Measurement of ventricular dimensions in WT and GPR55^−/− mice.

<p>Ventricular dimensions did not differ significantly between young WT and GPR55^−/− mice, however mature GPR55^−/− mice were characterised by significant myocardial remodelling; including a reduction in left ventricular (LV) free wall thickness, myocardial nuclei number, and HW∶BW, and increased collagen deposition. Data is expressed as mean±s.e.m. (n = 14–15).</p><p>*P<0.05 vs. WT (Young);</p>#<p>P<0.05 vs. GPR55^−/− (Young);</p>†<p>P<0.05 vs. WT (Mature).</p><p>Measurement of ventricular dimensions in WT and GPR55^−/− mice.</p

Load-independent (ESPVR, EDPVR, and <i>E</i>_max) haemodynamic parameters in both WT and GPR55^−/− mice.

<p>In mature mice with a genetic deletion for GPR55 (GPR55^−/−), baseline systolic function, but not diastolic function, was adversely affected. In particular, significant reductions in both ESPVR (A) and <i>E</i>_max (B) indicate attenuated cardiac contractility, while EDPVR (indicative of relaxation rate) was unaffected (C) in mature GPR55^−/− mice. Data is expressed as mean±s.e.m. (n = 14–15) *P<0.05 vs. WT (Young); #P<0.05 vs. GPR55^−/− (Young); †P<0.05 vs. WT (Mature).</p

Effect of GPR55 gene deletion on contractile reserve in young (10 week old) and mature (8 month old) mice.

<p>Contractile reserve, assessed by the change from baseline cardiac function in response to the α₁/β₁-adrenoceptor agonist dobutamine, was significantly attenuated in both young and mature mice with a gene deletion for GPR55. Data is expressed as mean±s.e.m. (n = 14–15).</p><p>*P<0.05 vs. WT (Young);</p>†<p>P<0.05 vs. WT (Mature).</p><p>Effect of GPR55 gene deletion on contractile reserve in young (10 week old) and mature (8 month old) mice.</p

Expression of GPR55 in ventricular tissue from WT and GPR55^−/− mice.

<p>Photomicrographs taken at ×200 demonstrate positive staining for GPR55 in ventricular tissue (localised to the cardiomyocytes) from WT mice (A), but not GPR55^−/− mice (B).</p

Representative left ventricular pressure volume loops from all experimental groups are included and illustrate the emerging systolic dysfunction (i.e. downward and rightward shift in the ESPVR curve) associated with mature GPR55^−/− mice.

<p>Representative left ventricular pressure volume loops from all experimental groups are included and illustrate the emerging systolic dysfunction (i.e. downward and rightward shift in the ESPVR curve) associated with mature GPR55^−/− mice.</p

Influence of GPR55 gene deletion on cardiac collagen deposition.

<p>Representative photomicrographs (×400) demonstrating cardiac collagen deposition in young WT (A), young GPR55^−/− (B), mature WT (C), and mature GPR55^−/− (D) mice. Collagen deposition was significantly increased in the left ventricle of mature GPR55^−/− mice (E). Data is expressed as mean±s.e.m. (n = 14–15) #P<0.05 vs. GPR55^−/− (Young); †P<0.05 vs. WT (Mature).</p

Load-dependent haemodynamic parameters in control (WT) mice and those with a genetic deletion for GPR55 (GPR55^−/−).

<p>Cardiac function is unaffected by age in WT mice, but undergoes a significant deterioration in GPR55 deficient mice. Data is expressed as mean±s.e.m. (n = 14–15).</p><p>*P<0.05 vs. WT (Young);</p>#<p>P<0.05 vs. GPR55^−/− (Young);</p>†<p>P<0.05 vs. WT (Mature).</p><p>Load-dependent haemodynamic parameters in control (WT) mice and those with a genetic deletion for GPR55 (GPR55^−/−).</p