Because systole and diastole are coupled and systolic ventricular-vascular coupling has been characterized, we hypothesize that diastolic ventricular-vascular coupling (DVVC) exists and can be characterized in terms of relaxation and stiffness. To characterize and elucidate DVVC mechanisms we introduce dP/dt vs P(t) (pressure phase-plane, PPP) derived analogs of ventricular and vascular 'stiffness' parameters. Although dV=0 during isovolumic periods, and time-varying LV stiffness expressed as dP/dV is undefined, our formulation allows determination of PPP derived stiffness-analog during isovolumic contraction and relaxation. Similarly, an aortic stiffness-analog is also derivable from the PPP. LV relaxation was characterized via , the time-constant of isovolumic relaxation, and vascular (aortic) relaxation was characterized in terms of its equivalent (Windkessel) exponential decay time-constant . Results show that systolic (ejection phase) and diastolic ventricular and vascular stiffness are coupled (K_Ao+=1.7(K_LV+)+154.1 r=0.86, K_Ao-=0.7(K_LV-)-5.5 r=0.86). In support of the DVVC hypothesis, a strong linear correlation between relaxation (rate of pressure decay) indexes and (=9.9-90.3 r=0.81) was also observed. The correlations observed underscore the role of long term, steady-state DVVC as a diastolic function determinant. Our validation of the PPP derived DVVC parameters provides insight into mechanisms, and facilitates quantification of arterial stiffening and associated increase in diastolic chamber stiffness. The PPP method provides a tool for quantitative assessment and determination of the functional coupling of the vasculature to diastolic function.