Abstract Several studies have shown that GH can enhance cardiac performance in rats after experimental myocardial infarction and in humans with congestive heart failure. In the present study, the hemodynamic effects of hexarelin (Hex), an analog of GH-releasing peptide-6 and a potent GH secretagogue, were compared with the effects of GH. Four weeks after ligation of the left coronary artery male rats were treated sc twice daily with hexarelin [10 μg/kgday (Hex10) or 100 μg/kgday (Hex100)], recombinant human GH (2.5 mg/kgday), or 0.9% NaCl for 2 weeks. Transthoracic echocardiography was performed before and after the treatment period.

GH, but not Hex, increased body weight gain. GH and Hex100 decreased total peripheral resistance ( P. GH SECRETAGOGUES (GHS) are a heterogeneous group of synthetically produced peptides [GH-releasing peptides (GHRP)] and nonpeptides that stimulate GH secretion in both animals and human subjects. A pair of specific, G protein-coupled GHS receptors (GHS-R) were recently cloned in human and rat (, ), but new data suggest that there are other GHS-R types, possibly related to the cloned receptors ().

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With cloning of GHS-R the idea of an as yet unidentified endogenous ligand as an additional regulator of GH secretion is supported. The functional type Ia GHS-R is expressed in the hypothalamus and the pituitary, and there seems to be a negative feedback of GH on expression of the GHS-R (). GHRP-6, which is the most extensively studied GHS, exerts its effect at both hypothalamic and pituitary sites. The main action is exerted in the hypothalamus, where the release of GH-releasing hormone (GHRH) is increased by GHRP-6, and somatostatin is functionally antagonized (–). In addition, GHRP-6 promotes the release of GH directly from rat and human pituitary cells (, ). However, the mechanisms behind the GH-releasing properties of GHS are not completely understood. The hexapeptide hexarelin (Hex) is chemically more stable and a more potent GH secretagogue than its analog GHRP-6 ().

Its actions have been investigated in both experimental and clinical studies (–). The results of many studies have shown that Hex increases GH secretion, but there are few studies of the clinical long term effects. However, Hex has been reported to accelerate growth in short children, influence parameters of bone formation and muscle morphology in aged dogs, and restore sodium channel properties in skeletal muscle in aged rats (–). The myocardium expresss functional receptors for both GH and insulin-like growth factor I (IGF-I), and it is now well known that the GH/IGF-I axis has an important role during cardiac development and for maintaining the structure and function of the heart (). In GH deficiency one of the clinical signs is an impaired cardiovascular performance, which may be reversed after GH substitution therapy, particularly in terms of increased stroke volume and reduced peripheral resistance ().

GH has also been shown to improve systolic function in normal subjects (). In recent studies of patients with congestive heart failure due to dilated cardiomyopathy, both acute administration of GH and more chronic treatment have been shown to exert major hemodynamic effects (, ).

The most important findings in these studies were improved parameters of systolic heart performance, decreased peripheral resistance, and enhanced ventricular work despite a reduction in oxygen consumption and energy production. These promising results could not be confirmed in a small placebo-controlled study despite increased levels of serum IGF-I (). However, there is also abundant experimental evidence for enhanced cardiac performance by GH, among them several studies using a rat model of experimental myocardial infarction (MI) (–). Besides a pronounced vasodilatation and lowering of total peripheral resistance by GH/IGF-I, enhanced myocardial contractility is likely to contribute (–).