Tomofumi Otsuki

Factors determining sodium chloride sensitivity of patients with essential hypertension: evaluation by multivariate analysis

Factors which determine sodium chloride sensitivity, defined as the difference between the mean blood pressure after 1 week of a low sodium chloride diet (3 g/day) and that after 1 week of a high sodium chloride diet (20 g/day), were studied in 60 inpatients with essential hypertension using a multivariate analysis. The sodium chloride sensitivity was independently correlated with the change in erythrocyte sodium concentration (r = 0.47) and with the change in plasma renin activity (r = 0.29); but it was not related to basal blood pressure, the change in plasma volume of the change in plasma norepinephrine concentration. These data suggest that both intracellular sodium accumulation and inadequate suppression of the renin-angiotensin system may be independently involved in the elevation of blood pressure after sodium chloride loading. We could not find the independent importance of volume retention, hyperadrenergic activity or basal blood pressure in the sodium chloride sensitivity.

Periarteritis of coronary arteries with severe eosinophilic infiltration. A new pathologic entity (eosinophilic periarteritis)

A 40 year-old male presented symptoms of angina pectoris for about nine years and expired with symptoms of unstable angina, changing pattern at the terminal stage. At autopsy, both right and left coronary arteries of the subepicardial region were grayish white and elastic hard. Histologically, inflammatory infiltration was localized in adventitia of coronary arteries located in the subepicardial region. Inflammatory cells infiltrated into the adventitia were mostly eosinophiles. The medial smooth muscle cells were well preserved and the intima showed irregular thickening with fibrosis. Vascular obstruction or recanalization could not be observed. As a result of these findings, it was considered that these inflammatory changes of the coronary arteries could be termed eosinophilic periarteritis. These inflammatory changes could not be found in the intramural coronary arteries. Rather extensive fibrosis could be seen in the muscle layer centering about the posterior wall of the left ventricle. No findings of angiitis could be detected in the blood vessels except subepicardial coronary arteries.

Relationship of cellular calcium to salt sensitivity in patients with essential hypertension.

The significance of cellular calcium metabolism and systemic calcium balance in sodium chloride sensitivity was studied in 16 patients with essential hypertension and in 13 normotensive subjects. With changes in sodium chloride intake from 3 to 20 g/day, mean blood pressure, lymphocyte [Ca2+]i and the acute hypotensive response to nifedipine were increased in the hypertensive patients, but not in the normotensive subjects. Serum calcium concentration was decreased and urinary calcium excretion was increased in both groups. In the hypertensive patients, elevation of mean blood pressure was positively correlated with the increase in lymphocyte [Ca2+]i and with the enhancement of the hypotensive response to nifedipine, but it was not related to the change in serum or urinary calcium. These results suggest that enhancement of cellular-calcium-dependent vasoconstriction may lead to increased blood pressure following sodium chloride loading in patients with essential hypertension.

Role of Intracellular Free Calcium in the Hypotensive Response to Nifedipine

The acute antihypertensive effect of 10 mg of sublingual nifedipine was investigated in patients with essential hypertension in comparison with that in normotensive controls and in relation to intracellular free calcium concentration ([Ca2 +]i) in lymphocytes. Parameters predictive of the response to nifedipine such as age, pretreatment blood pressure, plasma norepinephrine concentration and plasma renin activity were also assessed. The fall in mean blood pressure with nifedipine was greater, and [Ca2+]i in lymphocytes was higher in patients with essential hypertension than in normotensive controls. In patients with essential hypertension, the hypotensive response to nifedipine was positively correlated with lymphocyte [Ca2+]i (r = 0.82) and negatively linked with plasma renin activity (r = -0.65), but unrelated to age, pretreatment mean blood pressure or plasma norepinephrine concentration. [Ca2+]i in lymphocytes was inversely correlated with plasma renin activity (r = -0.66). In normotensives, the mean blood pressure response to the drug had no relation to the variables studied. These results suggest that the acute hypotensive response to nifedipine may involve [Ca2+]i abnormalities and that calcium-influx-dependent vasoconstriction may be enhanced in essential hypertensive patients with suppressed plasma renin activity.