Search

Net Na+ and K+ fluxes were measured in Na+ -loaded red cells from 19 normotensive control subjects, 22 essential hypertensive patients, and 8 secondary hypertensive patients. The ratio of Na+/K+ net fluxes was significantly lower in essential hypertensive patients than in normotensive control subjects. However, by the addition of the patients' own plasma, the net Na+ efflux rate was significantly increased in essential hypertensive patients, which caused the increment in the ratio of Na+/K+ net fluxes. This resulted in disappearance of the difference between normotensive and hypertensive subjects in the ratio of cation fluxes. It was possible that the abnormalities of cation transport in red cells from essential hypertensive patients might be compensated for by humoral factors in the plasma.

A 24-yr-old woman with hypertension, hypokalemic alkalosis, low plasma renin and hypoaldosteronism was studied. Plasma aldosterone, renin and potassium returned to normal and blood pressure fell after sodium restriction or the administration of triamterene. Thiazide therapy also normalized her blood pressure while dexamethasone, spironolactone and furosemide did not improve her symptoms. Plasma aldosterone levels were low and responded poorly to a short term ACTH injection, but responded well to the maximal adrenal stimulation by ACTH-Z. Plasma levels of cortisol, corticosterone and deoxycorticosterone were within the normal range. Adrenal scintigram with 131I-adosterol and abdominal computed axial tomography did not reveal the presence of a sizeable adrenal tumor. In addition, the urinary kallikrein excretion was low after sodium restriction and showed no response to saline infusion. These findings suggest that the excessive secretion of unusual mineralocorticoids may not exist in this case. From these observations and the results of the therapeutic responses to the diuretic agents, we conclude that the primary cause of the disorder of this patient seems to be a renal defect in the distal tubule in handling sodium and potassium which is similar to that in Liddle's syndrome.

This study was performed to determine whether there is any difference in cation transport of red blood cells from normotensive subjects and hypertensive patients in Japan. Net Na+ efflux and net K+ influx rates were measured in sodium-loaded red cells from 19 normotensive subjects, 22 essential hypertensive patients, and 8 secondary hypertensive patients. The ratio of Na+/K+ net fluxes and the net cation flux rate were compared between these groups. The ratio of Na+/K+ net fluxes was significantly lower in essential hypertensive patients than in normotensive subjects. Parameters such as age, sex, blood pressure, plasma renin activity, and plasma aldosterone concentration were also examined in 2 groups of essential hypertensive patients, divided on the basis of their Na+/K+ net fluxes. However, there is no significant difference between the groups. These results suggest that the ratio of cation flux is related to hypertension independently of these parameters.

To investigate the roles of the sympatheticoadrenomedullary system and the renin-angiotensin system in the pathogenesis of essential hypertension, the levels of plasma catecholamine and plasma renin activity (PRA) after glucagon-stimulation were evaluated. In 9 patients with essential hypertension whose levels of PRA were either normal or high (NHREH), iv bolus injection of 1 mg glucagon caused a rapid and significant increase in plasma epinephrine concentration from the basal values of 170 ± 25 pg/ml, mean ± sem to 314 ± 30 pg/ml (P < 0.05) at 5 min after the injection, reaching the mean peak values of 358 ± 87 pg/ml (P < 0.05). Plasma norepinephrine also rose from the basal values of 357 ± 50 pg/ml to the peak values of 1065 ± 231 pg/ml (P < 0.02) while increase in PRA was detected in 4 of 9 patients. In 7 patients with low renin essential hypertension (LREH), plasma epinephrine failed to increase after glucagon stimulation whereas plasma norepinephrine increased significantly from the basal values of 391 ± 77 pg/ml, reaching 1212 ± 274 pg/ml at their peak values (P < 0.01). There was no discernible response of PRA to glucagon. These results suggest that both epinephrine secretion from adrenal medulla and renin release from juxtaglomerular (JG) cells after glucagon injection are impaired in LREH in contrast to their significant responses observed in NHREH. It also indicates that glucagon load may be useful for the simultaneous assessment of the reserve of both renin secretion and sympatheticoadrenomedullary function in essential hypertension.

Clinical blood pressures measured at clinic by physician were higher than home blood pressures measured at home by patients in the majority of untreated patients with essential hypertension, but equivalent or lower in some patients. Clinic minus home blood pressure (delta P) were correlated with the levels of clinic blood pressure (r = 0.51, p less than 0.005 for systolic; r = 0.35, p less than 0.02 for diastolic blood pressure, respectively). The systolic delta P might be greater in the middle-aged women, especially in the fifties of females than the age-matched males (p less than 0.05). The delta P could not be altered by any antihypertensive drugs with the exception of systolic delta P with diuretic alone. The blood pressure tended to remain more stable throughout the 24-hour period in proportion as the severity of hypertension increased. The observation of circadian variation in blood pressure disclosed that the blood pressure was lower in the morning, but increased gradually, resulting in the relatively high blood pressure between the afternoon and evening in the low renin and volume expanded type of hypertension. On the contrary, the blood pressure was already high in the early morning in hypertensive patients characterized by the accelerated renin-angiotensin system and contracted volume factor.