Comparisons of body fluid volumes, plasma renin activity, hemodynamics and pressor responsiveness between juvenile and aged patients with essential hypertension.

Body fluid volumes, cardiac output, PRA and pressor responses to angiotensin II (AT) and norepinephrine (NE) were compared between untreated patients with essential hypertension aged younger than 35 (EH-I) and those aged older than 36 years (EH-II). Men blood volume, total body water and extracellular volume were not significantly different between the patients with essential hypertension and normotensive subjects. There were no difinite differences in each volume between the EH-I and EH-II patients either. However, the distribution of blood volume was significantly larger in the essential hypertensive patients than in the normotensive subjects, suggesting that the changes in blood volume might not be homogenous in essential hypertension. In addition, blood volume was noted to have a significant inverse correlation with PRA. Cardiac output at rest was slightly but not significantly less in the EH-I and EH-II groups than in the normotensive group. A decline in blood pressure following 'bed-rest' was accompanied by a decrease in total peripheral resistance index (TPRI). Thus, elevated peripheral vascular resistance seems to be responsible for the mild to moderate hypertension even in the younger patients. PRA and its increases in response to standing or furosemide were normal in the EH-I patients, while they were markedly suppressed in the EH-II patients as compared to the age-matched normotensive subjects. In addition, PRA had a significant inverse correlation with the blood pressure and the scores of the severity of hypertension in the patients with essential hypertension. Thus, it seems likely that low renin in essential hypertension is secondary to long-lasting hypertension. Pressor response to AT significantly correlated with mean blood pressure and that to NE did so with 24 hours' urinary sodium excretion in essential hypertensive patients. The influence of aging on the pressor responses were obscure: the relationships of the pressore responses to blood pressure or to urinary sodium excretion were not different between the EH-I and EH-II groups. The examinations were repeated in 16 patients with essential hypertension (16 to 48 year-old) in 11 to 30 days after the initial study. Twelve of the 16 patients had declines in blood pressure and TPRI at the second study. In 7 of the patients whose blood pressure declined following 'bed-rest', there were significant decreases in pressor response to AT and in blood volume and a significant increase in PRA (group A). The other 5 patients showed a significant decrease in PRA and an enhanced pressor response to NE (group B). The blood volume in the group A was significantly larger than that in the group B at the initial study. It is suggested that the cause of essential hypertension is not homogeneous in that the increased vascular resistance may have been attributed to sodium excess in some patients and to an increased sympathetic activity in others. Some additional factors remain to be taken into account to clarify the complicated aspects of essential hypertension.