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Biomedical subjects

K Ikegami

Publications and source records attributed to K Ikegami.

At least 91 records · Page 5Linked to original sources
PubMed1986

Effects of prostaglandin E2 and I2 on renal cortical and medullary blood flow in rabbits.

The effects of intra-aortic administrations of prostaglandin (PG) E2 and I2 on the renal regional blood flow were investigated in rabbits. Mean arterial blood pressure (MABP) was monitored by the direct method and total renal blood flow (TRBF) was measured using the electromagnetic method. Renal cortical and medullary blood flows (RCBF and RMBF) were measured by the hydrogen gas clearance method. Both PGE2 and PGI2 caused a dose-dependent reduction of MABP. At doses having no significant effect on MABP, PGE2, and PGI2 increased TRBF and decreased renal vascular resistance (RVR). The maximum reduction in RVR induced by PGI2 was significantly greater than that by PGE2. PGE2, produced significant increases in RCBF and in particular in RMBF, while PGI2 induced similar changes in RCBF and RMBF. The results suggest that PGE2, which is a weaker vasodilator than PGI2, mainly acts as a medullary vasodilator, and that PGI2 has similar vasodilatory effects on the cortex and medulla.

Animals↗
PubMed1985

Comparison of the effects of primary prostaglandins on isolated human urinary bladder.

The effects of primary prostaglandins (PGs) on the dome and trigone of the human urinary bladder were investigated in vitro. In the dome preparations, PGE1 (10(-9) to 10(-6) gm./ml.) showed a weak contractile effect, while PGE2 (10(-9) to 10(-6) gm./ml.) produced dose-dependent contractions. PGF2 alpha (10(-9) to 10(-6) gm./ml.) induced contractions greater than those induced by PGE1 and PGE2. In the trigone preparations, PGE1 (10(-9) to 10(-6) gm./ml.) had no effect, and PGE2 (10(-9) to 10(-6) gm./ml.) produced only a weak contractile response. PGF2 alpha (10(-9) to 10(-6) gm./ml.) showed a greater contractile potency than PGE2. Contractile responses of both preparations to PGE1, PGE2 and PGF2 alpha were not affected by pretreatments of atropine, hexamethonium and phentolamine. These results suggest that the order of potency of primary PGs to induce contractile responses is PGF2 alpha greater than PGE2 greater than PGE1 in both the dome and the trigone preparations, and that the contractile effects of PGE1, PGE2 and PGF2 alpha may not be mediated by activation of muscarinic, nicotinic or adrenergic alpha-receptors.

Acetylcholine↗
PubMed1985

A blue-green alga from Okinawa contains aplysiatoxins, the third class of tumor promoters.

The causative agents of swimmer's itch were isolated from the marine blue-green alga, Lyngbya majuscula, which grows off the coast of the Okinawa islands, Japan. Nuclear magnetic resonance and mass spectral studies revealed that these agents were identical with aplysiatoxin and debromoaplysiatoxin, which were previously shown to be the causative agents of swimmer's itch in Hawaii. Aplysiatoxin and debromoaplysiatoxin were recently found to be potent tumor promoters in two-stage carcinogenesis in mouse skin. This is the first report that humans are directly affected by these potent environmental tumor promoters in Japan.

Animals↗
PubMed1984

Role of the renal prostaglandins in furosemide-induced diuresis.

The role of the renal prostaglandin (PG) system in the renal effects of furosemide was assessed by using indomethacin, an inhibitor of PG synthetase, in conscious rats under conditions of vasopressin infusion (or dehydration). Urinary PGE and PGF2 alpha were measured by radioimmunoassay under conditions of furosemide-induced diuresis. The diuretic and natriuretic effects of furosemide were accompanied by a concomitant increase in the urinary excretion of PGE. In normal rats the pretreatment of indomethacin at 10 mg/kg failed to alter the diuretic effect of furosemide (5 mg/kg). In contrast, the diuretic effect of furosemide in vasopressin (2 U/kg)-infused (or dehydrated) rats was greatly inhibited by indomethacin. In regard to the natriuretic effect of furosemide, indomethacin did impair this response to furosemide both in normal and vasopressin-infused (or dehydrated) rats, but inhibited more strongly in the latter than in the former. These results suggest that the renal PGE is necessary for furosemide to produce optimal diuretic and natriuretic effects under conditions of vasopressin infusion (or dehydration).

Animals↗
PubMed1984

Interrelationships between the renal kallikrein-kinin and prostaglandin systems in furosemide-induced diuresis.

The relationships between the renal kallikrein-kinin (K-K) and prostaglandin (PG) systems under conditions of furosemide-induced diuresis were studied in normal rats. Urinary PGE and PGF2 alpha were measured by radioimmunoassay, and urinary kallikrein by enzymatic activity. The diuretic and natriuretic effects of furosemide were accompanied by a concomitant increase in the urinary excretion of kallikrein and PGE. The urinary excretion of kallikrein and PGE was closely related to the urinary excretion of sodium, potassium and chloride. The urinary excretion of kallikrein also showed a highly significant correlation with the urinary excretion of PGE. Pretreatment of the animal with indomethacin or aprotinin inhibited furosemide-induced diuresis and natriuresis. Aprotinin inhibited the urinary excretion of PGE, while indomethacin did not exert any inhibitory action on the urinary excretion of kallikrein. Although the urinary excretion of kallikrein was closely related to the urinary excretion of potassium, both indomethacin and aprotinin had no effect on the urinary excretion of potassium. The results indicate that the potassium-sodium exchange caused by furosemide in the distal nephron might stimulate the renal K-K system to result in increasing synthesis of PGE, which would, at least in part, participate in the diuretic and natriuretic effects of furosemide.

Animals↗
PubMed1984

Actions of some autonomic drugs on spontaneous contractions of isolated dog ureter.

Effects of some autonomic drugs on the isolated dog ureteral preparations showing spontaneous contractions were investigated quantitatively. Noradrenaline, adrenaline and phenylephrine produced increases in frequency and tension of the contractions which were reversed to decreases or depressed by phentolamine. Isoproterenol abolished the spontaneous contractions. Acetylcholine did not significantly change frequency and tension of the contractions. The results indicate that ureteral spontaneous contractions may be enhanced through an activation of alpha-adrenoceptors and be attenuated through an activation of beta-adrenoceptors. However, acetylcholine will not display an important role on the ureteral contractions.

Animals↗
PubMed1984

Carcinosarcoma of the ureter.

A rare case of carcinosarcoma of the ureter is reported. Histologically, this neoplasia was an unusual heterologous carcinosarcoma of the ureter. 2 years after the initial total nephroureterectomy, the patient died from recurrence.

Aged↗
PubMed1983

Effects of some prostaglandins on urinary bladder and urethra isolated from the dog.

Effects of prostaglandins (PGs) E1, E2, E2 and F2 alpha on the vesical and urethral smooth muscles of dogs were isometrically investigated in vitro. In vesical smooth muscles, 10(-8)-10(-6) PGE1/ml produced biphasic responses in the dome preparations; relaxation at 10(-8) g/ml and contractions at 10(-7)-10(-6) g/ml. In the trigone preparations, 10(-8)-10(-6) g PGE1/ml caused dose-dependent contractions. 10(-8)-10(-6)M g PGE2/ml and 10(-7)-10(-6) g PGF2 alpha /ml induced dose-dependent contractions of the dome and the trigone preparations. In urethral smooth muscles, 10(-8)-10(-6) g PGE1/ml and 10(-8)-10(-6) g PGE2/ml produced dose-dependent relaxations, while 10(-8)-10(-6) g PGF2 alpha /ml caused dose-dependent contractions. Results indicate that PGE, particularly PGE2, is able to stimulate micturition through vesical contraction and urethral relaxation.

Alprostadil↗