Abstract
This review describes the positive effects of growth hormone (GH) on the cardiovascular system. We analyze why the vascular endothelium is a real internal secretion gland, whose inflammation is the first step for developing atherosclerosis, as well as the mechanisms by which GH acts on vessels improving oxidative stress imbalance and endothelial dysfunction. We also report how GH acts on coronary arterial disease and heart failure, and on peripheral arterial disease, inducing a neovascularization process that finally increases flow in ischemic tissues. We include some preliminary data from a trial in which GH or placebo is given to elderly people suffering from critical limb ischemia, showing some of the benefits of the hormone on plasma markers of inflammation, and the safety of GH administration during short periods of time, even in diabetic patients. We also analyze how Klotho is strongly related to GH, inducing, after being released from the damaged vascular endothelium, the pituitary secretion of GH, most likely to repair the injury in the ischemic tissues. We also show how GH can help during wound healing by increasing the blood flow and some neurotrophic and growth factors. In summary, we postulate that short-term GH administration could be useful to treat cardiovascular diseases.
Highlights
The hGH gene family is composed by two growth hormone (GH) genes (GH-N and GH-V), and three placental genes that are located in the chromosome 17 [1]
While total homocysteine levels (tHcy) was similar in both groups of patients, ET-1 was significantly higher in active acromegaly, suggesting that it contributes to premature atherosclerosis and cardiovascular affectations that were observed in this pathology, the role that is played by Insulin-like Growth Factor I (IGF-I) on these vascular affectations could not be discarded
It has been found that acromegaly raises the risk of atherosclerosis [227,228,229]. This argument is contrary to the fact that GH is an atherosclerotic protector, but it must be elucidated whether the latter is a consequence of the increase in cardiovascular risk factors, rather than a pure consequence of the hormone. Another adverse effect of the hormone is the development of carpal tunnel syndrome, but this is unlikely to occur during short-time treatments with GH as these that we propose for treating cardiovascular disease (CVD) and peripheral arterial disease (PAD)
Summary
The hGH gene family is composed by two growth hormone (GH) genes (GH-N and GH-V), and three placental genes that are located in the chromosome 17 [1]. Further studies in mice of the same group demonstrated that secreted Klotho promoted endothelial increase of NO in aorta and arterioles [40], and that adenovirus-mediated Klotho gene delivery to a typical rat model of multiple atherogenic risk (OLETF rat) improved endothelial dysfunction, increased NO production, reduced increased blood pressure, and prevented medial hypertrophy, meaning that Klotho was a clear positive regulator of vascular function [41] This was confirmed in Klotho mutant mice when observing that in these animals the density of blood capillaries was decreased at the tissue level and angiogenesis was impaired, as was the release of NO from the vascular endothelium [42]. These concepts support our idea about GH as a hormone that plays many more roles in the body than those of a merely metabolic hormone and responsible for longitudinal growth until puberty ends
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