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1. Acetylcholine and bradykinin induce paradoxically amplified hypotensive response in hypertensive NO-deficient rats

Creator:
Mária Gerová
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Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, fyziologie, physiology, NO synthase, long-term NO synthase inhibition, acetylcholine hypotension, bradykinin hypotension, L-NAME, 14, and 612
Language:
English
Description:
M. Gerová. and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

2. Acute and chronic role of nitric oxide, renin-angiotensin system and sympathetic nervous system in the modulation of calcium sensitization in wistar rats

Creator:
Brunová, A., Bencze, M., Michal Behuliak, and Josef Zicha
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Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, krevní tlak, oxid dusnatý, sympatický nervový systém, blood pressure, nitric oxide, sympathetic nervous system, calcium sensitization, rho-kinase, renin-angiotensin system, prostanoids, fasudil, L-NAME, captopril, guanethidine, pentolinium, indomethacin, 14, and 612
Language:
English
Description:
Principal vasoactive systems - renin-angiotensin system (RAS), sympathetic nervous system (SNS), nitric oxide (NO) and prostanoids - exert their vascular effects through the changes in calcium levels and/or calcium sensitization. To estimate a possible modulation of calcium sensitization by the above vasoactive systems, we studied the influence of acute and chronic blockade of particular vasoactive systems on blood pressure (BP) changes elicited in conscious normotensive rats by acute dose-dependent administration of Rho-kinase inhibitor fasudil. Adult male chronically cannulated Wistar rats were used throughout this study. The acute inhibition of NO synthase (NOS) by L-NAME enhanced BP response to fasudil, the effect being considerably augmented in rats deprived of endogenous SNS. The acute inhibition of prostanoid synthesis by indomethacin modified BP response to fasudil less than the acute NOS inhibition. The chronic NOS inhibition caused moderate BP elevation and a more pronounced augmentation of fasudilinduced BP changes compared to the effect of acute NOS inhibition. This indicates both short-term and long-term NOdependent attenuation of calcium sensitization. Long-term inhibition of RAS by captopril caused a significant attenuation of BP changes elicited by fasudil. In contrast, a long-term attenuation of SNS by chronic guanethidine treatment (in youth or adulthood) had no effect on BP response to fasudil, suggesting the absence of SNS does not affect calcium sensitization in vascular smooth muscle of normotensive rats. In conclusion, renin-angiotensin system contributes to the long-term increase of calcium sensitization and its effect is counterbalanced by nitric oxide which decreases calcium sensitization in Wistar rats., A. Brunová, M. Bencze, M. Behuliak, J. Zicha., and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

3. Captopril prevents NO-deficient hypertension and left ventricular hypertrophy without affecting nitric oxide synthase activity in rats

Creator:
Bernátová, I., Pecháňová, O., and Šimko, F.
Type:
article, model:article, and TEXT
Subject:
nitric oxide synthase, captopril, L-NAME, angiotensin II, hypertrophy, and hypertension
Language:
English
Description:
The aim of the study was to assess whether angiotensin converting enzyme (ACE) inhibition with captopril prevents the development of hypertension and myocardial hypertrophy and affects nitric oxide synthase (NOS) activity in rats. Animals were divided into five groups: control, two groups receiving NG-nitro-L-arginine methyl ester (L-NAME) 20 or 40 mg/kg/day, a group receiving captopril 100 mg/kg/day and a group concomitantly treated with 40 mg/kg/day L-NAME plus 100 mg/kg/day captopril. After four weeks, systolic blood pressure (SBP) significantly increased in both L-NAME groups by 30 % and 34 %, respectively. In the captopril group, SBP significantly decreased by 30 % and in the captopril plus L-NAME group SBP was not changed as compared to the controL Although left ventricular weight/body weight (LVW/BW) ratio in both L-NAME groups was significantly elevated by 19 % and 29 %, respectively, no alterations in LVW/BW ratio were found in the captopril group and captopril plus L-NAME group. In both groups receiving L-NAME, NOS activity significantly decreased by 17 % and 69 % in the heart, by 14 % and 26 % in the aorta, by 60 % and 73 % in the brain and by 13 % and 30 % in the kidney, respectively. Captopril did not influence NO synthase activity in any of the studied tissues. We conclude that captopril prevents the development of hypertension and LV hypertrophy without affecting NO formation.
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http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

4. Changes of Sodium and ATP Affinities of Renal Na,K-ATPase During and After Nitric Oxide-Deficient Hypertension

Creator:
Vrbjar, N., Veronika Javorková, and Oľga Pecháňová
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Type:
article, studie, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, fyziologie člověka, human physiology, Sodium pump, Nitric oxide, Hypertension, L-NAME, Kidney, 14, and 612
Language:
English
Description:
The aim of this study was to assess the molecular basis of renal Na,K-ATPase disturbances in response to NO-deficient hypertension induced in rats by NO-synthase inhibition with 40 mg/kg/day NG-nitro-L-arginine methyl ester (L-NAME) for four weeks. After 4-week administration of L-NAME, the systolic blood pressure (SBP) increased by 30 %. Three weeks after terminating the treatment, SBP recovered to control value. When activating the Na,K-ATPase with its substrate ATP, a 36 % increase in Km and 29 % decrease in Vmax values were observed in NO-deficient rats. During activation with Na+, the Vmax was decreased by 20 % and the KNa was increased by 111 %, indicating a profound decrease in the affinity of the Na+-binding site in NO-deficient rats. After spontaneous recovery from hypertension, the Vmax remained at the level as in hypertension for both types of enzyme activation. However, in the presence of lower concentrations of substrate which are of physiological relevance an improvement of the enzyme activity was observed as documented by return of Km for ATP to control value. The KNa value for Na+ was decreased by 27 % as compared to hypertension, but still exceeded the corresponding value in the control group by 55 % thus resulting in a partial restoration of Na+ affinity of Na,K-ATPase which was depressed as a consequence of NO-dependent hypertension., N. Vrbjar, V. Javorková, O. Pecháňová., and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

5. Effect of captopril on cyclic nucleotide concentrations during long-term NO synthase inhibition

Creator:
Oľga Pecháňová and Iveta Bernátová
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, oxid dusnatý, hypertenze, nitric oxide, hypertension, NO synthase, cyclic nucleotides, L-NAME, ACE inhibitor, 14, and 612
Language:
English
Description:
The aim of the present study was to determine the effect of angiotensin-converting enzyme inhibitor captopril on cGMP and cAMP concentration in the left ventricle and aorta after NO synthase inhibition by 4-week-lasting NG-nitro-L-arginine-methyl ester (L-NAME) treatment. Five groups of rats were investigated: controls, L-NAME in the dose 20 mg/kg/day (L-NAME 20), L-NAME in the dose 40 mg/kg/day (L-NAME 40), captopril in the dose 100 mg/kg/day, L-NAME 40 mg/kg/day together with captopril 100 mg/kg/day. Captopril completely prevented L-NAME-induced hypertension and LV hypertrophy development. Compared to the controls, cGMP concentration in the L-NAME 20 and L-NAME 40 groups was decreased by 13 % and 22 %, respectively, in the left ventricle and by 27 % and 56 % in the aorta, respectively. Captopril did not influence this decrease of cGMP concentration. Cyclic AMP concentration in the aorta of L-NAME 20 group increased by 17 %. In the L-NAME 40 group, cAMP concentration increased by 17 % in the left ventricle and by 34 % in the aorta compared to controls. This increase was enhanced in rats given L-NAME together with captopril. Captopril alone had no effect on cAMP concentration. We conclude that captopril does not affect the concentration of cGMP, however, it has more than the additive effect on the cAMP concentration increase in the cardiovascular system during long-term NO synthase inhibition., O. Pecháňová, I. Bernátová., and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

6. Effect of long-term NO synthase inhibition on cyclic nucleotide content in rat tissues

Creator:
Pecháňová, O. and Bernátová, I.
Type:
article, model:article, and TEXT
Subject:
NO synthase, L-NAME, cGMP, cAMP, and hypertrophy
Language:
English
Description:
The effect of 4 weeks’ inhibition of NO synthase by nitro-L-arginine methyl ester (L-NAME) on haemodynamic parameters and cGMP and cAMP content was studied in rat tissues. L-NAME in both 20 mg/kg/day and 40 mg/kg/day doses significantly increased systolic blood pressure by 28 % and 30 % and decreased the heart rate by 14 % and 23 %, respectively, after the first week. These changes persisted during the following three weeks. Left ventricular weight/body weight (LVW/BW) ratio was significantly elevated in both L-NAME-treated groups by 19 % and 29 %, respectively. Radioimmunoassay was used to determine the cGMP and cAMP content Cyclic GMP content in animals treated by L-NAME (20 mg/kg/day and 40 mg/kg/day) decreased significantly by 13 % and 22 % in the left ventricle, by 28 % and 62 % in the aorta, by 20 % and 34 % in the brain, and by 10 % and 15 % in the kidney, respectively. On the other hand, the cAMP content increased in both L-NAME treated groups by 8 % and 9 % in the left ventricle, by 28 % and 46 % in the aorta, and by 23 % and 32 % in the brain, respectively. There were no significant changes in kidney cAMP content as compared to control animals. The results suggest a simultaneous decrease of cGMP and increase of cAMP content in the majority of studied tissues during NO-deficient hypertension.
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

7. Effect of losartan, an angiotensin II type 1 receptor antagonist on cardiac autonomic functions of rats during acute and chronic inhibition of nitric oxide synthesis

Creator:
Chaswal, M., Sakti Das, Prasad, J., Katyal, A., Mishra, A. K., and Fahim, M.
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, fyziologie člověka, human physiology, losartan, L-NAME, angiotensin II, baroreflex sensitivity, heart rate variability, 14, and 612
Language:
English
Description:
We studied the effect of losartan on baroreflex sensitivity (BRS) and heart rate variability (HRV) of adult Wistar rats during acute and chronic inhibition of nitric oxide synthesis by NG -nitro-Larginine methyl ester (L-NAME). Chronic L-NAME administration (50 mg/kg per day for 7 days, orally through gavage) increased mean arterial pressure (MAP), heart rate but significantly decreased BRS. In addition, a significant fall of standard deviation of normal RR intervals, total spectral power, high frequency spectral power and a rise of low frequency to high frequency (LF: HF) ratio was seen. Acute L-NAME administration (30 mg/kg, i.v. bolus dose) also raised MAP and impaired HRV but it was associated with augmented BRS for bradycardia reflex. Losartan treatment (10 mg/kg, i.v.) in both acute and chronic L-NAME treated rats, decreased MAP but the difference was not significant. On the other hand, losartan administration normalized depressed BRS for bradycardia reflex and significantly reduced LF to HF ratio in chronic L-NAME treated rats. But this improvement was not observed in acute L-NAME group. These results indicate importance of mechanisms other than renin-angiotensin system in the pressor response of both acute as well as chronic L-NAME. However, autonomic dysregulation especially following chronic L-NAME appears to be partly angiotensin dependent., M. Chaswal ... [et al.]., and Obsahuje seznam literatury
Rights:
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9. Inhibition of NO synthase activity in nervous tissue leads to decreased motor activity in the rat

Creator:
Lukáč Halčák, Oľga Pecháňová, Žigová, Z., Klemová, L., Novacký, M., and Iveta Bernátová
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, oxid dusnatý, nitric oxide, L-NAME, nervous tissue, spontaneous behavior, habituation tasks, 14, and 612
Language:
English
Description:
The nitric oxide/cGMP system has been shown to play a crucial role in the mechanism of learning and memory. The aim of the present study was to investigate whether the inhibition of NO synthase in brain regions leads to alterations of spontaneous behavior in rats. Male Wistar rats were treated with NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) at the dose of 40 mg/kg/day. After 4 weeks of L-NAME treatment, NO synthase activity was significantly decreased by 75 % in the cerebellum, by 71 % in the cerebral cortex and by 72 % in the thoracic spinal cord. Decreased NO synthase activity in the nervous tissue was associated with decreased motor horizontal and vertical activities as well as by lowered frequency of sniffing, cleaning and defecation. It is concluded that the inhibition of NO synthase activity has a suppressive effect on spontaneous behavior of rats., L. Halčák, O. Pecháňová, Z. Žigová, L. Klemová, M. Novacký, I. Bernátová., and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

10. Ivabradine does not impair anxiety-like behavior and memory in both healthy and L-NAME-induced hypertensive rats

Creator:
Krajcirovicova, K., Aziriova, S., Baka, T., Repova, K., Adamcova, M., Paulis, L., and Simko, F.
Format:
bez média and svazek
Type:
model:article and TEXT
Subject:
ivabradine, L-NAME, hypertension, heart rate, and behavior
Language:
English
Description:
Cardiovascular pathologies are frequently associated with anxiety and other behavioral disturbances. Ivabradine, an inhibitor of the hyperpolarization-activated cyclic nucleotide-gated channels in the sinoatrial node, decreases heart rate and provides cardiovascular protection. Although ivabradine is increasingly used in cardiovascular medicine, the data on its behavioral effects are lacking. The aim of this work was to show ivabradine’s potential effect on behavior in healthy and hypertensive rats. After a four-week treatment period, systolic blood pressure was increased in the N(G)-nitro-L-arginine methyl ester (L-NAME)-group and ivabradine significantly reduced it. Furthermore, it reduced the heart rate in both the control and L-NAME-group. In the control group, ivabradine enhanced the time spent in and transition to the open arms of the elevated plus maze test (EPM). In the L-NAME-group, ivabradine does not show a significant effect on the time spent in the EPM open arms and the number of transitions into them. Furthermore, ivabradine has no impact on cognitive function in both control and L-NAME groups. We conclude that ivabradine showed no undesirable effects on anxiety, locomotion or learning; in fact, some of these parameters were even improved. For the first time it has been shown that ivabradine is a safe cardiovascular drug regarding its effect on psycho-behavioral manifestations.
Rights:
http://creativecommons.org/publicdomain/mark/1.0/ and policy:public