Search

Start Over Subject NO synthase

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

Creator:
Mária Gerová
Format:
print, bez média, and svazek
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. Alterations of NO synthase isoforms in brain and kidney of rats with genetic and salt hypertension

Creator:
Silvie Hojná, Jaroslav Kuneš, and Jan Zicha
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, ledviny, kidneys, brainstem, diencephalon, NO synthase, genetic hypertension, 14, and 612
Language:
English
Description:
Both brain and peripheral nitric oxide (NO) play a role in the control of blood pressure and circ ulatory homeostasis. Central NO production seems to counteract angiotensin II-induced enhancement of sympathetic tone. The aim of our study was to evaluate NO synthase (NOS) activity and protein expression of its three isoforms - neuronal (nNOS), endothelial NOS (eNOS) and inducible (iNOS) - in two brain regions involved in blood pressure control (diencephalon and brainstem) as well as in the kidney of young adult rats with either genetic (12-week-old SHR) or salt- induced hypertension (8-week-old Dahl rats). We have demonstrated reduced nNOS and iNOS expression in brainstem of both hypertensive models. In SHR this abnormality was accompanied by attenuated NOS activity and was corrected by chronic captopril treatment which prevented the development of genetic hypertension. In salt hypertensive Dahl rats nNOS and iNOS expression was also decrea sed in the diencephalon where neural structures important for salt hypertension development are located. As far as peripheral NOS activity and expression is concerned, renal eNOS expression was considerably reduced in both genetic and salt-induced hypertension. In conclusions, we disclosed similar changes of NO system in the brainstem (but not in the diencephalon) of rats with genetic and salt-induced hypertension. Decreased nNOS ex pression was associated with increased blood pressure due to enhanced sympathetic tone., S. Hojná, J. Kuneš, J. Zicha., and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

3. 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

4. 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

5. Hypotensive Effect of Agmatine, Arginine Metabolite, is Affected by NO Synthase

Creator:
Gerová, M. and Török, J.
Type:
article, model:article, and TEXT
Subject:
Agmatine, Hypotension, NO synthase, NO-deficient hypertension, and Aorta relaxation
Language:
English
Description:
The metabolites of arginine were recently shown to be involved in cardiovascular control. The study addresses the general cardiovascular response of anaesthetized rats to agmatine, a decarboxylated arginine. The relation between two arginine metabolic pathways governed by arginine decarboxylase and nitric oxide synthase was investigated. Intravenous administration of agmatine 30 and 60 μM/0.1 ml saline elicited remarkable hypotension of 42.6±4.6 and 70.9±6.5 mm Hg, respectively. The hypotension was characterized by long duration with half-time of return 171.6±2.9 and 229.2±3.8 s, respectively. The time of total blood pressure (BP) recovery was about 10 min. Dose-dependent relaxation to agmatine was also found in aorta rings in vitro. Both doses of agmatine administered 60-180 min after NO synthase inhibition (L-NAME 40 mg/kg i.v.) caused greater hypotension 59.0±7.6 and 95.8±8.8 mm Hg (P<0.01 both) compared to animals with intact NO synthase, but this was accompanied by a significant shortening of the half-time of BP return. If agmatine was administered to hypertensive NO-deficient rats (treated with 40 mg/kg/day L-NAME for 4 weeks), similar significant enhancement of hypotension was observed at both agmatine doses, again with a significant shortening of half-time of BP return. It can be summarized that the long-lasting hypotension elicited by agmatine was amplified after acute or chronic NO synthase inhibition, indicating a feedback relation between the two metabolic pathways of arginine.
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

7. Muscle NMDA receptors regulate the resting membrane potential through NO-synthase

Creator:
Urazaev, A. Kh., Magsumov, S. T., Poletayev, G. I., Nikolsky, E. E., and Vyskočil, F.
Type:
article, model:article, and TEXT
Subject:
denervation, resting membrane potential, neuromuscular junction, NO synthase, and NMDA receptor
Language:
English
Description:
The early postdenervation depolarization of rat diaphragm muscle fibres (8-10 mV) is substantially smaller (3 mV) when muscle strips are bathed with 1 mM L-glutamate (GLÜ) or N-methyl-D-aspartate (NMDA). The effects of GLÜ and NMDA are not seen in the presence of aminophosphonovaleric acid (APV), a blocker of NMDA-subtype of glutamate receptors, 5 mM Mg2+ (which blocks NMDA-controlled ion channels) and L-nitroarginine methylester (NAME), an inhibitor of NO-synthase. This indicates that NMDA-subtype of GL(J receptors might be involved in the regulation of the membrane potential in muscle fibres, most probably through the NO-synthase system.
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

8. Non-quantal acetylcholine release is increased after nitric oxide synthase inhibition

Creator:
Mukhtarov, M. R., Vyskočil, F., Urazaev, A. Kh., and Nikolsky, E. E.
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, acetylcholin, acetylcholine, rat diaphragm, NO synthase, non-quantal release, 14, and 612
Language:
English
Description:
M. R. Mukhtarov, F. Vyskočil, A. Kh. Urazaev, E. E. Nikolsky. and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public