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Normotensive Rats (normotensive + rat)

Distribution by Scientific Domains

Medical Sciences	70%

Selected Abstracts

Role of GABAergic neurones in the nucleus tractus solitarii in modulation of cardiovascular activity

EXPERIMENTAL PHYSIOLOGY, Issue 9 2010
Jasenka Zubcevic
GABAergic neurones are interspersed throughout the nucleus tractus solitarii (NTS), and their tonic activity is crucial to the maintenance of cardiorespiratory homeostasis. However, the mechanisms that regulate the magnitiude of GABAergic inhibition in the NTS remain unknown. We hypothesized that the level of GABAergic inhibition is proportionally regulated by the level of excitatory synaptic input to the NTS from baroreceptors. Using the in situ working heart,brainstem preparation in normotensive and spontaneously hypertensive rats, we blocked GABAA receptor-mediated neurotransmission in the NTS with gabazine (a specific GABAA receptor antagonist) at two levels of perfusion pressure (low PP, 60,70 mmHg; and high PP, 105,125 mmHg) while monitoring the immediate changes in cardiorespiratory variables. In normotensive rats, gabazine produced an immediate bradycardia consistent with disinhibition of NTS circuit neurones that regulate heart rate (HR) which was proportional to the level of arterial pressure (,HR at low PP, ,57 ± 9 beats min,1; at high PP, ,177 ± 9 beats min,1; P < 0.001), suggesting that GABAergic circuitry in the NTS modulating heart rate was arterial pressure dependent. In contrast, there was no significant difference in the magnitude of gabazine-induced bradycardia in spontaneously hypertensive rats at low or high PP (,HR at low PP, ,45 ± 10 beats min,1; at high PP, ,58 ± 7 beats min,1). With regard to thoracic sympathetic nerve activity (tSNA), at high PP there was a significant reduction in tSNA during the inspiratory (I) phase of the respiratory cycle, but only in the normotensive rat (,,tSNA =,18.7 ± 10%). At low PP, gabazine caused an elevation of the postinspiration phase of tSNA in both normotensive (,,tSNA = 23.7 ± 2.9%) and hypertensive rats (,,tSNA = 44.2 ± 14%). At low PP, gabazine produced no change in tSNA during the mid-expiration phase in either rat strain, but at high PP we observed a significant reduction in the mid-expiration phase tSNA, but only in the spontaneously hypertensive rat (,,tSNA =,25.2 ± 8%). Gabazine at both low and high PP produced a reduction in the late expiration phase of tSNA in the hypertensive rat (low PP, ,,tSNA =,29.4 ± 4.4%; high PP, ,tSNA =,22.8 ± 3%), whereas in the normotensive rat this was only significant at high PP (,,tSNA =,42.5 ± 6.1%). Therefore, in the spontaneously hypertensive rat, contrary to the GABAA receptor-mediated control of HR, it appears that GABAA receptor-mediated control of tSNA in the NTS is arterial pressure dependent. This study provides new insight into the origin of GABAergic inhibition in NTS circuitry affecting heart rate and sympathetic activity. [source]

Peroxynitrite/Nitric Oxide Balance in Ischemia/Reperfusion Injury-Nanomedical Approach

ELECTROANALYSIS, Issue 4 2006
Ruslan Kubant
Abstract Electrochemical nanosensors were used to simultaneously monitor in vitro (a single endothelial cell) and in vivo (vasculature of rat) the concentrations of NO (vasorelaxant), cytotoxic O (oxidative stress) and ONOO, (nitroxidative stress). A balance of [NO]/[ONOO,]=(K) was applied as the diagnostic marker of dysfunctional endothelium and cardiovascular disease. In the isolated endothelium of normotensive rats, K=,2.8±0.1 while in hypertensive rats, K=0.4±0.1. During ischemia, K dropped from 7±1 to 1.4±0.2 and further decreased to 0.05±0.01 during reperfusion. The edema and vasoconstriction, indicators of vascular injury, correlated directly with the decrease in K. [source]

Role of GABAergic neurones in the nucleus tractus solitarii in modulation of cardiovascular activity

Possible mechanisms of action of the neutral extract from Bidens pilosa L. leaves on the cardiovascular system of anaesthetized rats

PHYTOTHERAPY RESEARCH, Issue 10 2003
T. Dimo
Abstract The aim of this study was to investigate the hypotensive and cardiac effects of the neutral extract from Bidens pilosa leaves. Intravenous administration of the extract resulted in a biphasic dose-related hypotensive activity. In normotensive rats (NTR), B. pilosa decreased systolic blood pressure by 18.26%, 42.5% and 30% at doses of 10, 20 and 30 mg/kg, respectively. In spontaneously hypertensive rats (SHR), the decrease in systolic blood pressure was 25.77%, 38.96% and 28.64% at the above doses, respectively. These doses induced hypotension by 27%, 34.13% and 18.73% respectively in salt-loaded hypertensive rats. In NTR, B. pilosa reduced heart rate by 23.68% and 61.18% at doses of 20 and 30 mg/kg, respectively. The force of contraction of the heart was only affected at 30 mg/kg. The initial phase of hypotensive response was partially inhibited by atropine while propranolol increased this effect. These results suggest that B. pilosa exhibited its ,rst hypotensive effects by acting on the cardiac pump ef,ciency and secondly through vasodilation. [source]

Cardiovascular effects of the methanol and dichloromethanol extracts from Mentha suaveolens Ehrh.

PHYTOTHERAPY RESEARCH, Issue 5 2001
Dr R. Bello
Abstract Methanol and dichloromethanol extracts of the leaves and stems of Mentha suaveolens Ehrh. have been tested for their effects on resting arterial blood pressure, heart rate and noradrenaline induced hypertension. Both extracts administered by i.v. bolus to urethane anaesthetized normotensive rats reduced the mean arterial blood pressure and heart rate, while only the dichloromethanol extract prevented the noradrenaline induced hypertension. Copyright © 2001 John Wiley & Sons, Ltd. [source]

Erectile Function in Two-Kidney, One-Clip Hypertensive Rats is Maintained by a Potential Increase in Nitric Oxide Production

THE JOURNAL OF SEXUAL MEDICINE, Issue S3 2009
A. Elizabeth Linder PhD
ABSTRACT Introduction., Hypertension is closely associated with erectile dysfunction (ED) as it has been observed in many experimental models of hypertension. Additionally, epidemiological studies show that approximately a third of hypertensive patients have ED. Aim., To test the hypothesis that the two-kidney, one-clip (2K-1C) rat model of hypertension displays normal erectile function due to increased nitric oxide (NO) production in the penis. Methods., Ganglionic-induced increase in intracavernosal pressure (ICP)/mean arterial pressure (MAP) ratio was used as an index of erectile function in 2K-1C and in normotensive sham-operated (SHAM) anesthetized rats. Cavernosal strips from hypertensive and normotensive rats were used for isometric tension measurement. The contraction induced by alpha-adrenergic agonist phenylephrine and the relaxation induced by the NO donor sodium nitroprusside (SNP) and by the Rho-kinase inhibitor Y-27632 were performed in the absence and in the presence of the NO synthase inhibitor N, -nitro-L-arginine (L-NNA). Results., Changes in ICP/MAP induced by ganglionic stimulation were not different between 2K-1C and SHAM rats. The contractile response induced by phenylephrine as well as the relaxation induced by SNP or the Y-27632 were similar in cavernosal strips from both groups. However, in the presence of L-NNA, the relaxation induced by Y-27632 was significantly impaired in 2K-1C compared to SHAM. Conclusions., These data suggest that hypertension and ED could be dissociated from high levels of blood pressure in some animal models of hypertension. Erectile function in 2K-1C hypertensive rats is maintained in spite of the increased Rho-kinase activity by increased NO signaling. Linder AE, Dorrance AM, Mills TM, Webb RC, and Leite R. Erectile function in two-kidney, one-clip hypertensive rats is maintained by a potential increase in nitric oxide production. J Sex Med 2009;6(suppl 3):279,285. [source]

Acute hypertension reveals depressor and vasodilator effects of cannabinoids in conscious rats

BRITISH JOURNAL OF PHARMACOLOGY, Issue 1 2009
W-S Vanessa Ho
Background and purpose:, The cardiovascular effects of cannabinoids can be influenced by anaesthesia and can differ in chronic hypertension, but the extent to which they are influenced by acute hypertension in conscious animals has not been determined. Experimental approach:, We examined cardiovascular responses to intravenous administration of anandamide and the synthetic cannabinoid, (R)-(+)-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl)pyrrolo[1,2,3-de]-1,4-benzoxazin-6-yl]-1-naphthalenylmethanone (WIN55212-2), in conscious male Wistar rats made acutely hypertensive by infusion of angiotensin II (AII) and arginine vasopressin (AVP). Rats were chronically instrumented for measurement of arterial blood pressure and vascular conductances in the renal, mesenteric and hindquarters beds. Key results:, Anandamide dose-dependently decreased the mean arterial blood pressure of rats made hypertensive by AII-AVP infusion, but not normotensive rats. Interestingly, acute hypertension also revealed a hypotensive response to WIN55212-2, which caused hypertension in normotensive animals. The enhanced depressor effects of the cannabinoids in acute hypertension were associated with increased vasodilatation in hindquarters, renal and mesenteric vascular beds. Treatment with URB597, which inhibits anandamide degradation by fatty acid amide hydrolase, potentiated the depressor and mesenteric vasodilator responses to anandamide. Furthermore, haemodynamic responses to WIN55212-2, but not to anandamide, were attenuated by the CB1 receptor antagonist, AM251 [N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophen yl)-4-methyl-1H-pyrazole-3-carboxamide]. Conclusions and implications:, These results broadly support the literature showing that the cardiovascular effects of cannabinoids can be exaggerated in hypertension, but highlight the involvement of non-CB1 receptor-mediated mechanisms in the actions of anandamide. [source]

ROLE OF HYPOTHALAMIC ,2 -ADRENOCEPTOR ACTIVITY IN FRUCTOSE-INDUCED HYPERTENSION

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 10 2006
Marcos A Mayer
SUMMARY 1The aim of the present study was to investigate the effects of the ,2 -adrenoceptor antagonist yohimbine on blood pressure and heart rate (HR) regulation, as well as on adrenergic and serotoninergic neurotransmission, in fructose hypertensive (F) rats. 2The anterior hypothalamic area of control (C) and F rats was perfused with Ringer's solution containing 10 and 100 µg/mL yohimbine through a microdialysis concentric probe. The effects of yohimbine on mean arterial pressure (MAP) and HR, as well as on hypothalamic dihydroxyphenylacetic acid (DOPAC) and 5-hydroxyindole acetic acid (5-HIAA) levels, were measured according to perfusion time. 3Although intrahypothalamic perfusion of yohimbine increased blood pressure in C rats (,MAP 9 ± 1 and 11 ± 2 mmHg for 10 and 100 µg/mL yohimbine, respectively; P < 0.05 vs Ringer's perfusion), the ,-adrenoceptor antagonist did not modify MAP in F. Intrahypothalamic yohimbine had no effect on HR at either concentration tested. Intrahypothalamic perfusion of 10 and 100 µg/mL yohimbine increased DOPAC levels in C rats (135 ± 6 and 130 ± 5% of basal levels, respectively; both n = 6; P < 0.05 vs Ringer's perfusion), but not in F animals (115 ± 6 and 102 ± 6% of basal levels, respectively; both n = 6). In both C and F rats, yohimbine administration induced an increase in 5-HIAA dialysate levels. 4The results of the present study support the notion that ,2 -adrenoceptor tone of the anterior hypothalamus of normotensive rats, which contributes to normal blood pressure regulation, is not involved in the control of HR in either normotensive C or hypertensive F rats. The absence of changes in MAP after yohimbine perfusion in F rats suggests that the ,2 -adrenoceptor tone could be decreased in this group of rats and that this may be responsible for the maintenance of hypertension in this model. Intrahypothalamic perfusion of yohimbine increased DOPAC in the dialysate only in C rats, suggesting changes in presynaptic ,2 -adrenoceptor activity in fructose-overloaded rats. Conversely, increased 5-HIAA levels did not differ between C and F groups. [source]

COMPARISON OF ANGIOTENSIN II-INDUCED BLOOD PRESSURE AND STRUCTURAL CHANGES IN FISCHER 344 AND WISTAR KYOTO RATS

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 7 2004
Jocelyne Blanc
SUMMARY 1.,The purpose of the present study was to evaluate the blood pressure (BP) response, the BP and heart rate (HR) components of the startle reaction and the structure of the carotid artery and the aorta during chronic infusion of angiotensin (Ang) II in Fischer 344 (F344) compared with Wistar Kyoto (WKY) rats, two in-bred normotensive contrasted strains. 2.,Osmotic mini-pumps filled with saline vehicle or AngII (120 ng/kg per min) were implanted subcutaneously in 8-week-old normotensive rats and infused for 4 weeks in F344 rats (saline, n = 10; AngII, n = 10) and WKY rats (saline, n = 10; AngII, n = 9). Basal BP, HR and the responses to an acoustic startle stimulus (duration 0.7 s, 115 dB) were recorded in conscious rats. The structure of the carotid artery and aorta was determined in 4% formaldehyde-fixed arteries. 3.,Compared with WKY rats, vehicle-treated F344 rats had lower bodyweight (BW; 266 ± 7 vs 299 ± 9 g; P < 0.05) and heart weight (0.80 ± 0.02 vs 0.98 ± 0.04 g; P < 0.05) and higher aortic systolic BP (SBP; 131 ± 1 vs 123 ± 5 mmHg; P < 0.001) and diastolic BP (98 ± 3 vs 89 ± 2 mmHg; P < 0.001). In F344 rats, compared with the WKY rats, the wall thickness/BW ratio was increased in the carotid artery (156 ± 9 vs 131 ± 6 nm/g; P < 0.05) and abdominal aorta (264 ± 13 vs 217 ± 12 nm/g; P < 0.05) and decreased in the thoracic aorta (246 ± 13 vs 275 ± 8 nm/g; P < 0.05). There was no difference in elastin and collagen density. Angiotensin II differentially enhanced BP in both strains: (SBP: 163 ± 5 and 132 ± 4 mmHg in F344 and WKY rats, respectively; Pstrain × treatment < 0.05). Circumferential wall stress was increased in the aorta of F344 rats compared with WKY rats (1176 ± 39 vs 956 ± 12 kPa (P < 0.001) and 1107 ± 42 vs 813 ± 12 kPa (P < 0.001) in thoracic and abdominal aortas, respectively). The startle response was amplified in F344 rats, with enhanced increases in SBP and pulse pressure (PP) and bradycardia compared with responses of WKY rats (+44 ± 9 mmHg, +10 ± 2 mmHg and ,40 ± 17 b.p.m., respectively, in F344 rats vs+28 ± 4 mmHg, + 4 ± 2 mmHg and ,19 ± 10 b.p.m. in WKY rats, respectively; Pstrain < 0.05 for BP and PP). The startle response was not affected by AngII. 4.,These results indicate a higher BP producing an increase in wall thickness in F344 rats compared with WKY rats. We propose that an increase in sympathetic nervous activity causes these haemodynamic differences, as suggested by the excessive increase in BP during an acoustic startle stimulus. Angiotensin II increased BP in F344 rats, but did not exaggerate the increase in BP during the startle reaction. [source]

Enalapril Prevents Aortic Hyperreactivity And Remodelling In One-Kidney, One-Clip Hypertensive Rats Without Reducing Arterial Pressure

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 7 2000
Valdeci Cunha
SUMMARY 1. The present study was designed to evaluate the blood pressure-independent effects of angiotensin-converting enzyme (ACE) inhibition on cardiovascular structure and function in one-kidney, one-clip (1K1C) hypertensive rats. 2. The study was conducted in four groups of rats: (i) uninephrectomized normotensive rats (1K); (ii) 1K1C hypertensive rats; (iii) 1K rats treated with enalapril; and (iv) 1K1C rats treated with enalapril. Enalapril treatment (20 mg/kg per day, p.o.) was started after surgery to induce hypertension or nephrectomy and continued for 5 weeks. 3. The increase in blood pressure of 1K1C rats was associated with activation of cardiac and aortic, but not plasma, ACE activity and with hypertrophy of both heart and aorta. No difference in cardiac output and in vitro systolic function was observed among the groups. Hypertrophied aorta isolated from 1K1C rats displayed increased sensitivity to phenylephrine (PE) and unaltered responses to both acetylcholine (ACh) and sodium nitroprusside compared with the 1K group. 4. Enalapril treatment effectively inhibited plasma and tissue ACE activity in 1K1C and 1K rats. Enalapril did not prevent the development of hypertension and cardiac hypertrophy nor did it change haemodynamic parameters in 1K1C rats. However, enalapril prevented the increase in aortic media thickness and cross-sectional area and restored the hypersensitivity to PE in aortic rings of 1K1C rats. The endothelium-dependent response to ACh was enhanced by enalapril in the aorta of 1K but not 1K1C rats. 5. These results suggest a role for activated local angiotensin II generation in aortic but not cardiac hypertrophy secondary to 1K1C hypertension. [source]