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- W2899009496 abstract "Objectives: GPR37L1 is one of ∼140 orphan G protein-coupled receptors, and its physiological function is not fully understood. We have previously shown that receptor knockout causes an 11mmHg increase in systolic blood pressure (SBP), specifically in female mice, by both radiotelemetry and invasive catheterisation. As such, we hypothesise that dysfunction of this receptor may be a causative factor for hypertension and its sequelae, and aim to characterise effects of GPR37L1 deficit during cardiovascular dysregulation. Methods: Wildtype and GPR37L1−/− mice (C57Bl/6J background) of both sexes were subjected to 7-day angiotensin II (2 mg/kg/day) or vehicle administration via osmotic mini-pump, followed by haemodynamic measurements by catheterisation and tissue harvest. Maladaptive cardiac remodelling was assessed by left ventricular (LV) weight, cardiomyocyte density, RT-qPCR for hypertrophy hallmark genes, and intramyocardial fibrosis. Results: In males, despite comparable AngII-induced SBP rises in both genotypes, GPR37L1−/− mice had significantly greater LV hypertrophy (p < 0.0001). Even with higher baseline SBP, GPR37L1−/− females responded to AngII similarly to wildtype controls on measures of haemodynamics and hypertrophy, but were protected against fibrosis (p = 0.0158). Conclusion: These findings demonstrate that GPR37L1 is critical for sustaining adaptive responses to cardiovascular dysfunction in males. We are currently undertaking ageing and sympathetic nervous system activation studies in mice to elucidate the mechanism for GPR37L1 control of blood pressure and cardiovascular homeostasis. Understanding the sexually dimorphic role of GPR37L1 will benefit our knowledge of sex differences in the cardiovascular system, leading to more effective, personalised treatments for cardiovascular disease." @default.
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- W2899009496 date "2018-10-01" @default.
- W2899009496 modified "2023-09-25" @default.
- W2899009496 title "A7665 Sexually dimorphic roles for GPR37L1, an orphan GPCR in the cardiovascular system" @default.
- W2899009496 doi "https://doi.org/10.1097/01.hjh.0000548013.63617.a8" @default.
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