Hypertensive patients with left ventricular hypertrophy had significantly higher baseline plasma renin activity and suppressed vasopressin levels during exercise compared to those without hypertrophy.
Observational (n=19)
Do pressor hormone profiles during exercise stress differ between hypertensive patients with and without left ventricular hypertrophy?
Differences in vasopressin and plasma renin activity profiles during stress suggest these hormones may be causally related to the development of left ventricular hypertrophy in hypertensive patients.
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.
Manolis et al. (Fri,) conducted a observational in Hypertension (n=19). Exercise testing (treadmill, Bruce protocol) vs. Patients with LVH vs without LVH was evaluated on Pressor hormone profiles (PRA, catecholamines, AVP) at baseline, peak exercise, and post exercise. Hypertensive patients with left ventricular hypertrophy had significantly higher baseline plasma renin activity and suppressed vasopressin levels during exercise compared to those without hypertrophy.