Reduced vascular excitatory responses to cardiopulmonary unloading in hypertensive patients with left ventricular diastolic dysfunction.

Physiological consequences of altered peak left ventricular diastolic filling rate in hypertension have not yet been fully assessed. The hypothesis that altered left ventricular diastolic filling rate interferes with inhibitory cardiopulmonary reflexes was tested. Normalized peak left ventricular diastolic filling rate was calculated from radionuclide ventriculography. Haemodynamic changes during lower body negative pressure (-5 to -40 mmHg) in nine hypertensive patients with slow normalized left ventricular filling rate (Group A) were compared with 16 hypertensive patients with normal normalized peak left ventricular diastolic filling rate and ten normal volunteers of the same age group. Baseline total peripheral resistance was higher in essential hypertension compared to normals but did not differ significantly between the two hypertensive groups. For data analysis, the levels of lower body negative pressure were grouped as low levels of -5 to -10, and -15 to -20 mmHg, an intermediate level of -25 mmHg, and high levels of -30 to -40 mmHg; the change in total peripheral resistance (from baseline) was less prominent in Group A compared to Group B and to normals (-1.4 +/- 1.7 [SE], -0.06 +/- 1.4, 1.1 +/- 1.2 and 4.5 +/- 2 u.M2 in Group A at the four consecutive levels of lower body negative pressure vs. 0.9 +/- 0.7, 3.8 +/- 0.9, 7.2 +/- 1.6, and 8.2 +/- 1.4 in Group B, and 2.0 +/- 0.7, 3.3 +/- 0.8, 4.9 +/- 0.8, and 5.6 +/- 1.0 in normals). The reductions in central venous pressure and in pulmonary wedge pressure were not significantly different among the three groups at the different levels of lower body negative pressure, but the reduction in cardiac output was smaller in patients with reduced dv/dt ratio than in the other two groups. The responses to the cold pressor test were similar in all subjects. We conclude that patients with essential hypertension and diastolic dysfunction have impaired total peripheral resistance responses to lower body negative pressure. This abnormality may reflect an alteration in cardiac baroreflexes secondary to left ventricular diastolic dysfunction, an influence of baseline sympathetic activity on the observed vascular responsiveness to lower body negative pressure, or primary differences among groups in the changes in cardiac output induced by similar levels of lower body negative pressure.