Linked Life Data

8931832

Source:http://linkedlifedata.com/resource/pubmed/id/8931832

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1997-2-18
pubmed:abstractText
The effects of the administration of either the angiotensin converting enzyme (ACE) inhibitor, quinapril (10 mg/kg/day, orally), or the calcium antagonist, diltiazem (100 mg/kg/day, orally), on blood pressure (BP), renal function, and vascular reactivity in isolated perfused mesenteric beds were studied in rats treated for 8 weeks with the nitric oxide (NO) synthesis inhibitor, NG-nitro-L-arginine methyl ester (LNAME, 40 mg/kg/day). The oral administration of LNAME significantly increased systolic BP values, which reached the levels of 186 +/- 7 mm Hg at week 8. Both quinapril and diltiazem reduced this, although the ACE inhibitor was more effective than the calcium antagonist. The chronic inhibition of NO resulted in an increase in water excretion whether or not the increase in systolic BP was prevented by the coadministration of either quinapril or diltiazem. At the end of the experiment, LNAME-treated rats presented higher proteinuria than control rats (140 +/- 4 mg/24 hours v 21 +/- 1 mg/24 hours, P < .05). This elevated protein excretion was normalized by both antihypertensive drugs. None of the treatments was able to modify either natriuresis or plasma creatinine levels. Endothelium-dependent relaxations to acetylcholine (10(-12) to 10(-8) mol/L) were comparable in all groups. However, the vasoconstriction induced by either the continuous infusion of phenylephrine (10(-5) mol/L) or by a bolus of angiotensin II (1 nmol) was higher in the animals that received LNAME than in control ones. The antihypertensive therapy normalized the response to phenylephrine but not to angiotensin II. These data suggest that both quinapril and diltiazem are not only able to reduce BP elevation induced by the chronic administration of LNAME in rats, but also to prevent the renal damage and the hyperresponsiveness to phenylephrine induced by this NO synthesis inhibitor.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0895-7061
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1077-83
pubmed:dateRevised
2009-2-24
pubmed:meshHeading
pubmed-meshheading:8931832-Angiotensin-Converting Enzyme Inhibitors, pubmed-meshheading:8931832-Animals, pubmed-meshheading:8931832-Antihypertensive Agents, pubmed-meshheading:8931832-Blood Pressure, pubmed-meshheading:8931832-Calcium Channel Blockers, pubmed-meshheading:8931832-Diltiazem, pubmed-meshheading:8931832-Diuresis, pubmed-meshheading:8931832-Dose-Response Relationship, Drug, pubmed-meshheading:8931832-Enzyme Inhibitors, pubmed-meshheading:8931832-Isoquinolines, pubmed-meshheading:8931832-Kidney, pubmed-meshheading:8931832-Male, pubmed-meshheading:8931832-NG-Nitroarginine Methyl Ester, pubmed-meshheading:8931832-Nitric Oxide Synthase, pubmed-meshheading:8931832-Random Allocation, pubmed-meshheading:8931832-Rats, pubmed-meshheading:8931832-Rats, Sprague-Dawley, pubmed-meshheading:8931832-Splanchnic Circulation, pubmed-meshheading:8931832-Tetrahydroisoquinolines
pubmed:year
1996
pubmed:articleTitle
Renal and vascular consequences of the chronic nitric oxide synthase inhibition. Effects of antihypertensive drugs.
pubmed:affiliation
Department of Physiology, School of Medicine, University Complutense, Madrid, Spain.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't