Vascular function and blood pressure in GH transgenic mice

Acromegaly is associated with cardiovascular disease. We studied vascular f unction and mean arterial blood pressure in transgenic mice overexpressing bovine GH. Mean arterial blood pressure was measured in conscious, unrestrained male a nd female bovine GH and littermate control mice during normal as well as hi gh salt intake using telemetric devices. Structure in artificially perfused maximally dilated hindquarter vascular beds and vascular reactivity and en dothelial function in small mesenteric vessels were studied in female bovin e GH and control mice. Mean arterial blood pressure was increased in female bovine GH transgenic ( 126 +/- 3 min Hg) and male bovine GH transgenic (129 +/- 4 mm Hg) compared with female (109 +/- 3 min Hg, P < 0.05) and male (111 +/- 3 min Hg, P < 0. 05) controls respectively. Increased salt intake had no effect on mean arte rial blood pressure. Perfusion studies showed a significant decrease in the average diameter of the female bovine GH transgenic hindquarter vascular b ed (P < 0.05). The responses of isolated resistance arteries to nor-epineph rine, potassium-induced depolarization, acetylcholine, or sodium-nitropruss ide did not significantly differ between bovine GH transgenic and control m ice. We conclude that the phenotype of the bovine GH transgenic mice includes a salt-resistant form of hypertension. Furthermore, the increase in mean arte rial blood pressure is accompanied by a significant structural narrowing of the resistance vasculature without changes in vascular reactivity or endot helial function. The results imply that hypertension in bovine GH transgeni c mice is maintained mainly by a structurally based increase in peripheral vascular resistance.