Why the study?
Does a -10 degrees head-down tilt induce different hemodynamic and neurohormonal responses in patients with sustained essential hypertension compared to normotensive controls?
Does a -10 degrees head-down tilt induce different hemodynamic and neurohormonal responses in patients with sustained essential hypertension compared to normotensive controls?
Hypertensive patients exhibit an exaggerated increase in cardiac output and local flow during head-down tilt, likely due to decreased venous distensibility leading to higher central venous pressure.
Answers are grounded in this paper and cite their sources.
Hypertensives show blunted venous tone response to tilt; hypothesis-generating for reduced compliance and requires prospective validation before any clinical inference.
Central and forearm arterial and venous hemodynamics, arterial baroreflex sensitivity, plasma renin activity, and catecholamines were studied in supine position and after -10 degrees head-down tilt in 29 patients with sustained essential hypertension and in 29 normotensive controls of the same age and sex. In both populations, blood pressure, heart rate, and arterial baroreflex sensitivity did not change during the maneuver. Head-down tilt induced a similar increase in cardiopulmonary blood volume in controls and hypertensives, whereas the increase in central venous pressure, cardiac output, and forearm blood flow was higher in hypertensives. Forearm venous tone decreased in controls (from 16.6 +/- 0.8 to 13.8 +/- 0.9 mmHg X ml-1 X 100 g-1; P less than 0.01) but did not change in hypertensive patients (24.9 +/- 1.6 vs. 25.1 +/- 1.9. The magnitude of forearm vascular resistance changes induced by head-down tilt were significantly related to the basal venous tone in the overall population (P less than 0.01). The decrease in plasma renin activity and plasma catecholamines was similar in the two groups. The study provides the evidence that the higher increase in cardiac output and local flow observed in head-down tilt in hypertensive patients is probably due to a higher change in central venous pressure related to a decrease in venous distensibility.
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London et al. (1983) studied this question.
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