Biomedical subjects

N Sakamoto

Publications and source records attributed to N Sakamoto.

At least 451 records · Page 25Linked to original sources

PubMed1981

Isthmic afferent neurons identified by the retrograde HRP method in a teleost, Navodon modestus.

Isthmic afferent neurons were investigated by the retrograde horseradish peroxidase (HRP) method in a teleost, Navodon modestus. Following HRP injections into the nucleus isthmi, large pyriform neurons are labeled in the ipsilateral optic tectum. Very large and multipolar neurons are also labeled in the ipsilateral nucleus pretectalis. No labeled neurons were found in other areas.

Animals↗

PubMed1981

Identification of hyaluronidase activity in rabbit dental pulp.

A hyaluronidase activity was demonstrated in rabbit dental pulp. The optimum pH of the enzyme was 3.8. The enzyme activity was enhanced by protamine and poly-L-lysine and was inhibited by iodoacetamide, ferric ion, and ferrous ion in decreasing order. The product of the enzyme reaction was identified as tetrasaccharide. From these results it was concluded that the enzyme exists in pulp tissue and is functioning for degradation of proteoglycans in situ.

Animals↗

PubMed1981

Home blood pressure and circadian variation of blood pressure in the evaluation of hypertensive patients.

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.

Adrenal Gland Neoplasms↗

PubMed1981

Hypertension, hypokalemia and hypoaldosteronism with suppressed renin: a clinical study of a patient with Liddle's syndrome.

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.

Adrenocorticotropic Hormone↗

PubMed1981