Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions |
umls-concept:C0003483,
umls-concept:C0018792,
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0027481,
umls-concept:C0034493,
umls-concept:C0035028,
umls-concept:C0122426,
umls-concept:C0205314,
umls-concept:C0205409,
umls-concept:C0231491,
umls-concept:C0332206,
umls-concept:C0439659,
umls-concept:C0597421,
umls-concept:C0599840,
umls-concept:C0679622,
umls-concept:C1564522
|
pubmed:issue |
6
|
pubmed:dateCreated |
1993-2-8
|
pubmed:abstractText |
HS-142-1, a specific nonpeptide antagonist for the atrial natriuretic peptide (ANP) receptor, equally blocked rat ANP (rANP)-, porcine brain natriuretic peptide-, or porcine C-type natriuretic peptide-stimulated GMP production in cultured bovine aortic smooth muscle (BASM) and bovine aortic endothelial (BAE) cells in a concentration-dependent fashion, at concentrations of 1-300 micrograms/ml. But, even at 300 micrograms/ml, HS-142-1 only weakly inhibited the specific binding of 125I-rANP to the BASM and BAE cells, where only a small portion of the binding sites are linked to guanylyl cyclase. Further, with BAE cell membranes, HS-142-1 recognized only the 135-kDa ANP receptor, which is thought from 125I-rANP affinity cross-linking studies to be the guanylyl cyclase-linked receptor. HS-142-1 also, if anything, inhibited the labeling of 135-kDa ANP receptors in the affinity cross-linking studies with BASM membranes, suggesting that a major portion of the 135-kDa ANP receptors are HS-142-1 insensitive and only a small portion of the 135-kDa ANP receptors are responsible for the blockade by HS-142-1 of GMP production in BASM cells. At a concentration of 100 micrograms/ml, HS-142-1 reversibly prevented ANP-induced relaxation of the isolated rabbit thoracic aorta induced to contract with 3 x 10(-7) M phenylephrine, but not the relaxation induced by sodium nitroprusside, isoproterenol, or papaverine. These results suggest that HS-142-1 specifically inhibits natriuretic peptide-induced vasorelaxation through the blockade of guanylyl cyclase-linked natriuretic peptide receptors. HS-142-1 thus will be a powerful tool for understanding the physiological roles, in vasculature, of natriuretic peptides, which contribute to the homeostasis of blood pressure and intravascular volume.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Atrial Natriuretic Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Cross-Linking Reagents,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic GMP,
http://linkedlifedata.com/resource/pubmed/chemical/Guanylate Cyclase,
http://linkedlifedata.com/resource/pubmed/chemical/HS 142-1,
http://linkedlifedata.com/resource/pubmed/chemical/Polysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Atrial Natriuretic Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Vasodilator Agents
|
pubmed:status |
MEDLINE
|
pubmed:month |
Dec
|
pubmed:issn |
0026-895X
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
42
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
982-90
|
pubmed:dateRevised |
2006-11-15
|
pubmed:meshHeading |
pubmed-meshheading:1362244-Animals,
pubmed-meshheading:1362244-Aorta,
pubmed-meshheading:1362244-Atrial Natriuretic Factor,
pubmed-meshheading:1362244-Cattle,
pubmed-meshheading:1362244-Cells, Cultured,
pubmed-meshheading:1362244-Cross-Linking Reagents,
pubmed-meshheading:1362244-Cyclic GMP,
pubmed-meshheading:1362244-Guanylate Cyclase,
pubmed-meshheading:1362244-Male,
pubmed-meshheading:1362244-Polysaccharides,
pubmed-meshheading:1362244-Rabbits,
pubmed-meshheading:1362244-Receptors, Atrial Natriuretic Factor,
pubmed-meshheading:1362244-Vasodilator Agents
|
pubmed:year |
1992
|
pubmed:articleTitle |
Inhibition by HS-142-1, a novel nonpeptide atrial natriuretic peptide antagonist of microbial origin, of atrial natriuretic peptide-induced relaxation of isolated rabbit aorta through the blockade of guanylyl cyclase-linked receptors.
|
pubmed:affiliation |
Tokyo Research Laboratories, Kyowa Hakko Kogyo Co., Ltd., Japan.
|
pubmed:publicationType |
Journal Article,
In Vitro
|