In 21 hospitalized patients with benign essential hypertension, pressor responses to angiotensin were significantly correlated with levels of mean blood pressure, and pressor responses to each of angiotensin, norepinephrine and tyramine were correlated significantly with urinary sodium excretion. Sixteen of the 21 patients were studied twice with an averaged interval of 21 days without changes in daily salt intake during the hospitalization. Twelve of the 16 patients exhibited a decline in blood pressure at the second study, and the blood pressure reduction was due to a decrease in total peripheral resistance. At the same time, in 7 of the 12 patients (group A), there were a significant decrease in response to angiotensin, a marked increase in plasma renin activity and insignificant decreases in urinary sodium excretion and plasma volume. The other 5 patients (group B) showed a decrease in plasma renin activity, an enhanced response to norepinephrine, insignificant increases in urinary sodium excretion and plasma volume, and invariable or rather increased responses to angiotensin, when blood pressure was declined at the time of the second study. It is suggested that the hypertension in the group A may have been related to sodium excess, while that in the group B may have been associated with an increased sympathetic activity.

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Kidney extract (I), (II) and (III) were obtained from rats which were adrenalectomized and given tap water, adrenalectomized and given 10 g/l NaCl, and intact, respectively. When each extract was subcutaneously injected every 12 hours into uninephrectomized rats, the blood pressure was gradually elevated. This hypertension-inducing action was observed more or less in every extracts. The potency was (I) > (II) > (III) while no apparent disparity was found in renin content of the three extracts. During and after the development of hypertension, plasma renin level was not increased 12 hours after the injection except in the recipients of extract (I), even in the presence of a high blood pressure. However, from an aspect of changes following each individual injection, the effect of the kidney extract on the plasma renin level appeared to be parallel with its hypertension-inducing effect. The latter effect, therefore, could be attributed to a cumulative effect of an excessive fluctuation of the renin-angiotensin level or the blood pressure, although implication of other renal substances than renin would not be excluded. Continuous high level of plasma renin or angiotensin may accelerate the development of hypertension.

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Cardiac myofibrils isolated from the hearts of Okamoto-Aoki hypertensive rat (SHR) and normotensive Wistar rat (NR) showed essentially the same ATPase activity either in the absence or presence of Ca²⁺. On the other hand, Ca²⁺ activated ATPase activity of relaxed preparation of cardiac myofibrils from SHR was significantly lower than that from NR. ATPase activity and Ca²⁺ binding ability of cardiac sarcoplasmic reticulum (cardiac SR) and arterial subcellular membrane (arterial SR) isolated from SHR and NR were measured. The maximum Ca²⁺ binding capacity of cardiac SR from SHR (8.80±0.33 nmoles/mg) was significantly lower than that from NR (11.95±0.55). Also, cardiac SR from SHR had significantly elevated Ca²⁺ activated ATPase activity (0.171±0.009 μmoles/mg/min) compared with that of NR (0.100±0.009). And, the maximum Ca²⁺ binding capacity of arterial SR from SHR (23.55±0.72 nmoles/mg) was significantly lower than that from NR (39.35±4.89). ATPase activity of arterial SR from SHR (2.94±0.18 μmoles/mg/min) was significantly elevated compared with that of NR (2.22±0.14). Reduction of Ca²⁺ binding capacity of both cardiac and arterial SR may result in increase of intracellular free Ca²⁺ concentration which probably be one of the important factor for increase of muscular tone. If this abnormal intracellular distribution of Ca²⁺ is associated with the vascular smooth muscle, it would cause the increase of vascular resistance resulting in hypertension.

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