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Biomedical subjects

H Usui

Publications and source records attributed to H Usui.

At least 145 records · Page 8Linked to original sources
PubMed1987

Possible role of endothelial thromboxane A2 in the resting tone and contractile responses to acetylcholine and arachidonic acid in canine cerebral arteries.

The amount of immunoreactive thromboxane B2 (iTXB2) released from isolated canine arteries was determined by radioimmunoassay. The amount of iTXB2 released from the cerebral, coronary, mesenteric, and saphenous arteries was 47.0 +/- 7.2, 4.0 +/- 0.6, 4.9 +/- 0.5, and 2.7 +/- 0.4 pg/mg wet weight tissue/30 min, respectively. The release of iTXB2 from the cerebral artery was decreased to less than 50% by the administration of indomethacin (10(-5) M) or OKY-046 (10(-4) M), and by intimal rubbing. The release of iTXB2 was enhanced nearly twofold by the addition of arachidonic acid (AA) (10(-5) M) to the medium, but not by the addition of acetylcholine (ACh) (10(-6) M). The cerebral arterial strips maintained the resting tone, which was reduced maximally by papaverine (10(-4) M). The resting tone was also reduced dose dependently by a cyclooxygenase inhibitor (indomethacin), a thromboxane A2 (TXA2) synthetase inhibitor (OKY-046), and a TXA2 antagonist (ONO-3708). The resting tone of rubbed strips was about half that of intact strips. ACh and AA induced similar transient contractions in the cerebral artery. Contractions produced by these agents were attenuated by indomethacin (10(-7) M), aspirin (5 X 10(-5) M), OKY-046 (10(-6) M), and ONO-3708 (10(-8) M), and abolished by intimal rubbing. From these results, it is concluded that TXA2 is produced in the endothelial cells and may be involved in maintaining the resting tone and contractile response to AA in the canine cerebral artery.

Acetylcholine↗
PubMed1987

Regional differences of reactivity to stimulants in the dog portal tree.

We studied the regional differences both of reactivity to various stimulants and of neurogenic responses elicited by transmural stimulation in the longitudinal and circular muscles of the truncal portal vein, mesenteric vein, splenic vein and gastric vein of the dog portal tree. Strong spontaneous activity appeared in the longitudinal muscle of the truncal portal vein (96% of preparations tested). Weak spontaneous activity sometimes appeared in the circular muscle of the truncal portal vein (41%) and rarely in the longitudinal muscle of the mesenteric vein (12%). It did not appear in other segments. The splenic vein and the gastric vein showed similar patterns in the relationship between resting tension and response to noradrenaline; that is, the responsiveness of either longitudinal or circular muscle of these two veins increased and then decreased almost parallel as resting tension increased and reached a maximum under the same resting tension. The longitudinal muscle of both the truncal portal vein and the mesenteric vein was more responsive to noradrenaline, acetylcholine, histamine and KCl than the circular muscle; for example 2.02 and 1.44 times more responsive to noradrenaline, respectively. On the other hand, the longitudinal muscle of the splenic vein and the gastric vein responded less well than the circular muscle; for example 0.36 and 0.16 times as responsive to noradrenaline, respectively. Acetylcholine and histamine caused marked contractions which were comparable to those elicited by noradrenaline in the longitudinal muscle of the truncal portal vein. Acetylcholine also elicited similar contractions in the longitudinal muscle of the mesenteric vein but the responses induced in preparations of other segments were small. 6 The longitudinal muscle of the truncal portal vein responded well even to low-frequency stimulation of 2 Hz, while the circular muscles of the truncal portal and splenic veins gave marked responses only to high-frequency stimulation of 10 or 20 Hz or more. These contractile responses were attenuated by phentolamine (10-6 M) or atropine (10-6 M). The longitudinal muscle of the splenic vein showed no significant response to stimuli of any frequency. 7 It seems that the portal tree receives not only adrenergic but also cholinergic innervation. In addition, the longitudinal muscle of the truncal portal vein may receive non-adrenergic, noncholinergic innervation as well. 8 The longitudinal muscle of the portal vein may be crucial to venous return in assisting movement of the blood it contains. If this is the case in man, then the regional differences in the portal tree demonstrated in this study may explain why varicose changes during portal hypertension occur preferentially in the oesophagogastric region and rarely in other regions, as blood stasis may occur more readily in the regions of the gastric and splenic veins where the longitudinal muscle is not very active.

Acetylcholine↗
PubMed1987

A possible role of thromboxane A2 in endothelium in maintaining resting tone and producing contractile response to acetylcholine and arachidonic acid in canine cerebral arteries.

Endothelial thromboxane A2 (TXA2) in maintaining the resting tone and producing the contractile response to acetylcholine (ACh) and arachidonic acid was studied in canine cerebral artery. The spontaneous release of TXB2 from cerebral artery was about tenfold higher than that of coronary, mesenteric and saphenous arteries. The resting tone, the release of TXB2 and the contraction produced by arachidonic acid were decreased by the presence of cyclooxygenase inhibitor, TXA2 synthetase inhibitor, TXA2 antagonist and rubbing of the luminal side of preparations. The contraction produced by ACh was inhibited by the presence of the above inhibitors and rubbing of the preparations without decreasing the release of TXB2. These results suggest that the resting tone of canine cerebral artery and the contractile response to arachidonic acid are related to activation of TXA2 synthesis in the endothelium.

Acetylcholine↗
PubMed1987

Endothelium-dependent vasocontraction in response to noradrenaline in the canine cerebral artery.

In the canine basilar artery, noradrenaline-induced contraction was markedly decreased by intimal rubbing. Scanning electron microscopic studies showed that the rubbing procedure had scrapped away the endothelial cells from the intimal surface of the artery. Prazosin (10(-7) M) reduced the noradrenaline-induced contraction in intact arteries, but did not significantly affect the contraction in the scrapped arteries. Yohimbine (10(-7) M) strongly inhibited the contraction in both intact and scrapped arteries. The endothelium-dependent vasocontraction produced by noradrenaline was inhibited by aspirin (5 X 10(-5) M), OKY-046 (10(-5) M) and ONO-3708 (5 X 10(-9) M). The present experiments provided evidence for endothelium-dependence of the vasocontraction produced by noradrenaline in canine basilar arteries, and they suggested that the endothelium-derived contracting factors might be arachidonic acid metabolites such as TXA2; they also suggested that alpha 1 adrenoceptors might be preferentially distributed on the endothelium, while alpha 2 adrenoceptors are preferentially located in smooth muscle.

Animals↗
PubMed1987

Nitroglycerin-sensitive and -resistant contractions mediated by receptor-operated calcium channels in rabbit ear artery.

In isolated rabbit ear arteries incubated in a Ca2+-free medium with EGTA and nifedipine in the presence of norepinephrine, serotonin or histamine, an addition of Ca2+ induced a tonic contraction which is due to Ca2+ entry through receptor-operated Ca2+ channels (ROCs). Nitroglycerin (10(-4) M) significantly inhibited the ROCs-dependent contractions produced by serotonin or histamine, but failed to inhibit the ROCs-dependent contraction by norepinephrine. These results suggest the possible existence of two types of receptor-operated Ca2+ channels in rabbit ear artery.

Animals↗
PubMed1987

ID sequences in the genes of three brain-specific proteins.

We characterized the brain-specific gene coding for rat S-100 protein beta-subunit and found three "brain identifier (ID)" elements, which have been proposed to regulate the gene expression in rat brain. The nucleotide sequences of these elements corresponded well with that of the consensus ID element and were clearly different from those of "ID-like" elements in rat beta B1-crystallin gene, etc. ID elements were also observed in the flanking regions of rat neuron-specific enolase and cholecystokinin genes, which were expressed in the neuronal cells. Direct repeats were observed in the regions flanking ID elements.

Animals↗
PubMed1987

Tissue distribution of rat S-100 alpha and beta subunit mRNAs.

Using Southern blot analysis it is demonstrated that S-100 alpha and beta genes were found as single copies in the rat genome. S-100 alpha mRNA was not found at all in rat brain during the developmental period, but it was slightly detectable in muscle and kidney. S-100 beta mRNA was detected in rat brain, and its mRNA level increased during the developmental period. The different localizations of the subunits may be due to the specific expression of each gene in various tissues.

Aging↗
PubMed1986

Molecular cloning of cDNA of S100 alpha subunit mRNA.

The primary structure of the bovine S-100 alpha mRNA on the basis of molecular cloning and sequence analysis of the cDNA are described. The sequence is composed of 532 bp which include the 282 bp of the complete coding region, 89 bp at the 5'-noncoding region, 161 bp at the 3'-noncoding region, polyadenylation signal, ATTAAA and poly(A) tail. Northern blot analysis shows that the size of S-100 alpha mRNA is about 700-800 bases long and a single mRNA occurs in bovine brain. Bovine brain contains both S100 alpha and beta subunits and their mRNAs. In contrast, the rat brain contains only S100 beta subunit and its mRNA.

Animals↗
PubMed1986

Developmental and regional changes of cholecystokinin mRNA in rat brains.

Since the nucleotide sequence of cholecystokinin (CCK) cDNA was found in the rat gene, we applied cDNA to quantitate the CCK mRNA. The size of the mRNA for a CCK precursor was 850 nucleotides in length using brain cytoplasmic RNA. There were no bands except CCK mRNA by Northern blot analysis. We also examined the developmental changes and regional distribution of CCK mRNA in rat brains by dot-blot and gel-blot hybridization using CCK cDNA as a probe. CCK mRNA was barely detectable in the fetal brain, but started to increase postnatally and attained the plateau level after 20-30 days. Further, the level of CCK mRNA was highest in the frontal cortex, followed by those of the hippocampus and striatum. The cerebellum contained only negligible CCK mRNA. These results are in agreement with those of CCK concentration in the corresponding brain areas and suggest a transcriptional control of CCK concentration.

Aging↗
PubMed1986

Sympathetic denervation and alpha adrenoceptors in dog cerebral arteries.

The magnitude of the noradrenaline-induced contractions of dog middle cerebral arteries was less than that seen in the vertebral, common carotid, femoral and renal arteries. Noradrenaline and clonidine produced a similar magnitude of maximum contractions in the middle cerebral arteries, whereas methoxamine produced no significant contractions in the same arteries. In the extracranial arteries, noradrenaline and methoxamine produced significantly larger contractions than clonidine. Binding studies revealed no specific 3H-prazosin binding sites in the cerebral arteries, though such binding sites were evident in the case of extracranial arteries. 3H-Yohimbine binding studies revealed the presence of two classes of binding sites with high and low affinities in both cerebral and extracranial arteries. After superior cervical ganglionectomy, noradrenaline- and clonidine-induced contractions of the denervated middle cerebral arteries were not altered, compared with the control arteries. A 3H-yohimbine binding study was also performed using the denervated cerebral arteries. This study revealed that there was a low affinity 3H-yohimbine binding site, whereas high affinity 3H-yohimbine binding site was not detectable. These results suggest the presence of two different binding sites with high and low affinity for alpha 2 adrenoceptors, which we are classifying into alpha 2H and alpha 2L subtypes. The high affinity sites, alpha 2H adrenoceptors, are presynaptically located while the low affinity sites, alpha 2L adrenoceptors, located postsynaptically. The noradrenaline-induced contractions are probably mediated by postsynaptic low affinity sites of alpha 2 adrenoceptors (alpha 2L adrenoceptors) in the cerebral arteries and mainly by alpha 1 adrenoceptors in the extracranial arteries.

Animals↗