Related Experiment Videos
Pressor hormone profile during stress in hypertension: does vasopressin interfere with left ventricular hypertrophy?
A Manolis1, G Athanasopoulos, G Karatasakis
1Department of Cardiology, Tzanion Hospital, Piraeus, Greece.
Insights
Hypertension patients with left ventricular hypertrophy (LVH) show distinct neurohormonal profiles during exercise. Lower vasopressin and higher plasma renin activity may contribute to LVH development in hypertension.
Area of Science:
- Cardiology
- Endocrinology
- Hypertension Research
Background:
- Neurohormonal factors may explain varying degrees of left ventricular hypertrophy (LVH) in patients with similar hypertension.
- Understanding these hormonal differences is crucial for managing hypertensive heart disease.
Purpose of the Study:
- To compare pressor hormone profiles during exercise testing in hypertensive patients with and without LVH.
- Investigate the roles of plasma renin activity (PRA), catecholamines, and vasopressin (AVP) in LVH development.
Main Methods:
- Nineteen hypertensive patients were divided into two groups based on echocardiographic LVH presence or absence.
- Subjects underwent treadmill exercise testing (Bruce protocol) with measurements of PRA, catecholamines, and AVP at rest, peak exercise, and post-exercise.
Main Results:
- Group I (no LVH) exhibited suppressed PRA and higher baseline AVP, which increased with exercise.
- Group II (with LVH) showed higher baseline PRA and suppressed AVP levels.
- Norepinephrine increased in both groups, but was higher in Group I. A negative correlation existed between AVP increments and double product increments.
Conclusions:
- Lower baseline AVP, higher PRA, and blunted AVP response to exercise may be linked to LVH development in hypertension.
- These hormonal differences suggest distinct pathophysiological pathways contributing to hypertensive heart disease.
Abstract:
Neurohormonal factors may account for the fact that patients with similar severity and duration of hypertension develop different degrees of left ventricular hypertrophy (LVH). The purpose of this work was to compare the pressor hormone profiles of hypertensive subjects off medication during exercise testing. Nineteen patients, stratified according to echocardiographically diagnosed absence (Group I n = 6) or presence (Group II n = 13) of LVH, underwent testing on the treadmill according to the Bruce protocol. Both groups were comparable in age, severity and duration of hypertension and reached similar double product at peak exercise. Measurements of plasma renin activity (PRA), plasma catecholamines and vasopressin (AVP) at baseline, peak exercise and post exercise revealed significant differences between groups: Group I had suppressed PRA levels throughout and had significantly higher baseline AVP levels, which increased further at peak effort. Group II had significantly higher baseline PRA levels, which tended to increase further at peak effort, and had suppressed AVP levels throughout. There was a significant negative correlation between percent increments in AVP and increments in double product. Norepinephrine increased significantly with effort in both groups, but the levels attained were higher in Group I. In view of the known negative inotropic action of AVP and the trophic effect of angiotensin, we speculate that lower baseline AVP and higher PRA, together with inability of AVP to increase with effort, may be causally related to development of LVH.