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K Sunaga

Publications and source records attributed to K Sunaga.

At least 37 records · Page 2Linked to original sources
PubMed1993

Autoradiographic demonstration of an increase in muscarinic cholinergic receptors in cerebellar granule cells treated with tetrahydroaminoacridine.

The neurotrophic and neurosurviving effects of 9-amino-1,2,3,4-tetrahydroacridine (THA), a putative antidementia agent, were studied in cultured granule cells using biochemical and morphological methods. The addition of 30 microM THA to cultures grown in 15 mM K(+)-containing media markedly increased cell survival and enhanced [3H]N-methylscopolamine binding to muscarinic cholinergic receptors (mAChRs). Furthermore, receptor autoradiographic studies revealed that neuronal cells were labelled over both cell bodies and fibers by the [3H]receptor ligand. These observations provide direct evidence that THA promotes the expression of mAChR binding sites in differentiating cerebellar granule cells.

Animals↗
PubMed1993

Influence of lisinopril on urinary electrolytes excretion after furosemide in healthy subjects.

It has been reported that the urinary excretions of chloride (Cl), potassium (K), and magnesium (Mg), but not sodium (Na), after furosemide, a loop diuretic, were decreased by pretreatment with lisinopril, an ACE inhibitor in hypertensive subjects. The electrolytes disturbance induced by furosemide might be ameliorated by lisinopril. The present study re-examines this potential drug interaction in healthy subjects. Lisinopril (20 mg) or its matching placebo was given orally using a double-blind, crossover design. Four hours after lisinopril administration, furosemide (20 mg) was injected intravenously and urine was collected during the following intervals: 0-0.5, 0.5-1, 1-1.5, 1.5-2, 2-3, 3-4, and 4-6 hours. Blood samples for plasma furosemide concentration were obtained at 0.5, 1, 1.5, 2, 3, 4, and 6 hours after the agent. There were no significant differences between the two trials in plasma concentrations of furosemide or urinary excretions of the agent. Urine volume and urinary excretions of electrolytes (Na, Cl, K, and Mg) after the furosemide with lisinopril administration were not significantly different from those of placebo at any observation period. These results suggest that the urinary excretions of electrolytes after furosemide administration are not influenced by pretreatment with lisinopril.

Adult↗
PubMed1993

Tetrahydroaminoacridine is neurotrophic and promotes the expression of muscarinic receptor-coupled phosphoinositide turnover in differentiating cerebellar granule cells.

We have investigated whether 9-amino-1,2,3,4-tetrahydroacridine (THA), a drug with potential antidementia activity, has a trophic action on differentiating cerebellar granule cells by using the method of [3H]inositol incorporation into inositol-containing phospholipid. Addition of THA (30-50 microM) prevented the extensive neuronal degeneration which occurred in the growth medium containing "low" K+ (15 mM). These effects were similar to the neuroprotective action caused by the presence of 100 microM N-methyl-D-aspartate (NMDA). Neurotrophic effects of THA and NMDA on cells grown in low K+ were also demonstrated by direct microscopic examination of cellular morphology. Measurement of phosphoinositide (PI) response in the rescued cells indicated that NMDA modestly promoted the PI response to carbachol and norepinephrine but markedly stimulated the activity induced by glutamate. In contrast, although THA had little or no influence on the maturation of the norepinephrine- and glutamate-induced PI response, it selectively enhanced the activity stimulated by carbachol. Furthermore, the THA treatment drastically increased the Vmax value of carbachol-induced PI turnover with no significant alteration in the EC50 value. Scatchard analysis of the binding of N-[3H]methylscopolamine to intact granule cells indicated a selective increase in the maximum binding value in cells grown in THA-supplementing medium. These observations suggest that THA seems to selectively up-regulate muscarinic cholinergic receptors.

4-Aminopyridine↗
PubMed1990

Effects of calcium channel blockers and hydralazine on epinephrine-induced stimulation of glucose output from primary cultured rat hepatocytes.

Effects of calcium channel blockers from structurally different classes and hydralazine on epinephrine-induced stimulation of glucose output from primary cultured rat hepatocytes were examined in vitro. Diltiazem, verapamil, and nifedipine dose-dependently inhibited the epinephrine-induced stimulation of glucose output from the primary cultured rat hepatocytes. In contrast to these agents, nicardipine caused decreases in the basal and epinephrine-stimulated glucose output from rat hepatocytes in primary culture. Hydralazine treatment was found to reduce the response in a dose-dependent manner. These results indicate that the calcium channel blockers and hydralazine did not potentiate but reduce the epinephrine-induced stimulation of glucose output from primary cultures of rat hepatocytes in vitro.

Animals↗
PubMed1990

Effects of calcium channel blockers and hydralazine on plasma glucose levels in streptozotocin-induced diabetic rats in vivo.

Effects of calcium channel blockers from structurally different classes and hydralazine on plasma glucose levels were examined in streptozotocin-induced diabetic rats in vivo. Non-dihydropyridine calcium channel blockers (verapamil, diltiazem, 1.0-10 mg/kg, i.p.) did not significantly affect the basal plasma glucose level, and dihydropyridine calcium channel blockers (nifedipine, 0.1-0.3 mg/kg, i.p,; nicardipine, 0.35-0.70 mg/kg, i.p.) caused mild hyperglycemia, which was blocked by the administration of the beta-adrenoceptor antagonist propranolol. In contrast, hydralazine markedly produced hyperglycemia, which was also inhibited by the combined administration of propranolol. The selective alpha 1-adrenoceptor antagonist prazosin greatly potentiated the hydralazine-induced hyperglycemia. Isoproterenol alone showed hyperglycemia similar to that of hydralazine. Hexamethonium (40 mg/kg, i.p.), a ganglionic blocker, blocked the hydralazine-induced hyperglycemia. There was a negative correlation between the hyperglycemic effect and the blood pressure lowering effect by different doses of hydralazine in streptozotocin-diabetic rats, but not in normal rats. These results suggest that endogenous catecholamines are involved in the hydralazine-induced hyperglycemia through the interaction with beta-adrenoceptors in streptozotocin-diabetic rats in vivo.

Animals↗
PubMedDate not supplied

Antioxidative activity of Allium victorialis L. extracts.

Allium victorialis L. (Liliaceae, "Hon-Gyoujya Nin-Niku" in Japanese) was successively extracted with hexane, acetone, methanol and 70% methanol and the extracts were further separated into a total of twenty-five fractions by silica gel and ODS column chromatographies. The biological activities of these four extracts and 25 column fractions were compared. The cytotoxic activity of all extracts and fractions against two oral tumor cell lines was significantly higher than that against normal human gingival fibroblasts, suggesting their tumor-specific action. Three methanol column fractions [M2, M3, M6] and a 70% methanol column fraction [70M6] most effectively reversed the multidrug resistance (MDR) against L5178 mouse T cell lymphoma. The electron spin resonance (ESR) spectroscopy showed that methanol column fractions and 70% methanol extracts produced the highest amount of radical(s) and most efficiently scavenging O2*-, generated by the hypoxanthine-xanthine reaction system, suggesting that the same substances in these fractions display both prooxidant and antioxidant properties. They showed no anti-human immunodeficiency virus (HIV) or anti-Helicobacterpylori activity. These data suggest the medicinal efficacy of Allium victorialis extract.

Allium↗
PubMedDate not supplied

Usefulness of circadian amplitude of blood pressure in predicting hypertensive cardiac involvement.

Twenty-four-hour blood pressure (BP) profiles of 56 patients diagnosed as 'hypertensive' by WHO criteria were analyzed by the fit of a 24-hour cosine curve according to the single cosinor method. A left ventricular mass index (LVMI) was also assessed by two-dimensional echocardiography on each patient as a gauge of target organ involvement. LVMI and the BP MESOR correlates positively for systolic, S (r = 0.324), mean arterial, MA (r = 0.334) and diastolic, D (r = 0.267) BP (P less than 0.05), yet no statistically significant linear correlation between LVMI and the circadian BP amplitude (one-half of predictable change) was found. When a second-degree polynomial regression was fitted to the circadian BP amplitudes, an association was found (SBP: R2 = 0.138, P = 0.02; MAP: R2 = 0.167, P = 0.01; DBP: R2 = 0.128, P less than 0.01). The corresponding curves were characterized by peaks in the circadian amplitudes of SBP, MAP and DBP around a value of LVMI between 110 and 120 g/m2. For further scrutiny, three subgroups had been formed on the basis of literature, a priori with respect to the LVMI (group 1: LVMI less than 100); group 2: 100 less than LVMI less than 130; group 3: 130 less than LVMI). For MESORs, there was no difference between groups 1 and 2, whereas the MESOR of group 3 were larger than the other two groups. The circadian BP amplitudes of group 2 were larger than those of the other two groups for SBP, MAP and DBP. An increasing LVMI precedes a definitive increase of BP MESOR and coincides with an increase in the circadian BP amplitude; thus an increase in extent of circadian changes can alert the self-monitoring population of a target organ involvement.

Adolescent↗