Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1999-9-15
pubmed:abstractText
Kinins have been implicated in the hemodynamic adaptation to postnatal life. The present study examined the impact of bradykinin B(2) receptor (B(2)R) gene disruption on the postnatal changes in blood pressure (BP) and the susceptibility to early onset salt-sensitive hypertension in mice. B(2)R null (-/-) and wild-type (+/+) mice were fed normal (NS, 1% NaCl) or high (HS, 5% NaCl) salt diets during pregnancy. After birth, the pups remained with their mothers until they were weaned and were subsequently continued on the respective maternal salt intake until 4 months of age. The age-related changes at 3 and 4 months in tail-cuff BP and anesthetized mean arterial pressure at 4 months were not different in NS/B(2)R(-/-) and NS/B(2)R(+/+) mice. However, there was a mild increase in BP in NS/B(2)R(-/-) at 2 months versus NS/B(2)R(+/+). In contrast, HS/B(2)R(-/-) mice manifested early onset and persistent elevations of tail-cuff BP (P<0.05) at 2, 3, and 4 months versus other groups. MAP was also higher in HS/B(2)R(-/-) than HS/B(2)R(+/+), NS/B(2)R(-/-), and NS/B(2)R(+/+) (91+/-3 versus 75+/-5, 74+/-2, and 70+/-2 mm Hg, respectively; P<0.05). Kidney renin and angiotensin type 1 receptor mRNA levels were not different. Additional studies showed that a delay in the initiation of HS until after birth was accompanied by later development of hypertension, although postnatal discontinuation of HS resulted in a gradual return of BP to normal values by 4 months of age. The results demonstrate that (1) kinins protect the developing animal from salt-sensitive hypertension, (2) lack of B(2)R from early development does not alter the maturation of BP under conditions of normal sodium intake, and (3) exposure to a HS diet during fetal life is not sufficient in itself to induce long-term hypertension in either wild-type or B(2)R null mice.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0194-911X
pubmed:author
pubmed:issnType
Print
pubmed:volume
34
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
176-80
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:10454437-Age Factors, pubmed-meshheading:10454437-Angiotensin II, pubmed-meshheading:10454437-Animals, pubmed-meshheading:10454437-Animals, Newborn, pubmed-meshheading:10454437-Blood Pressure, pubmed-meshheading:10454437-Blotting, Northern, pubmed-meshheading:10454437-Body Weight, pubmed-meshheading:10454437-Data Interpretation, Statistical, pubmed-meshheading:10454437-Female, pubmed-meshheading:10454437-Hypertension, pubmed-meshheading:10454437-Kallikrein-Kinin System, pubmed-meshheading:10454437-Kidney, pubmed-meshheading:10454437-Male, pubmed-meshheading:10454437-Mice, pubmed-meshheading:10454437-Mice, Knockout, pubmed-meshheading:10454437-Pregnancy, pubmed-meshheading:10454437-RNA, Messenger, pubmed-meshheading:10454437-Radioimmunoassay, pubmed-meshheading:10454437-Receptors, Angiotensin, pubmed-meshheading:10454437-Receptors, Bradykinin, pubmed-meshheading:10454437-Renin-Angiotensin System, pubmed-meshheading:10454437-Sodium Chloride, Dietary
pubmed:year
1999
pubmed:articleTitle
Early onset salt-sensitive hypertension in bradykinin B(2) receptor null mice.
pubmed:affiliation
Department of Pediatrics, Tulane University School of Medicine, New Orleans, LA, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't