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Biomedical subjects

K Nakata

Publications and source records attributed to K Nakata.

At least 559 records · Page 31Linked to original sources
PubMed1981

Prostaglandins and the contractility of the guinea pig biliary system.

The effects of exogenously applied prostaglandins on the contractile responses of the gallbladder and sphincter of Oddi isolated from guinea pigs were examined in normal and indomethacin-treated preparations. Indomethacin reduced the tone and the contractile responses to transmural stimulation and to exogenously applied ACh of the gallbladder, while the tone and contractile responses of the sphincter of Oddi were little affected by indomethacin. Prostaglandins E1, E2 and F2 alpha potentiated the contractile responses of the gallbladder to transmural stimulation and ACh, and furthermore, treatment with indomethacin enhanced the potentiating effects of prostaglandins E1 and E2 but not the effect of PGF2 alpha. The reduced tone and contractility of the gallbladder were restored to the control level by addition of PGE1 and PGE2 but not by PGF2 alpha. These results suggest that endogenous PGE1 and PGE2 may play an important role in neurogenic control of contractility of the gallbladder, but not of the sphincter of Oddi.

Acetylcholine↗
PubMed1981

Effects of indomethacin on prostaglandin synthesis and on contractile response of the guinea pig gallbladder.

In studies on prostaglandin (PG) synthetase activity in the guinea pig gallbladder, prostaglandin E2 and F2 alpha (PGE2 and PGF2 alpha) were enzymatically formed from arachidonic acid using the 105,000-g precipitate fraction. The amount of PGE2 synthesized was about four times larger than PGF2 alpha. Indomethacin (1-3 microM) inhibited both the PG synthesis and the contractile response to transmural stimulation in the gallbladder. These findings suggest that the inhibitory effect of indomethacin on the contractility of the gallbladder is related to the inhibition of PG synthesis, and that endogenous PGE2 is involved in the contractility of this tissue.

Animals↗
PubMed1981

Tissue and blood cell concentration of methylguanidine in rats and patients with chronic renal failure.

Methylguanidine concentration in blood cell of nondialysed patients with chronic renal failure was quantitatively determined by the method of the present authors. We also determined tissue methylguanidine concentrations in the liver, blood cell, kidney, colon, muscle and brain of uremic rat experimentally produced by Platt's method. Methylguanidine concentrations in blood cell and tissues except the brain of the uremic rats and in blood cell of the uremic patients were 5--7 times higher than those in their serums. An increased methylguanidine concentration in the liver of the uremic rat receiving 40% protein diet was observed. These results imply that methylguanidine acts as one of the important uremic toxins in the intracellular space except for the brain, and suggest that the liver specifically affects the formation of methylguanidine.

Animals↗
PubMed1981

Effects of C-terminal octapeptide of cholecystokinin and prostaglandins on adrenergic functions in the guinea-pig gallbladder and sphincter of Oddi.

Effects of C-terminal octapeptide of cholecystokinin (C8-CCK) and prostaglandins E1, E2 and E alpha on noradrenaline-induced responses and 3H-noradrenaline release in the gallbladder and sphincter of Oddi of guinea pigs were examined. In the sphincter of Oddi, noradrenaline in low concentrations induced a relaxation which was blocked by either phentolamine or propranolol, while noradrenaline in high concentrations induced a contraction which was blocked by phentolamine. These results suggest the existence of excitatory and inhibitory alpha-receptors and inhibitory beta-receptors in the sphincter of Oddi. In the gallbladder, the adrenergic receptors are alpha-excitatory and beta-inhibitory. C8-CCK (10(-9) g/ml) potentiated both contractile and relaxing responses to noradrenaline, in the gallbladder. The same concentration of prostaglandins potentiated only contractile response to noradrenaline. In the sphincter of Oddi, noradrenaline-induced responses were not affected by C8-CCK and prostaglandins. Prostaglandins inhibited 3H-efflux evoked by electrical stimulation, while C8-CCK had no effect on the 3H-efflux from both preparations. These results suggest that C8-CCK enhances the contractile and relaxing responses to noradrenaline, and that prostaglandins act in a similar way on the postsynaptic response and, in addition, inhibit presynaptically the release of noradrenaline in the gallbladder. In the sphincter of Oddi, only prostaglandins inhibit the presynaptic event.

Ampulla of Vater↗
PubMed1981

A new potent inhibitor of converting enzyme: (2R,4R)-2-(2-hydroxyphenyl)-3-(3-mercaptopropionyl)-4-thiazolidinecarboxylic acid(SA446).

(2R, 4R)-2-(2-Hydroxyphenyl)-3-(3-mercaptopropionyl)-4-thiazolidinecarboxylic acid (SA446) is a novel potent converting enzyme inhibitor having a sulfhydryl group in the molecule. SA446 inhibited the activity of semi-purified rabbit lung converting enzyme (IC50 = 6 nM). The contractile response of isolated guinea pig ileum to angiotensin I (AI) was markedly inhibited by SA446 (IC50 = 28 nM). On the other hand, SA446 augmented the contraction to bradykinin (BK) (AC50 = 0.7 nM), but did not affect the contraction caused by angiotensin II (AII), acetylcholine and histamine. These in vitro potencies of SA446 were 4 to 5 times larger than those of captopril. SA446 inhibited the pressor response to AI in rats (ID50 = 0.06 mg/kg, i.v., 0.48 mg/kg, p.o.) and dogs (ID50 = 0.01 mg/kg, i.v.). SA446 augmented the depressor response to BK (AD50 = 0.009 mg/kg, i.v.), but did not affect the pressor responses to AII and norepinephrine in rats. These in vivo activities of SA446 in dogs were more potent than those of captopril, but the reverse was seen in rats. Oral administration of SA446 had a hypotensive effect on two-kidney, one-clip renal hypertensive rats and spontaneously hypertensive rats, at doses over 3 and 10 mg/kg, respectively. However, the blood pressure of normotensive and DOCA-salt hypertensive rats was not affected by SA446, in doses up to 100 mg/kg. These results indicate that oral SA446 is a potent active inhibitor of converting enzyme and may be classed as an antihypertensive agent.

3-Mercaptopropionic Acid↗
PubMed1981

Insulin binding to erythrocytes in diabetes mellitus.

Insulin binding to erythrocytes was studied in diabetic patients. Insulin binding was lower in untreated diabetics and diabetic patients treated with diet or insulin than in normal subjects. Binding variation was mainly due to decreased binding site concentration in untreated and insulin-treated patients, and to lowered insulin binding site affinity in diet-treated patients. Several patients treated with hypoglycemic agents showed higher insulin binding due to increased binding site concentration. Insulin binding to erythrocytes may not always reflect the insulin binding status of insulin sensitive tissues.

Diabetes Mellitus↗