Document Detail


Systemic blood pressure response to the inhibition of two hyperpolarizing pathways: a comparison to NO-synthase inhibition.
MedLine Citation:
PMID:  16497109     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The impact on blood pressure of two vasodilating mechanisms, underlied by vascular smooth muscle hyperpolarization, was studied and compared to that induced by nitric oxide NO mechanism. Systemic blood pressure, after inhibitory intervention in arachidonic acid metabolism cytochrome P-450 inhibition by miconazole 0.5 mg/100 g b.w. , one of the hyperpolarizing pathways, did not change. After the inhibition of the action voltage-dependent K(+) channels operator by 4-aminopyridine 0.1 mg/100 g b.w. , the other hyperpolarizing pathway, blood pressure declined slightly from 132.3+/-3.2 mm Hg to 116.5+/-5.0 mm Hg, P<0.05 . Inhibition of nitric oxide production L-NAME 5 mg/100 g b.w. increased blood pressure considerably 123.5+/-2.7 mm Hg to 155.4+/-3.1 mm Hg, P<0.001 . After inhibition of the hyperpolarizing pathway by miconazole, hypotension induced by acetylcholine (Ach, 10 microg represented 63.0+/-1.9 mm Hg vs control value 78.6+/-5.2 mm Hg P<0.001 , by bradykinin (BK) 100 microg 59.4+/-3.9 mm Hg vs control value 71.2+/-6.1 mm Hg P<0.05 . After inhibition of the hyperpolarizing pathway by 4-aminopyridine, hypotension induced by ACh 10 microg achieved 64.6+/-2.5 mm Hg vs control value 78.4+/-2.8 mm Hg P<0.001 and that induced by BK 100 microg 56.6+/-5.3 mm Hg vs control value 72.3+/-2.5 mm Hg P<0.001 . ACh or BK hypotension after the inhibition of the above hyperpolarizing pathways was significantly attenuated. On the contrary, after NO-synthase inhibition the hypotension to ACh was significantly enhanced. Blood pressure decrease after ACh 10 microg hypotension was 91.8+/-4.1 mm Hg vs control value 79.3+/-3.3 mm Hg P<0.01 , and after BK 100 microg it was 78.4+/-7.1 mm Hg vs control value 68.3+/-5.2 mm Hg. A different basal BP response, but equally attenuated hypotension to Ach and BK, was detected after the inhibition of two selected hyperpolarizing pathways. In cotrast, the inhibition of NO production elicited an increase in systemic BP and augmentation of ACh and BK hypotension. The effectiveness of further hyperpolarizing mechanisms in relation to systemic BP regulation and nitric oxide level remains open.
Authors:
M Gerová; M Kittová
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Physiological research / Academia Scientiarum Bohemoslovaca     Volume:  55     ISSN:  0862-8408     ISO Abbreviation:  Physiol Res     Publication Date:  2006  
Date Detail:
Created Date:  2006-12-20     Completed Date:  2007-02-15     Revised Date:  2008-04-02    
Medline Journal Info:
Nlm Unique ID:  9112413     Medline TA:  Physiol Res     Country:  Czech Republic    
Other Details:
Languages:  eng     Pagination:  603-10     Citation Subset:  IM    
Affiliation:
Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, Bratislava, Slovak Republic. maria.gerova@savba.sk
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MeSH Terms
Descriptor/Qualifier:
4-Aminopyridine / pharmacology
Acetylcholine / pharmacology
Animals
Arachidonic Acid / metabolism
Biological Factors / metabolism*
Blood Pressure / drug effects
Bradykinin / pharmacology
Carotid Arteries / drug effects,  metabolism*
Cytochrome P-450 Enzyme System / antagonists & inhibitors,  metabolism*
Dose-Response Relationship, Drug
Enzyme Inhibitors / pharmacology
Male
Miconazole / pharmacology
Muscle, Smooth, Vascular / drug effects,  metabolism*
NG-Nitroarginine Methyl Ester / pharmacology
Nitric Oxide Synthase / antagonists & inhibitors,  metabolism*
Potassium Channel Blockers / pharmacology
Potassium Channels, Voltage-Gated / drug effects,  metabolism*
Rats
Rats, Wistar
Vasodilator Agents / pharmacology
Chemical
Reg. No./Substance:
0/Biological Factors; 0/Enzyme Inhibitors; 0/Potassium Channel Blockers; 0/Potassium Channels, Voltage-Gated; 0/Vasodilator Agents; 0/endothelium-dependent hyperpolarization factor; 22916-47-8/Miconazole; 504-24-5/4-Aminopyridine; 506-32-1/Arachidonic Acid; 50903-99-6/NG-Nitroarginine Methyl Ester; 51-84-3/Acetylcholine; 58-82-2/Bradykinin; 9035-51-2/Cytochrome P-450 Enzyme System; EC 1.14.13.39/Nitric Oxide Synthase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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