Abstract
BackgroundThe 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.ResultsHypophysectomy 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.ConclusionGH 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.
Highlights
The aim of the study was to evaluate the acute and continuous 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
Growth hormone causes a transient decrease in mean arterial blood pressure and a transient increase in heart rate, Fig 1 and 2 Hypophysectomy per se, caused a 17% decrease in MAP and HR before onset of hormonal treatment
After 14 days of GH therapy, the MAP returned to pre-treatment levels, indicating that GH had a transient effect on BP regulation
Summary
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. As in human adult GHD, these rats show endothelial dysfunction and impaired vascular reactivity [10,11], while aortic endothelial nitric oxide synthase (eNOS) expression is not affected [12]. These rats display decreased heart weights [12,13], and reduced vasculature mass in the muscle vascular bed suggesting an hypotropic remodelling of the cardiovascular system [13]. Previous studies on BP regulation in Hx rats [10,12,13] have used less precise techniques to measure BP i.e. tail-cuff technique and showed imprecise GH effect on acute and continuous BP regulation
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