| pubmed-article:8203622 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8203622 | lifeskim:mentions | umls-concept:C0020538 | lld:lifeskim |
| pubmed-article:8203622 | lifeskim:mentions | umls-concept:C0028128 | lld:lifeskim |
| pubmed-article:8203622 | lifeskim:mentions | umls-concept:C0003009 | lld:lifeskim |
| pubmed-article:8203622 | lifeskim:mentions | umls-concept:C2003941 | lld:lifeskim |
| pubmed-article:8203622 | lifeskim:mentions | umls-concept:C0205191 | lld:lifeskim |
| pubmed-article:8203622 | pubmed:issue | 5 Pt 2 | lld:pubmed |
| pubmed-article:8203622 | pubmed:dateCreated | 1994-7-5 | lld:pubmed |
| pubmed-article:8203622 | pubmed:abstractText | Nitric oxide (NO) is a tonically produced vasodilator that maintains blood pressure (BP) in the normal animal. In these studies, we produced chronic NO blockade by oral administration of the NO synthesis inhibitor nitro-L-arginine methyl ester (L-NAME), which produced sustained hypertension and increased renal vascular resistance (RVR) in conscious rats. Acute blockade of the angiotensin II type 1 (AT1) receptor with losartan had little effect on BP and RVR in either chronically NO-blocked or normal conscious rats. Acute blockade of the alpha 1-adrenoceptor with prazosin produced moderate similar falls in BP in both chronically NO-blocked and normal rats. The combination of AT1 and alpha 1-adrenoceptor blockade was profoundly antihypertensive and was particularly effective in lowering BP in chronically NO-blocked rats where the hypertension was obliterated. In contrast, the increased RVR persisted in chronically NO-blocked rats receiving combined acute AT1 and alpha 1-adrenoceptor blockade. These observations indicate that, in the sustained phase of chronic NO blockade, the hypertension is largely due to the combined activities of alpha 1-adrenoceptor and AT1 stimulation. | lld:pubmed |
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| pubmed-article:8203622 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8203622 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8203622 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8203622 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8203622 | pubmed:month | May | lld:pubmed |
| pubmed-article:8203622 | pubmed:issn | 0002-9513 | lld:pubmed |
| pubmed-article:8203622 | pubmed:author | pubmed-author:BaylisCC | lld:pubmed |
| pubmed-article:8203622 | pubmed:author | pubmed-author:EngelsKK | lld:pubmed |
| pubmed-article:8203622 | pubmed:author | pubmed-author:QinHH | lld:pubmed |
| pubmed-article:8203622 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8203622 | pubmed:volume | 266 | lld:pubmed |
| pubmed-article:8203622 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8203622 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8203622 | pubmed:pagination | R1470-6 | lld:pubmed |
| pubmed-article:8203622 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:8203622 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:8203622 | pubmed:articleTitle | Angiotensin II and alpha 1-adrenergic tone in chronic nitric oxide blockade-induced hypertension. | lld:pubmed |
| pubmed-article:8203622 | pubmed:affiliation | Department of Physiology, West Virginia University, Morgantown 26506-9229. | lld:pubmed |
| pubmed-article:8203622 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8203622 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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