiple regression analysis showed that the decrease in left ventricular hypertrophy was most closely correlated (or associated) with the increase in BRS, whereas the decrease in aortic hypertrophy was most closely associated with the decrease in diastolic BPV and the amelioration in renal lesion, with the increase in BRS and the decrease in diastolic BPV. In conclusion, low-dose ketanserin produces organ protection independently of its BP-lowering action in SHR, and this organ protection was importantly attributable to the enhancement of BRS and decrease in BPV.

Animals↗

PubMed2005

Synergism of atenolol and nitrendipine on hemodynamic amelioration and organ protection in hypertensive rats.

OBJECTIVE: This study was designed to investigate the possible synergism of atenolol and nitrendipine on blood pressure (BP) and blood pressure variability (BPV) reductions, baroreflex sensitivity (BRS) amelioration, and organ protection in hypertensive rats. METHOD: The dose was 20 mg/kg for atenolol, 10 mg/kg for nitrendipine and 20 + 10 mg/kg for the combination of these two drugs. In an acute study, a single dose was given via a catheter previously inserted into the stomach in spontaneously hypertensive rats (SHR). In a subacute study, SHR, deoxycorticosterone acetate (DOCA)-salt rats, and two-kidney, one-clip (2K1C) rats were used. They received the same dose by gavage daily for 10 days. BP was measured 24 h after drug administration. In chronic studies, these drugs at the aforementioned dose were mixed into rat chow. SHR were treated for 4 months. BP was then continuously recorded for 24 h. After the determination of BRS, rats were killed for organ-damage evaluation. RESULTS: In the acute study, it was found that the combination of atenolol and nitrendipine had an obviously greater and longer BP reduction than treatment with each of these two drugs separately. In the subacute study, an effective decrease in BP 24 h after administration was found only in the rats treated with the combination. In chronic studies, it was found that the combination possessed the obvious synergism on BP and BPV reduction, BRS amelioration and organ protection in SHR. Multiple-regression analysis showed that the decrease in left ventricular hypertrophy was most significantly related to the decrease in systolic BPV and BP, the decrease in aortic hypertrophy was most significantly related to the increase in BRS and the decrease in systolic BPV, and amelioration in the renal lesion was most significantly associated with the restoration of BRS. CONCLUSION: Treatment with a combination of atenolol and nitrendipine exhibited a rapid and persistent antihypertensive effect and possessed an obvious synergism on BP and BPV reduction, BRS restoration and organ protection in hypertensive rats. The decrease in BPV and the restoration of BRS may importantly contribute to organ protection in SHR with chronic treatment.

Animals↗

PubMed2005

Diminished responses to nifedipine imply severe end-organ damage in spontaneously hypertensive rats.

This study was designed to investigate the effect of end-organ damage (EOD), the initial blood pressure levels, and baroreflex sensitivity (BRS) on the blood pressure-lowering effect of nifedipine in spontaneously hypertensive rats (SHRs). Nifedipine was intravenously administered at a dose of 1 mg/kg. BP was continuously recorded in the conscious state before and after nifedipine administration. BRS was determined before drug administration. Two days after the blood pressure (BP) recording, rats were killed for organ-damage evaluation. Univariate correlation analysis showed that BP changes induced by nifedipine injection were negatively correlated with EOD score and aortic weight/length but positively correlated with left kidney weight/body weight and basal BP levels. Stepwise multiple linear regression analysis demonstrated that increase in overall end-organ damage was most significantly related to the decrease in hypotensive effect of nifedipine; increase in aortic hypertrophy was also related to a decreased fall in systolic and diastolic BP induced by nifedipine, whereas increase in initial BP levels was associated with increased hypotensive effect of nifedipine. In conclusion, the severity of overall EOD contributed more than basal BP levels to the diminished responses to nifedipine, and aortic hypertrophy was also involved in diminished drug responses.

Animals↗

PubMed2005

Blood pressure variability, cardiac baroreflex sensitivity and organ damage in experimentally hypertensive rats.

1. The present study was designed to investigate the haemodynamic features and morphological changes in experimentally hypertensive rat models. 2. Sprague-Dawley rats were used to prepare the experimentally hypertensive models, including two-kidney, one-clip renovascular hypertensive (2K1C) rats, deoxycorticosterone acetate salt hypertensive (DOCA) rats and N(G)-nitro-l-arginine methyl ester-induced hypertensive (l-NAME) rats. Six weeks after the induction of hypertension, 24 h blood pressure was recorded and blood pressure variability (BPV) expressed by 24 h (or 12 h in the daytime and night-time study) standard deviation of the variables was calculated. Then, cardiac baroreflex sensitivity (BRS) was determined and four endogenous factors (tumour necrosis factor-alpha, interleukin-1beta, angiotensin II and endothelin-1) were measured. Finally, morphological changes were examined. 3. It was found that an increase in BPV and a decrease in BRS were accompanied by an elevation of blood pressure in all three hypertensive models. The DOCA rats had the highest BPV, whereas the l-NAME rats had the lowest BRS. 4. Morphological changes were similar in DOCA and l-NAME rats and the cardiac changes were relatively slight in 2K1C rats. Tumour necrosis factor-alpha was increased in all the three models, especially in DOCA rats. Endothelin-1 was higher in DOCA rats and angiotensin II was increased in 2K1C rats and decreased in DOCA rats. 5. In conclusion, increased BPV and decreased BRS accompanied the elevation of blood pressure in all three hypertensive models. The DOCA rats had the highest BPV and the l-NAME rats had the lowest BRS. Obvious organ damage was seen in all three hypertensive models 6 weeks after the induction of hypertension.

Angiotensin II↗

PubMed2004

Inhibition of inflammation contributes to organ protection of atenolol in sinoaortic-denervated rats.

The present study was designed to test the hypothesis that inhibition of inflammation contributes to the protective effects of atenolol on the organ damage induced by sinoaortic denervation (SAD) in rats. SAD was performed in male Sprague-Dawley rats at the age of 10 weeks. Atenolol (20 mg/kg/d, po) was administered for 12 weeks beginning from 4 weeks after SAD. Organ damage evaluation and the determination of plasma TXB2, serum IL-1, TNF-alpha and tissue reactive oxygen species (ROS) were performed at 16 weeks after SAD. It was found that there existed obvious organ damage including increased cardiac and aortic collagen, and glomerular injury, in SAD rats. Plasma TXB2, serum TNF-alpha IL-1, and tissue ROS increased significantly after SAD. Long-term treatment with atenolol significantly prevented the organ damage with a decrease in left ventricular weight, cardiac and aortic collagen contents, and glomerular injury score in SAD rats. Plasma TXB2, serum IL-1, and tissue ROS were found to be significantly decreased by the long-term treatment with atenolol. Furthermore, it was found that the levels of inflammation-related factors were significantly related to all the organ-damage parameters studied in this experiment. These results suggest that inhibition of inflammation and oxygen stress contributes to the organ-protective effects of atenolol in SAD rats.

Animals↗

PubMed2004

Arterial baroreflex function determines the survival time in lipopolysaccharide-induced shock in rats.

Lipopolysaccharide (LPS) mimics many of the effects of septic shock. LPS-induced death has been attributed to systemic hypotension, hyporeactiveness to vasoconstrictors, metabolic acidosis, and organ damage. However, there is no research directed to the involvement of the baroreflex sensitivity (BRS) in LPS-induced death. The purpose of this study was to evaluate the effect of BRS on the survival time after lethal LPS challenge. Four groups of rats were used. Each rat received an equivalent dose of intravenous LPS (50 mg/kg). It was found that the anesthetized sinoaortic-denervated (SAD) rats (representative of the lowest BRS, BRS = 0.022 +/- 0.015 ms/mmHg) survived the shortest time (36 +/- 11.1 min). The conscious SAD rats (BRS = 0.198 +/- 0.035 ms/mmHg) and the anesthetized sham-operated rats (BRS = 0.304 +/- 0.072 ms/mmHg) were alive a relatively long time (101 +/- 11.5 min and 110 +/- 12.4 min, respectively). The conscious sham-operated rats (BRS = 0.943 +/- 0.097 ms/mmHg) survived the longest time (148 +/- 6.5 min). These results demonstrated that arterial baroreflex function determined the survival time in the LPS-induced lethal shock.

Anesthesia↗

PubMed2004

Greater hypertrophy in right than left ventricles is associated with pulmonary vasculopathy in sinoaortic-denervated Wistar-Kyoto rats.

1. Biventricular hypertrophy has been described in a high blood pressure variability (BPV) model of sinoaortic-denervated (SAD) rats without systemic hypertension. To explore the possible involvement of the lung in SAD-induced right ventricular hypertrophy (RVH), we examined lung morphology, in addition to systemic haemodynamics and ventricle morphology, in Wistar-Kyoto rats 32 weeks after SAD. 2. In Wistar-Kyoto rats 32 weeks after SAD, there existed a substantial elevation in BPV, with no change in the average level of arterial pressure. Biventricular hypertrophy following SAD was characterized by a greater hypertrophy in right than left ventricles; both absolute and normalized right ventricular weights were significantly increased by 22 and 27%, respectively, and only normalized left ventricular weight was significantly increased by 12%. No infarcts were found in any ventricles examined. 3. In the lung, the most prominent change following SAD was pulmonary vasculopathy, including wall thickening, perivascular fibrosis and cell infiltration. In pulmonary arteries with an internal diameter of 70-130 microm, the external diameter, wall thickness and wall thickness to internal diameter ratio were increased in SAD compared with control rats. 4. There was no correlation between right and left ventricular weights. In contrast with BPV-correlated left ventricular weight, right ventricular weight was correlated with the wall thickness of the pulmonary artery, but not with BPV. 5. These findings suggest that greater RVH following SAD is associated with pulmonary vasculopathy, but is not secondary to the left ventricular problems or high BPV.

Animals↗

PubMed2003

Ketanserin stabilizes blood pressure in conscious spontaneously hypertensive rats.

1. It has been demonstrated that blood pressure variability (BPV) is increased in hypertension and related to organ damage. It will be important to lower BPV in the treatment of hypertension. The present study was designed to investigate the effect of ketanserin, a 5-HT2A receptor antagonist with a weak alpha1-adrenoceptor blocking effect, on BPV in conscious spontaneously hypertensive rats (SHR). 2. It was found that ketanserin decreased blood pressure (BP) and BPV in SHR when administered intravenously (3 mg/kg, i.v.). Ketanserin decreased BPV, but not the BP level, when administered intracerebroventricularly (50 microg/rat, i.c.v.). 3. Prazosin, an alpha1-adrenoceptor antagonist, lowered BP but did not affect BPV when given either i.v. (0.5 mg/kg) or i.c.v. (30 microg/rat). Ritanserin (0.625 mg/kg, i.v.; 40 microg/rat, i.c.v.), a 5-HT2A receptor antagonist, decreased BPV only when administered i.c.v. and did not modify the BP level. 4. Ketanserin enhanced arterial baroreflex function in SHR when given either i.v. or i.c.v. 5. The stabilizing effect of ketanserin on BP was persistent when administered intragastrically. This administration route is similar to oral administration clinically. 6. It is concluded that ketanserin is an antihypertensive agent with an effect of reducing BPV. This effect is mainly mediated by central 5-HT2A receptors and is probably attributable to the restoration of arterial baroreflex function.

Animals↗

PubMed2003

Inflammation is involved in the organ damage induced by sinoaortic denervation in rats.

OBJECTIVE: The present study was designed to test the hypothesis that inflammation is involved in the end-organ damage (EOD) induced by sinoaortic denervation (SAD) in rats. METHOD: SAD was performed in male Sprague-Dawley rats at the age of 10 weeks. Under anaesthesia, aortic nerves were cut and the sinus region of the carotid artery was stripped and painted with 10% phenol. Pathological evaluation of EOD and the determination of plasma or tissue levels of the factors related to inflammation, including thromboxane B2 (TXB2) interleukin-1 (IL-1), tumour necrosis factor alpha (TNF-alpha) and reactive oxygen species (ROS) were performed at 16 weeks after SAD. Pathological evaluation of EOD included heart weight ratio, myocardial and blood vessel hydroxyproline and collagen volume fraction, glomerular injury score and number of infiltrating inflammatory cells. Indomethacin (20 mg/kg per day, orally) or vitamin E (100 mg/kg per day, orally) was administered for 12 weeks, beginning from 4 weeks after SAD, to observe their effects on SAD-induced EOD. RESULTS: There were significant fibrosis and inflammatory infiltration in the myocardium and blood vessels, represented by higher hydroxyproline and collagen volume fraction, and a large amount of inflammatory cells in the tissues of SAD rats. Heart weight and kidney glomerular injury score were significantly higher in SAD than in sham-operated rats. Plasma TXB2, TNF-alpha, IL-1 and tissue ROS increased significantly after SAD. Indomethacin and vitamin E significantly decreased the contents of some factors related to inflammation in SAD rats. Both drugs also alleviated myocardial and vessel fibrosis, inflammatory infiltration and kidney damage. CONCLUSION: Inflammation is involved in the organ damage induced by SAD in rats.

Animals↗

PubMed2003

Effects of long-term treatment with candesartan on organ damages in sinoaortic denervated rats.

The study was designed to observe the effects of long-term treatment with candesartan cilexetil (candesartan) on blood pressure (BP), blood pressure variability (BPV), baroreflex sensitivity (BRS) and end-organ damage (EOD) in sinoaortic denervated (SAD) rats. Candesartan was mixed in rat chow at an estimated dose of 3 mg/kg/day. After 12 weeks of drug administration, rats were instrumented to determine BP, BPV and BRS in conscious state. Organ damage was estimated by observation of morphologic changes. When compared with sham-operated rats, SAD rats exhibited increased BPV, decreased BRS, and normal BP and plasma angiotensin II level. Left ventricular and aortic hypertrophies and renal lesion were found in SAD rats. Candesartan significantly decreased BP and BPV, ameliorated impaired BRS, increased plasma angiotensin II level and obviously diminished the EOD in SAD rats. Multiple-regression analysis shows that decrease in left ventricular hypertrophy was mainly related to decrease in systolic BPV. Decrease in aortic hypertrophy was mainly determined by increase in BRS and decrease in systolic BP. Amelioration in renal lesion was predicted by increase in BRS and decrease in systolic BPV. BRS was the most important determinant for renal lesion and aortic hypertrophy in SAD rats. In addition, plasma angiotensin II level was higher in candesartan-treated rats. In conclusion, long-term treatment with candesartan prevented SAD-induced organ damage. Restoration of arterial baroreflex function, decrease in BPV, and blockade of activated renin-angiotensin system may contribute to the organ protective action of candesartan in SAD rats.

Animals↗

PubMed2003

Morphological evidence of reinnervation of the baroreceptive regions in sinoaortic-denervated rats.

1. The arterial baroreflex (ABR) plays an important role in the maintenance of the stability of blood pressure. Sinoaortic denervation (SAD) destroys the integrity of the reflex arc and produces severe organ damage in rats. However, partial recovery of ABR function has been observed following chronic denervation. The aim of the present study was to determine whether there was morphological evidence of reinnervation of the aortic arch and carotid sinus following SAD. 2. A substantial body of physiological and morphological evidence suggests that substance P (SP) may be a neurotransmitter contained in first-order sensory baroreceptor afferents; therefore, the patterns of vascular SP and neurofilament (NF) immunoreactive (IR) innervation of the aortic arch and carotid sinus were investigated in the present study. 3. Ten-week-old male Sprague-Dawley rats underwent SAD or sham operation. Whole mounts of carotid bifurcation and aortic arch were prepared for immunohistochemical study at various time points (1, 9 and 16 weeks after operation). 4. The results of computerized image analysis show that the mean density of NF- and SP-IR nerves of SAD rats 9 and 16 weeks after operation increased gradually and significantly compared with that of rats 1 week after operation. 5. In conclusion, the results indicate that there is reinnervation of the aortic arch and carotid sinus by NF- and SP-IR fibres in SAD rats, which may be the morphological basis for the partial restoration of ABR function over time after SAD.

Animals↗

PubMed2002

Candesartan inhibits sinoaortic denervation-induced cardiovascular hypertrophy in rats.

AIM: To study the effect of candesartan cilexetil (candesartan), a new AT1 receptor antagonist, on sinoaortic denervation (SAD)-induced cardiovascular hypertrophy and its potential mechanisms in rats. METHODS: For long-term treatment, candesartan (6 mg/kg/d) was given in rat food for 16 weeks after SAD surgery, and for acute treatment, a single dose of candesartan (3 mg/kg) was administrated intragastrically at 30 d after SAD. RESULTS: The indexes of left ventricular and aortic hypertrophy in candesartan-treated SAD rats were decreased when compared with untreated SAD rats, and similar to or less than those in normal rats. SAD-induced cardiomyocyte hypertrophy, myocardial fibrosis, wall thickening of intramyocardial arterioles and aortae, and destruction of vascular internal elastin membrane were almost inhibited by candesartan. The plasma angiotensin II levels were markedly increased in treated SAD rats and negatively correlated with the indexes of hypertrophy. Both blood pressure and its variability were reduced by a single dose of candesartan during 3 h of observation period. CONCLUSION: Candesartan can efficiently inhibit SAD-induced cardiovascular hypertrophy. In addition to known mechanisms, upregulation of circulating angiotensin II and stabilization of blood pressure may be involved in this cardiovascular protection of candesartan.

Angiotensin Receptor Antagonists↗