Research article

Short-term administration of growth hormone (GH) lowers blood pressure by activating eNOS/nitric oxide (NO)-pathway in male hypophysectomized (Hx) rats

Henrik C Nyström¹ , Natalia Klintland² , Kenneth Caidahl² , Göran Bergström^1,2 and Anna Wickman¹

¹  Department of Physiology, Institute of Physiology & Pharmacology, The Sahlgrenska Academy, Göteborg University, P.O. Box 432, SE-405 30 Göteborg, Sweden

²  Department of Clinical Physiology, Sahlgrenska University Hospital/SU, SE-413 45 Göteborg, Sweden

author email corresponding author email

BMC Physiology 2005, 5:17doi:10.1186/1472-6793-5-17

Published:	7 November 2005

Abstract

Background

The aim of the study was to evaluate the acute and continuous (up to 14 days of treatment) effect of growth hormone (GH) on blood pressure (BP) regulation and to investigate the interplay between GH, nitric oxide (NO) and BP.

In un-supplemented and GH supplemented hypophysectomized (Hx) male rats as well as intact rats, continuous resting mean arterial blood pressure (MAP) was measured using telemetry. Baroreceptor activity and the influences of NO on BP control were assessed during telemetric measurement. Furthermore, basal plasma and urine nitrate levels and aortic endothelial nitric oxide synthase (eNOS) expression were analysed. Endothelial function as well as vascular structure in the hindquarter vascular bed was estimated using an in vivo constant-flow preparation.

Results

Hypophysectomy was associated with decreased MAP (Hx: 83 ± 3 vs Intact: 98 ± 6 mmHg, p < 0.05) and heart rate (HR) (Hx: 291 ± 4 vs Intact: 351 ± 7 beat/min, p < 0.05). Endothelial dysfunction and reduced vasculature mass in the hindquarter vascular bed was found in Hx rats. GH substitution caused a further transient decrease in MAP and a transient increase in HR (14% and 16% respectively, p < 0.05). The reduction in MAP appeared to be NO dependent. Aortic eNOS expression was unchanged. GH substitution resulted in an impaired baroreceptor function. Two weeks of GH treatment did not normalise the BP, vascular structure and the endothelial function in the resistance vessels.

Conclusion

GH substitution seems to have a short lasting effect on lowering blood pressure via activation of the NO-system. An interaction between GH, NO-system and BP regulation can be demonstrated.