Biomedical subjects

Ding-Feng Su

Publications and source records attributed to Ding-Feng Su.

At least 37 records · Page 2Linked to original sources

PubMed2004

Interaction between clonidine and N-methyl-D-aspartate receptors in the caudal ventrolateral medulla of rats.

It is known that the caudal ventrolateral medulla (CVLM) plays an important role in controlling blood pressure and mediating the cardiovascular effects of centrally acting antihypertensive drugs such as clonidine. Recently, the effect of clonidine was believed to be related to the functional states of N-methyl-D-aspartate (NMDA) receptors. The present work was designed to observe the interactions between clonidine and NMDA receptor in the CVLM. Unilaterally injected clonidine (6 nmol) into the CVLM not only produced a pressor action, but also effectively (P<0.01, n=8) antagonized the decreases in both mean arterial pressure (MAP) (-22.3+/-5.0 to -7.9+/-2.3 mmHg) and heart rate (HR) (-31.9+/-5.9 to -10.3+/-2.7 beats/min) evoked by L-glutamate in the CVLM. Unilaterally injected NMDA receptor antagonist MK801 (200 pmol) into the CVLM significantly increased MAP by 26.5+/-3.7 mmHg and HR by 37.1+/-7.6 beats/min, and completely (P<0.01, n=10) abolished the pressor effect (16.1+/-6.6 to 1.5+/-2.8 mmHg) of clonidine in the CVLM. In conclusion, these findings show that NMDA receptors within the CVLM contribute to clonidine-induced action, and suggest that the CVLM plays an important role in the interaction between clonidine and NMDA receptors.

Animals↗

PubMed2004

High-level apoptosis is persistent in myocardiocytes of sinoaortic-denervated rats.

BACKGROUND: Arterial baroreflex plays an important part in the regulation of cardiovascular activity. Sinoaortic denervation (SAD) produces organ damage in rats. A previous study suggested that apoptosis in myocardium is involved in the organ damage induced by SAD. OBJECTIVE: To study the time course of cardiomyocyte apoptosis in SAD rats by evaluating apoptotic cells and expression of apoptosis-related genes in the left ventricles of SAD rats, 4, 8, 16 and 32 weeks after SAD operation. METHODS: Male Sprague-Dawley rats underwent SAD or sham operation at the age of 10 weeks. Four, 8, 16 or 32 weeks after operation, blood samples and heart tissues were taken for the following studies: determination of angiotensin II in plasma and heart, pathological evaluations, terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labelling and immunohistochemistry. Some observations were also made in rats 1 and 2 weeks after denervation. RESULTS: Loss of body weight gain, cardiac hypertrophy, an increase in left ventricular collagen volume and an increase in cardiac angiotensin II content were observed in SAD rats from 2 to 32 weeks after SAD operation. The apoptotic myocardiocytes were increased in SAD rats compared with sham-operated rats. The expression of Bcl-2 protein, an inhibiting factor of apoptosis, was markedly decreased in the myocardiocytes of SAD rats. In contrast, the expression of Bax, Fas and Fas-L proteins, promoting factors of apoptosis, was significantly increased in the myocardiocytes of SAD rats. All these modifications were persistent from 4 to 32 weeks after SAD operation. CONCLUSION: These findings demonstrate that a high level of apoptosis is persistent in myocardiocytes in SAD rats. We propose that apoptosis may be one of the mechanisms underlying the cardiac damage induced by SAD.

Angiotensin II↗

PubMed2004

Restoration of baroreflex function by ketanserin is not blood pressure dependent in conscious freely moving rats.

OBJECTIVE: Since the end of the 1980s, the pathological importance of baroreflex function has attracted the attention of many investigators. In our previous studies, it was found that ketanserin lowered blood pressure (BP), decreased BP variability and enhanced baroreflex sensitivity (BRS). The present work was designed to test the hypothesis that the restoration of BRS by ketanserin is not dependent on BP level in conscious rats. DESIGN AND METHODS: Spontaneously hypertensive rats (SHR) aged 8-12 months were used. Blood pressure was recorded for 60 min and BRS was determined separately before and after intragastric administration of ketanserin, with four doses. In a second experiment, 10-week-old Sprague-Dawley rats were used for preparing a myocardial infarction (MI) model by ligating the coronary artery. MI rats were treated with ketanserin for 5 weeks, with two doses. At the end of the treatment, BP and BRS of the MI rats were studied in conscious state. In addition, the effects of ketanserin on BRS in Sprague-Dawley rats with normal BRS and the effects of prazosin and ritanserin on BRS in SHR were also observed. RESULTS: It was found that ketanserin significantly decreased BP and improved BRS in the conscious SHR. The decrease in BP was dose-dependent but the improvement of BRS was not. At the smallest dose (0.3 mg/kg), ketanserin did not lower BP but enhanced BRS. In MI rats, the treatment with ketanserin did not significantly decrease BP, but it improved BRS at both doses administered (0.6 and 10 mg/kg). Ketanserin [3 and 10 mg/kg, intragastric (i.g.)] did not affect BRS in SD rats with normal BRS. Prazosin and ritanserin did not enhance BRS in SHR when administered intravenously. Ritanserin markedly and prazosin slightly enhanced BRS in SHR following intracerebroventricular administration. CONCLUSION: The restoration of baroreflex function by ketanserin is not BP dependent and this effect is mediated by central 5-HT2A receptor.

Animals↗

PubMed2004

Asynchronism of the recovery of baroreflex sensitivity, blood pressure, and consciousness from anesthesia in rats.

Anesthesia inhibits arterial baroreflex functions such as baroreflex sensitivity (BRS). The main objective of the present study was to determine the time course of BRS recovery from anesthesia and to determine whether BRS recovery is synchronous with the recovery of consciousness and blood pressure (BP). Experiments were performed in male Sprague-Dawley rats using different commonly used anesthetics at routine doses through intraperitoneal administration: (1) diazepam/ketamine, a mixture of diazepam (5 mg/kg) and ketamine (50 mg/kg); (2) chloral hydrate (0.3 g/kg); (3) sodium pentobarbital (30 mg/kg); and (4) urethane (1.0 g/kg). The anesthetic state, evaluated by algesthesia and cornea reflex, was maintained for 1-2.5 hours. The BRS, assessed by intravenous injection of phenylephrine, was inhibited rapidly and dramatically, with maximum depressions of 51%-80%. The BRS recovery time was approximately 5 hours for diazepam/ketamine, chloral hydrate, and pentobarbital, but more than 24 hours for urethane. Compared with BRS inhibition, BP reduction was less pronounced by 8% (not significant) for diazepam/ketamine and by 12%-30% for the others. The BP recovery time was approximately 2 hours, with the exception of chloral hydrate (>6 hours). In conclusion, after anesthesia, BRS inhibition is more obvious than BP reduction, and the recovery of BRS lags behind the recovery of consciousness or BP.

Anesthesia Recovery Period↗

PubMed2004

Changes of central norepinephrine, beta-endorphin, LEU-enkephalin, peripheral arginine-vasopressin, and angiotensin II levels in acute and chronic phases of sino-aortic denervation in rats.

We and others have demonstrated that impaired arterial baroreceptor reflex (ABR) function is one of the major causes of hypertension-associated end organ damage. The goal of this study was to clarify the potential neuro-humoral mechanisms responsible for impaired ABR-induced end organ damage. The sino-aortic denervated (SAD) rat was used as an animal model of ABR dysfunction. One-week SAD rats were characterized by hypertension, tachycardia, increased norepinephrine content, and decreased beta-endorphin and leu-enkephalin content in hypothalamus and medulla oblongata, and increased plasma levels of arginine-vasopressin. In 18-week SAD rats, the 24-hour average arterial pressure, heart rate, beta-endorphin, and leu-enkephalin content in hypothalamus and medulla oblongata and plasma levels of arginine-vasopressin and angiotensin II were not different from those measured in ABR-intact rats. However, blood pressure variability and angiotensin II content in kidney and left ventricle increased. When exposed to chronic stress, exaggerated changes in arterial pressure, blood pressure variability, the levels of central norepinephrine, beta-endorphin and leu-enkephalin, plasma arginine-vasopressin and angiotensin II, and tissue angiotensin II were found in 18-week SAD rats. These data indicate that a long-term impairment of ABR leads to chronic activation of central noradrenergic neurons and tissue renin-angiotensin system, and that stress induces exaggerated responses of neuro-humoral factors and hemodynamics in SAD rats. Thus, if the present results hold true for humans, one can expect abnormal neurotransmitter/neuromodulator responses to environmental insults in patients with impaired ABR function.

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

ATP-sensitive potassium channels are involved in adenosine-induced reduction of blood pressure variability in spontaneously hypertensive rats.

With a computerized analysis system, blood pressure was recorded continuously in conscious unrestrained spontaneously hypertensive rats. The effects of different adenosine receptor agonists and ATP-sensitive potassium channel opener and blocker on blood pressure variability in spontaneously hypertensive rats were studied. It was found that adenosine, 5'-N-cyclopropyl-carboxamidoadenosine (CPCA, a selective adenosine A2-receptor agonist) and pinacidil (a nonselective ATP-sensitive potassium channel opener) decreased blood pressure variability when one of them was used alone, whereas N -cyclopentyladenosine (CPA, a selective adenosine A1-receptor agonist) had no significant effects on blood pressure variability. When pretreated with glibenclamide (a nonselective ATP-sensitive potassium channel blocker), the inhibitory effects of adenosine and CPCA on blood pressure variability were significantly prevented. By itself, however, glibenclamide had no influence on blood pressure variability. These results suggest that the effect of adenosine on blood pressure variability in spontaneously hypertensive rats is due to activation of ATP-sensitive potassium channels mediated by adenosine A2-receptor.

Adenosine↗

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

Increased susceptibility of ventricular arrhythmias to aconitine in anaesthetized rats is attributed to the inhibition of baroreflex.

1. Aconitine is widely used to produce ventricular arrhythmias in anaesthetized rats. The present work was designed to test the hypothesis that anaesthesia may increase the susceptibility of ventricular arrhythmia to aconitine due to the inhibition of arterial baroreflex. In addition, the susceptibility of ventricular arrhythmia to aconitine at different times during the course of a whole day was also investigated. 2. Male Sprague-Dawley rats were used. Arrhthymias were induced by aconitine infusion at six time points (01.00, 05.00, 09.00, 13.00, 17.00 and 21.00 h) with rats in both anaesthetized and conscious states. In sinoaortic-denervated (SAD) rats, ventricular arrhythmias were induced by aconitine infusion between 09.00 and 13.00 h. 3. There was a significant difference in the lethal dose of aconitine between anaesthetized and conscious rats (99.6 +/- 30.1 vs 58.2 +/- 14.7 micro g/kg; P < 0.001). Anaesthesia did increase the susceptibility of rats to ventricular arrhythmias following aconitine. 4. In SAD rats, the lethal dose of aconitine was less than that for baroreflex-intact rats when determined in the conscious state. The difference in the lethal dose of aconitine between SAD and baroreflex-intact rats disappeared when it was determined in anaesthetized rats. 5. The time of day did not affect the susceptibility of either anaesthetized or conscious rats to ventricular arrhythmias following aconitine, except for a difference in the ventricullar fibrillation threshold dose between 13.00 and 17.00 h in anaesthetized rats. 6. In conclusion, anaesthesia may increase the risk of ventricular arrhythmias following aconitine. Intact arterial baroreflex function is necessary to prevent drug-induced ventricular arrhythmias.

Aconitine↗

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↗

PubMed2004

Synergism of atenolol and amlodipine on lowering and stabilizing blood pressure in spontaneously hypertensive rats.

This study was designed to investigate the possible synergism of atenolol and amlodipine on lowering and stabilizing blood pressure (BP) in spontaneously hypertensive rats. Sixty-four spontaneously hypertensive rats were randomly divided into eight groups. They were given 0.8% carboxymethylcellulose sodium (control), atenolol (10 mg/kg), amlodipine (0.5, 1 and 2 mg/kg) and the combinations of atenolol and amlodipine (10 + 0.5, 10 + 1 and 10 + 2 mg/kg), respectively. The drugs were given via a catheter of gastric fistula. BP was recorded for 25 h from 1 h before drug administration to 24 h after administration, in conscious, freely moving rats. It was found that combination of atenolol and amlodipine significantly decreased BP and systolic BP variability. From probability sum analysis it was found that the combination of atenolol and amlodipine, in a proportion as 10 : 1, was the best one (q = 1.54). In conclusion, the present work clearly demonstrated that there is a synergistic effect between atenolol and amlodipine in lowering and stabilizing the BP. The synergistic effect is highest when the dose proportion of the two drugs is 10 : 1.

Adrenergic beta-Antagonists↗

PubMed2003

Blockade of N-methyl-D-aspartate receptors within the rostral ventrolateral medulla antagonizes clonidine-induced cardiovascular effects.

There is wide agreement that the rostral ventrolateral medulla (RVLM) plays a crucial role in the regulation of blood pressure (BP), and that there may be a close correlation between the actions of centrally acting antihypertensive agents and N-methyl-D-aspartate (NMDA) receptor functional states. The present study was done to test the hypothesis that NMDA receptors within the RVLM were involved in the cardiovascular effects of centrally acting antihypertensive drug clonidine in anesthetized and paralyzed rats. Prior unilateral microinjection of NMDA receptor antagonist dizocilpine (MK801, 500 pmol) into the RVLM significantly attenuated (p<0.01, n=9) the reductions of BP (-24+/-6 to -8+/-4 mm Hg) and heart rate (-49+/-9 to -14+/-7 bpm) induced by unilaterally injected clonidine (5 nmol) into the RVLM. Prior bilateral microinjection of MK801 (500 pmol for each side) into the RVLM effectively (p<0.01, n=7) antagonized the hypotension (-25+/-5 to -8+/-2 mm Hg) and bradycardia (-43+/-7 to -11+/-4 bpm) of intravenously administered clonidine (10 microg kg(-1)). Importantly, iontophoretic application of MK801 (60 nA) significantly (p<0.01, n=9) prevented the inhibitory effect of intravenously (10 microg kg(-1)) injected clonidine on the discharge of presympathetic neurons in the RVLM (neuronal inhibition: -39+/-6 to -10+/-2%). In conclusion, the present study shows that the RVLM administrated MK801 effectively antagonizes clonidine-induced cardiovascular effects, and suggests that NMDA receptors within the RVLM contribute to clonidine actions.

Adrenergic alpha-Agonists↗

PubMed2003

[Angiotensin II contents in plasma, and cardiac and renal tissues of sinoaortic denervated rats].

Our previous data demonstrate that impairment of arterial baroreceptor reflex (ABR) plays an independent role in hypertension target organ damage. To elucidate the mechanisms responsible for the dysfunction of ABR associated organ damage, sinoaortic denervated (SAD) rats were used as an animal model of ABR dysfunction. Twenty-four-hour continuous blood pressure (SBP and DBP), blood pressure variability (BPV), heart rate (HR) and HR variability (HRV) were measured in conscious and unrestrained rats. Angiotensin II (Ang II) in plasma, heart and kidney was assayed by raio-immunological assay (RIA) 1 or 18 weeks after denervation. In short-term SAD rats, twenty-four-hour mean SBP and DBP increased compared with that of sham-operated rats and long-term SAD rats. No significant difference in SBP, DBP or HR was found between long-term SAD rats and sham-operated ones. Compared with the sham-operated rats, long-term SAD rats had elevated BPV. No significant change in Ang II levels of caridiac and renal tissues was found in short-term SAD rats. In long-term SAD rats, Ang II level of plasma was not increased while the Ang II content in the heart and kidney increased. Ang II contents of plasma and tissues in long-term SAD rats exposed to chronic stress were higher than those in the control rats. These results show (1) in short-term SAD rats blood pressure increased, while in long-term SAD rats 24 h mean blood pressure did not increase, although BPV elevated in long-term SAD rats; (2) in long-term SAD rats, secretion of Ang II in cardiac and renal tissues was enhanced and more Ang II released when the animals were exposed to chronic stress. These results suggest that elevated BPV and secretion of Ang II may be related to the development of organ damage induced by ABR dysfunction.

Angiotensin II↗

PubMed2003

Involvement of I(1)-imidazoline receptors in baroreceptor reflex in the caudal ventrolateral medulla of rats.

There is ample evidence to show the existence of center I(1)-imidazoline receptors that are involved in the regulation of cardiovascular activities. The purpose of this study was to examine the possible role of I(1)-imidazoline receptors and alpha(2)-adrenoceptors within the caudal ventrolateral medulla (CVLM) in mediating the baroreceptor reflex in anesthetized rats. Unilateral microinjection of idazoxan (2 nmol in 50 nl), a mixed antagonist of I(1)-imidazoline receptors and alpha(2)-adrenoceptors, into the CVLM significantly (P<0.01) decreased blood pressure (BP), heart rate (HR), and the firing rate of presympathetic neurons in the rostral ventrolateral medulla (RVLM) by 21+/-6 mmHg, 25+/-5 beats per min and 3.5+/-0.9 spikes/s, respectively. Moreover, unilateral injection of idazoxan into the CVLM significantly (P<0.01) reduced the inhibitory responses of the ipsilateral RVLM presympathetic neurons evoked by stimulation of aortic nerve and elevation of BP, and partially inhibited the neuronal cardiac cycle-related rhythm. Depressor responses evoked by aortic nerve stimulation were significantly (P<0.01) attenuated 10 and 20 min after bilateral microinjection of idazoxan (2 nmol in 50 nl for each side) into the CVLM (-20+/-4 and -30+/-4 vs. -40+/-1 mmHg). However, injection of yohimbine (500 pmol in 50 nl), a selective alpha(2)-adrenoceptor antagonist, into the CVLM did not affect the resting cardiovascular activities and baroreceptor reflex. It is concluded that the CVLM I(1)-imidazoline receptors are involved in maintenance of tonic cardiovascular activities and transmission of the baroreceptor reflex.

Action Potentials↗

PubMed2003

Comparative study of sinoaortic denervated rats and spontaneously hypertensive rats.

BACKGROUND: Both hypertension and high blood pressure variability (BPV) are involved in cardiovascular damage. This comparative study was designed to explore the possible effects of both of these phenomena on the cardiovascular system. METHODS: The high BPV model of 16-week sinoaortic denervated (SAD) rats and the hypertension model of spontaneously hypertensive rats (SHR) were used for comparison at the same age of 26 weeks. The comparison was focus on hemodynamics, cardiovascular hypertrophy, and hemodynamic responses to ketanserin. Linear regression analysis was performed to study the role of hemodynamics in cardiovascular hypertrophy. RESULTS: In SHR, hypertension was accompanied by a moderately high BPV, whereas in SAD rats, substantially high BPV existed alone, without hypertension. Left ventricular hypertrophy was severe in SHR but was mild in SAD rats. Aortic hypertrophy was present in SAD rats but was absent in SHR. In SAD rats, the hypertrophy was correlated with BPV but not with blood pressure (BP) level. However, in SHR, hypertrophy was correlated with both BP and BPV level. The BP-lowering effect of ketanserin was comparable in both models, whereas its BPV-lowering effect was greater in SAD rats than in SHR. This hypersensitivity was associated with basal BPV level in SAD rats. CONCLUSIONS: These results indicate that hypertension may be more important than high BPV in causing left ventricular hypertrophy, and that the aorta may be more sensitive to substantially 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

Effects of glucose-insulin-potassium on baroreflex sensitivity, left ventricular function and ventricular arrhythmia in the subacute phase of myocardial infarction in rats.

Glucose-insulin-potassium (GIK) is clinically used for reducing mortality in acute myocardial infarction (MI). It is known that ventricular arrhythmia, left ventricular dysfunction and impaired baroreflex sensitivity (BRS) are the three major determinants for predicting the mortality after acute MI. The present work was designed to study the effects of GIK on BRS, ventricular arrhythmia, and left ventricular function in rats with coronary artery ligature. Sprague-Dawley rats were used and the myocardial infarction was produced by ligature of the left anterior descending artery. Five weeks after coronary artery ligation, BRS was measured in conscious state with a computerized blood pressure monitoring system and left ventricular function and electrocardiogram were determined in the anaesthetized state in the subacute phase of myocardial infarction. It was found that GIK did not affect the blood pressure and heart period in both conscious and anaesthetized rats. GIK did not enhance BRS, but reduced ventricular arrhythmia and improved left ventricular function by reducing left ventricular end diastolic pressure in anaesthetized rats with MI. It is proposed that reducing ventricular arrhythmia and improving left ventricular function contribute to the effect of GIK on reducing the mortality after MI.

Animals↗

PubMed2003

Contribution of blood pressure variability to the effect of nitrendipine on end-organ damage in spontaneously hypertensive rats.

OBJECTIVE: It has been proposed that blood pressure variability (BPV) is positively related to end-organ damage (EOD) in hypertension. The present work was designed to observe the effects of long-term treatment with nitrendipine and hydralazine on BPV and EOD in spontaneously hypertensive rats (SHR), to examine the hypothesis that lowering BPV with an antihypertensive drug is an important factor in organ protection. DESIGN AND METHODS: Drugs were mixed in rat chow. After 4 months of drug administration, blood pressure was recorded continuously in conscious freely moving rats for 24 h. The heart, kidneys, and brain were then isolated and examined. RESULTS: It was found that nitrendipine significantly decreased blood pressure and BPV, and significantly decreased EOD score in SHR. Hydralazine decreased blood pressure, but did not lower BPV. No effect on EOD was found in hydralazine-treated rats. In control rats (n = 38), EOD score was weakly related to systolic blood pressure (r = 0.331, P < 0.05) and closely related to long-term systolic BPV (r = 0.551, P < 0.01). In nitrendipine-treated rats, EOD score was closely related to long-term systolic BPV (r = 0.602, P < 0.01), but not to BP level (r = 0.174, P > 0.05). CONCLUSION: BPV plays an important role in the organ-protecting effects of nitrendipine.

Animals↗