Hemodynamic effects of [Sar1, Ile8] All, an angiotensin II analog, were studied in 30 patients with essential hypertension, who were subdivided into 11 low renin, 10 normal renin and 9 high renin groups according to low, normal and high PRA values both before and after furosemide administration (80 mg, orally) plus 4 h of ambulation, respectively. [Sar1, Ile8] All infusion (600 ng/kg/min) produced significant increases in mean blood pressure (MBP) and total peripheral resistance index (TPRI) in normal renin and low renin groups and significant decreases in MBP and TPRI in high renin group, while the cardiac index and heart rate remained unchanged during the infusion in these three groups. Change in MBP at 30 min of [Sar1, Ile8] All infusion correlated significantly with alteration in TPRI in 23 patients with essential hypertension, who completed the 30-min infusion. The response of both MBP and TPRI to [Sar1, Ile8] All also correlated significantly with basal PRA. These results suggest that blood pressure response to [Sar1, Ile8] All in essential hypertension is primarily due to alteration in total peripheral resistance and that direction and amplitude of the response of both MBP and TPRI are practically dependent on basal PRA levels.
To study the role of volume factors in the pathogenesis of hypertension, total blood volume (TBV) was determined in 43 patients with essential hypertension, 10 with primary aldosteronism, 5 with Cushing's syndrome, 5 with renovascular hypertension and 23 age-matched normotensives. The radioisotope (131I) labeled plasma tracer technique was employed under conditions of constant sodium intake (200mEq/day). The TBV values obtained were expressed as % normal against the predicted values according to the formulae of Fujita and his co-workers. The results were as follows: (1) TBV was increased in patients with primary aldosteronism. (2) In essential hypertensive patients, with either normal or low plasma renin activity, TBV was normal. (3) There was no increment of TBV in patients with Cushing's syndrome. These results suggest that expanded intravascular volume plays a major role in the mechanism of hypertension with suppressed plasma renin activity in primary aldosteronism, whereas other unknown factors may be related to the causes of hypertension in patients with essential hypertension and Cushing's syndrome.
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