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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4-6
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pubmed:dateCreated |
2008-11-10
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pubmed:abstractText |
We studied the effect an inhibitor of Ras-GTPase (FPTIII, 1.5 mg/kg alt diem for 4 weeks) on mean arterial pressure (MAP), urine protein, vascular reactivity and cardiac function in streptozotocin (STZ)-induced diabetes in control normotensive (WKY) and spontaneously hypertensive rats (SHR). The increased urinary protein in STZ-treated WKY (D-WKY) and STZ-treated SHR (D-SHR) were significantly lower in FPTIII treated D-WKY and D-SHR. The abnormal vascular responsiveness to endothelin-1, angiotensin II, carbachol or histamine in isolated carotid artery from D-WKY and D-SHR was improved by chronic treatment with FPTIII. In isolated perfused hearts, recovery of left ventricular function from 40 min of global ischemia was significantly improved in FPTIII treated D-WKY and D-SHR. These results show that treatment with FPTIII can attenuate development of abnormal vascular reactivity and renal/cardiac dysfunction during simultaneous occurrence of hypertension and diabetes.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/2-(2-oxo-2-((3,7,11-trimethyl-2,6,10...,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/Carbachol,
http://linkedlifedata.com/resource/pubmed/chemical/Endothelin-1,
http://linkedlifedata.com/resource/pubmed/chemical/GTP Phosphohydrolases,
http://linkedlifedata.com/resource/pubmed/chemical/Histamine,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphonic Acids,
http://linkedlifedata.com/resource/pubmed/chemical/Streptozocin,
http://linkedlifedata.com/resource/pubmed/chemical/ras Proteins
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pubmed:status |
MEDLINE
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pubmed:issn |
1537-1891
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
49
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
151-7
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pubmed:meshHeading |
pubmed-meshheading:18706523-Angiotensin II,
pubmed-meshheading:18706523-Animals,
pubmed-meshheading:18706523-Blood Pressure,
pubmed-meshheading:18706523-Carbachol,
pubmed-meshheading:18706523-Cardiovascular Diseases,
pubmed-meshheading:18706523-Carotid Arteries,
pubmed-meshheading:18706523-Diabetes Mellitus, Experimental,
pubmed-meshheading:18706523-Drug Synergism,
pubmed-meshheading:18706523-Endothelin-1,
pubmed-meshheading:18706523-GTP Phosphohydrolases,
pubmed-meshheading:18706523-Histamine,
pubmed-meshheading:18706523-Hypertension,
pubmed-meshheading:18706523-Male,
pubmed-meshheading:18706523-Myocardial Reperfusion Injury,
pubmed-meshheading:18706523-Phosphonic Acids,
pubmed-meshheading:18706523-Rats,
pubmed-meshheading:18706523-Rats, Inbred SHR,
pubmed-meshheading:18706523-Rats, Inbred WKY,
pubmed-meshheading:18706523-Signal Transduction,
pubmed-meshheading:18706523-Streptozocin,
pubmed-meshheading:18706523-ras Proteins
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pubmed:articleTitle |
Inhibition of Ras-GTPase signaling by FPTIII ameliorates development of cardiovascular dysfunction in diabetic-hypertensive rats.
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pubmed:affiliation |
Department of Pharmacology & Toxicology, Faculty of Medicine, Kuwait University, Kuwait. mariam@hsc.edu.kw
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pubmed:publicationType |
Journal Article,
In Vitro
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