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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2001-7-18
pubmed:abstractText
Acromegaly is associated with cardiovascular disease. We studied vascular function and mean arterial blood pressure in transgenic mice overexpressing bovine GH. Mean arterial blood pressure was measured in conscious, unrestrained male and female bovine GH and littermate control mice during normal as well as high salt intake using telemetric devices. Structure in artificially perfused maximally dilated hindquarter vascular beds and vascular reactivity and endothelial function in small mesenteric vessels were studied in female bovine GH and control mice. Mean arterial blood pressure was increased in female bovine GH transgenic (126 +/- 3 mm Hg) and male bovine GH transgenic (129 +/- 4 mm Hg) compared with female (109 +/- 3 mm Hg, P < 0.05) and male (111 +/- 3 mm Hg, P < 0.05) controls respectively. Increased salt intake had no effect on mean arterial blood pressure. Perfusion studies showed a significant decrease in the average diameter of the female bovine GH transgenic hindquarter vascular bed (P < 0.05). The responses of isolated resistance arteries to nor-epinephrine, potassium-induced depolarization, acetylcholine, or sodium-nitroprusside did not significantly differ between bovine GH transgenic and control mice. We conclude that the phenotype of the bovine GH transgenic mice includes a salt-resistant form of hypertension. Furthermore, the increase in mean arterial blood pressure is accompanied by a significant structural narrowing of the resistance vasculature without changes in vascular reactivity or endothelial function. The results imply that hypertension in bovine GH transgenic mice is maintained mainly by a structurally based increase in peripheral vascular resistance.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
142
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3317-23
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:11459773-Animals, pubmed-meshheading:11459773-Blood Pressure, pubmed-meshheading:11459773-Blood Vessels, pubmed-meshheading:11459773-Body Weight, pubmed-meshheading:11459773-Cattle, pubmed-meshheading:11459773-Female, pubmed-meshheading:11459773-Growth Hormone, pubmed-meshheading:11459773-Heart, pubmed-meshheading:11459773-Hemodynamics, pubmed-meshheading:11459773-Hindlimb, pubmed-meshheading:11459773-Kidney, pubmed-meshheading:11459773-Male, pubmed-meshheading:11459773-Mice, pubmed-meshheading:11459773-Mice, Inbred C57BL, pubmed-meshheading:11459773-Mice, Inbred CBA, pubmed-meshheading:11459773-Mice, Transgenic, pubmed-meshheading:11459773-Organ Size, pubmed-meshheading:11459773-Reference Values, pubmed-meshheading:11459773-Splanchnic Circulation, pubmed-meshheading:11459773-Vascular Resistance, pubmed-meshheading:11459773-Vasodilation
pubmed:year
2001
pubmed:articleTitle
Vascular function and blood pressure in GH transgenic mice.
pubmed:affiliation
Institute of Physiology and Pharmacology, Department of Physiology, Göteborg University, Sweden.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't