Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1985-1-18
pubmed:abstractText
The basic mechanism underlying the abnormal systemic vascular resistance in the spontaneously hypertensive rat (SHR) is poorly understood. To categorize the beta-receptor system in the lungs of these animals, we evaluated receptor number and affinity as an index of this subclass of beta receptors. The lung was chosen because it is not directly affected by the alteration in blood pressure and provides a ready supply of beta-receptors. The aortic blood pressure and heart rate were measured directly through cannulation of the carotid artery. Twenty-four hours later, lung membranes from the SHR and control animals were extracted and partially purified. The affinity and number of receptors were measured by saturation analysis employing 3H-dihydroalprenolol (3H-DHA). Scatchard analysis demonstrated that the number of receptors was identical and of a single class in both sets of animals. However, the beta-receptor from the SHR had a higher affinity than that of normal rats. It is not clear whether this represents an adaptive mechanism following the development of hypertension in the SHR or it represents a basic alteration in this strain of rat. Further studies aimed at categorizing the development of this defect during ontogeny as well as its physiologic consequences should prove valuable in understanding the mechanism of spontaneous hypertension.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0047-1828
pubmed:author
pubmed:issnType
Print
pubmed:volume
48
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1203-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1984
pubmed:articleTitle
The lung beta-receptor in the spontaneous hypertensive rat.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't