Abstract
Growth hormone secretagogue receptor (GHS‐R) signaling has been associated with growth hormone release, increases in food intake and pleiotropic cardiovascular effects. Recent data demonstrated that acute GHS‐R antagonism leads to increases in mean arterial pressure mediated by the sympathetic nervous system in rats; a highly undesirable effect if GHS‐R antagonism was to be used as a therapeutic approach to reducing food intake in an already obese, hypertensive patient population. However, our data in conscious, freely moving GHS‐R deficient mice demonstrate that chronic absence of GHS‐R signaling is protective against obesity‐induced hypertension. GHS‐R deficiency leads to reduced systolic blood pressure variability (SBPV); in response to acute high‐fat diet (HFD)‐feeding, increases in the sympathetic control of SBPV are suppressed in GHS‐R KO mice. Our data further suggest that GHS‐R signaling dampens the immediate HFD‐mediated increase in spontaneous baroreflex sensitivity. In diet‐induced obesity, absence of GHS‐R signaling leads to reductions in obesity‐mediated hypertension and tachycardia. Collectively, our findings thus suggest that chronic blockade of GHS‐R signaling may not result in adverse cardiovascular effects in obesity.
Highlights
Ghrelin is an acylated peptide hormone, mainly secreted from the gastrointestinal mucosa and it functions as the endogenous ligand to the growth hormone secretagogue receptor 1a (GHS-R) (Kojima et al 1999)
GHS-R deficiency leads to reduced systolic blood pressure variability
GHS-R deficiency had no effect on mean arterial pressure (MAP), heart rate (HR) or systolic blood pressure (SBP) (Fig. 1A–C)
Summary
Ghrelin is an acylated peptide hormone, mainly secreted from the gastrointestinal mucosa and it functions as the endogenous ligand to the growth hormone secretagogue receptor 1a (GHS-R) (Kojima et al 1999). GHS-Rs are expressed in various CNS areas and peripheral tissues. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.
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