Document Detail


Influences of carvedilol treatment on the effects of acetylcholine on regional haemodynamics in the spontaneously hypertensive rat.
MedLine Citation:
PMID:  9730849     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
1. In a previous report, we have shown that vasodilatation induced by acetylcholine is impaired in the kidney and the heart of the spontaneously hypertensive rat (SHR) in vivo. The present investigation was performed to study the influence of oral antihypertensive treatment with carvedilol for 6 to 10 weeks on acetylcholine-induced changes in regional haemodynamics in SHR in vivo. Cardiac output, regional blood flow and vascular resistance in organs of major importance in hypertensive disease, such as the kidney, heart, skeletal muscle, brain and eye, were measured with radioactively labelled microspheres in anaesthetized rats (aged 12-16 weeks).2. Mean arterial blood pressure was significantly lower in the carvedilol-treated SHR group (156+/-3 mmHg, n=17) than in an untreated SHR group (172+/-6 mmHg, n=13). Infusion of acetylcholine (2 microgram.min-1.kg-1) caused similar significant reductions in blood pressure in the two groups (-13+/-1% and -14+/-2%). However, acetylcholine induced a significant increase in total peripheral vascular resistance in the carvedilol group (29+/-10%, P<0.01), whereas no significant change was observed in the control group (0+/-11%).3. Acetylcholine significantly increased renal vascular resistance in the carvedilol group (+62+/-15%, P<0.01), but did not change vascular resistance in the control group (-6+/-6%). In the heart, acetylcholine did not affect vascular resistance in the carvedilol group, but reduced vascular resistance significantly in the control group (-17+/-8%, P<0.05). The circulatory changes induced by acetylcholine in the skeletal muscle, brain and ophthalmic circulation did not differ between the groups.4. In conclusion, the results demonstrate that long-term oral carvedilol treatment in the SHR did not enhance acetylcholine-induced vasodilatation, but instead pronounced renal vasoconstriction was induced by acetylcholine, which could partly be due to a decreased cardiac index.
Authors:
S O Granstam; B Fellström; L Lind
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Clinical science (London, England : 1979)     Volume:  95     ISSN:  0143-5221     ISO Abbreviation:  Clin. Sci.     Publication Date:  1998 Sep 
Date Detail:
Created Date:  1999-01-14     Completed Date:  1999-01-14     Revised Date:  2013-05-28    
Medline Journal Info:
Nlm Unique ID:  7905731     Medline TA:  Clin Sci (Lond)     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  303-9     Citation Subset:  IM    
Affiliation:
Department of Medicine, University Hospital of Uppsala, 75185 Uppsala, Sweden.
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MeSH Terms
Descriptor/Qualifier:
Acetylcholine / pharmacology*
Administration, Oral
Adrenergic Antagonists / pharmacology*
Animals
Blood Pressure / drug effects
Carbazoles / pharmacology*
Coronary Circulation / drug effects
Hemodynamics / drug effects*
Male
Propanolamines / pharmacology*
Rats
Rats, Inbred SHR
Regional Blood Flow / drug effects
Renal Circulation / drug effects
Vascular Resistance / drug effects
Vasodilator Agents / pharmacology*
Chemical
Reg. No./Substance:
0/Adrenergic Antagonists; 0/Carbazoles; 0/Propanolamines; 0/Vasodilator Agents; 0K47UL67F2/carvedilol; 51-84-3/Acetylcholine

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


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