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Vascular function and blood pressure in GH transgenic mice
M Bohlooly-Y1, L Carlson, B Olsson
1Institute of Physiology and Pharmacology, Department of Physiology, Göteborg University, Sweden.
Endocrinology
|July 19, 2001
Summary
Hypertension in bovine growth hormone (GH) transgenic mice involves structural narrowing of blood vessels. This vascular resistance increase causes salt-resistant hypertension, independent of endothelial function.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
- Vascular Biology
Background:
- Acromegaly, a condition linked to cardiovascular disease, is characterized by excess growth hormone (GH).
- Understanding the vascular mechanisms underlying GH-associated hypertension is crucial for managing cardiovascular risks.
Purpose of the Study:
- To investigate vascular function and blood pressure regulation in mice overexpressing bovine growth hormone (bGH).
- To determine if bGH overexpression leads to hypertension and identify underlying structural or functional vascular changes.
Main Methods:
- Mean arterial blood pressure was measured telemetrically in bGH transgenic and control mice under normal and high salt conditions.
- Vascular structure was assessed in perfused hindquarter beds.
- Vascular reactivity and endothelial function were studied in isolated mesenteric resistance arteries.
Main Results:
- bGH transgenic mice exhibited significantly elevated mean arterial blood pressure compared to controls, irrespective of salt intake.
- Perfusion studies revealed a structural narrowing of the hindquarter vascular bed in bGH transgenic mice.
- No significant differences in vascular reactivity or endothelial function were observed between transgenic and control mice.
Conclusions:
- bGH transgenic mice develop a salt-resistant form of hypertension.
- The hypertension is associated with structural narrowing of resistance vasculature.
- Increased peripheral vascular resistance, due to structural changes, is the primary mechanism maintaining hypertension in this model.