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M Yoshimura

Publications and source records attributed to M Yoshimura.

At least 739 records · Page 41Linked to original sources
PubMed1984

alpha 2 and alpha 1-Adrenoceptors mediate opposing actions on parasympathetic neurons.

We used intracellular recording methods to analyze the membrane responses to norepinephrine in cat vesical parasympathetic ganglia. In parasympathetic neurons, norepinephrine (NE) produces a membrane hyperpolarization, a membrane depolarization often accompanied by cell firing and a biphasic potential, a hyperpolarization followed by a depolarization. We found that the NE hyperpolarization is mediated through alpha 2-adrenoceptors while the NE depolarization is mediated through alpha 1-adrenoceptors. This situation is different than in sympathetic neurons where beta-adrenoceptors mediate a NE depolarization.

Animals↗
PubMed1984

[The effect of dopaminergic antagonists on plasma aldosterone in normal subjects and patients with hypopituitarism].

Although angiotensin II, ACTH and potassium are generally acknowledged as major factors in regulating the influences on aldosterone secretion, it has recently been reported that dopamine is a potent inhibitor of aldosterone secretion in man and animals. In the present study, we investigated the effect of two kinds of dopaminergic receptor antagonists, metoclopramide and sulpiride, on plasma aldosterone concentration (PAC) and serum prolactin (PRL) in man. Normotensive volunteers and patients with hypopituitarism were injected with metoclopramide (10 mg i.v.) or sulpiride (10 mg i.m.). In normal volunteers, metoclopramide increased both PAC and PRL levels, and showed a maximum level at 30 minutes after injection. In patients with hypopituitarism, PAC tended to increase without change of PRL, which suggested that the increase in PAC by metoclopramide might have a direct inhibitory effect on the dopaminergic receptor in the adrenal gland. Moreover another antagonist, sulpiride also increased PRL but contrary tended to decrease PAC. These results suggested that PRL responses to both inhibitors were mediated by dopaminergic antagonist activity at the level of pituitary receptors. However dopamine-induced modulation of aldosterone secretion may be different from that of PRL at dopaminergic receptors. These results suggested that modulatory inhibition of aldosterone secretion by dopamine may be affected by difference of affinity of dopamine to receptor as organ specificity, or different affinity of metoclopramide and sulpiride to adrenal dopamine receptor.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1984

Identification of transfer RNA suppressors in Escherichia coli. III. Ochre suppressors of lysine tRNA.

Transducing phages of lambda carrying suppressors, lysT (Su+ beta), supG and and supL, were isolated in vivo. Upon infection with each of these phages, the production of tRNALys and tRNAVal1 was markedly enhanced. Fingerprint analysis of these tRNAs revealed that they consisted of normal tRNALys, mutant tRNALys and tRNAVal1 in equimolar ratios. The mutant tRNALys carried a single-base alteration at the anticodon, from 5'-UUU-3' to 5'-UUA-3', which makes it an ochre suppressor. DNA sequence analysis of the entire transducing fragment (730 base-pairs) of lambda pSu+ beta revealed that three tRNA genes are tightly clustered within a transcription unit in the following order; i.e. promoter-(48 base-pairs)-wild-type tRNALys-(132 base-pairs)-tRNAVal1-(2 base-pairs)-Su+ beta tRNALys-. In wild-type bacteria there are two identical tRNALys genes in one operon. Although we have shown that in Su+ beta it is the distal tRNALys that has been mutated to the ochre suppressor by a single base change at the anticodon (U36 to A36), we have not determined which of the two genes bears the supG or the supL mutation. The sequences following both tRNALys genes are highly homologous: both are about 100 base-pairs long and both terminate with an 18 base-pair sequence homologous to the last 18 bases of each tRNA. The sequences of tRNALys and tRNAVal1 are also very similar. Thus, including the 3'-portions of these tRNA genes, the 18 base-pair sequence is more or less periodically repeated five times in the DNA sequence.

Bacteriophage lambda↗
PubMed1984

Identification of transfer RNA suppressors in Escherichia coli. IV. Amber suppressor Su+6 a double mutant of a new species of leucine tRNA.

An Escherichia coli DNA fragment containing an Su+6 amber suppressor gene (supP) was cloned into a lambda gt lambda Ch vector by the shotgun method, selecting a Su+6 transducing phage lambda pSu+6. Through prophage integration followed by induction occurring at the transducing region of the lambda pSu+6 in Su- E. coli, a counterpart transducing phage carrying the wild-type allele (Su degrees 6) was isolated (lambda pSu degrees 6). The fingerprint of a tRNA encoded by lambda pSu degrees 6 was identical to that of an unidentified tRNAE previously reported (Ikemura & Ozeki, 1977). The cloverleaf structure of this tRNA was determined by combining the results of tRNA analysis and DNA sequencing of the gene. Judging from the anticodon of 5'-CAA-3', Su degrees 6 tRNA was identified as a new type of leucine isoacceptor in E. coli. Unlike other suppressors analyzed, Su+6 tRNA differed by two nucleotides from Su degrees 6 tRNA; one at the anticodon (CAA to CUA) and the other at the junction of D- and anticodon-stem (A27 to G27). DNA sequence analysis revealed that a single stretch of tRNA is flanked by the putative sequences of promoter and terminator. Thus a single copy of the Su degrees 6 tRNA gene constitutes a solitary tRNA transcription unit. Southern blotting showed only one copy of Su degrees 6 tRNA gene per haploid genome of E. coli. Since this single gene can mutate to the Su+6 suppressor, the Su degrees 6 leucine tRNA may be accounted as a dispensable species among the leucine isoacceptor tRNAs. Two possible open reading frames are found immediately following the Su degrees 6 tRNA gene.

Bacteriophage lambda↗
PubMed1984

The possible applications of a composite skin and subcutaneous vein graft in the replantation of amputated digits.

A composite graft of skin and attached vein was taken from the dorsal aspect of the foot and used in the replantation of 6 amputated digits in 5 patients which were complicated by loss of skin and blood vessels and with exposed bone and tendon. The 5 replanted digits survived in 4 patients. Complete survival of the skin graft was achieved in two digits and partial necrosis occurred in three digits. The technique is put forward as a possible method of vascular reconstruction in which skin loss is complicated by exposure of the deeper structures i.e., bone, tendon and/or joint.

Adult↗
PubMed1984

Centrally-induced vasopressor responses to carbachol are augmented in DOCA-salt hypertensive rats.

Increased sympathetic nervous system activity and vasopressin release has been demonstrated in established DOCA-salt hypertension in the rat. To determine the importance of these mechanisms in centrally-mediated pressor responses in this model of hypertension, both awake rats and rats anaesthetised with urethane were given intracerebroventricular injections of carbachol. The systolic blood pressure after implanting a silicon rubber mould containing DOCA, and with subsequent substitution of 1% saline in tap water, increased from 112 +/- 3 mmHg to a stable 188 +/- 7 mmHg by the end of 4 weeks, measured using a tail-cuff method. The blood pressure consistently became elevated when carbachol was injected into the cerebral ventricles of awake rats. Of the three groups of normotensive rats (NTR), sham-operated rats (SHAM) and DOCA-salt hypertensive rats (DOCA), the magnitude of the pressor phase was largest in the DOCA rats. The heart rate in all three groups of rats decreased similarly. When the rats were later anaesthetised with urethane to allow recording of abdominal sympathetic nerve activity, the carbachol injections caused biphasic blood pressure responses and sympathetic nerve discharge consisting of initial vasodepression and sympathetic nerve inhibition of short duration. This was followed by a sustained pressor phase accompanied by a corresponding increase in sympathetic nerve activity. The magnitude of the pressor response was again larger in the DOCA than in the SHAM rats. Spinal section abolished the initial depressor phase but did not much affect the sustained pressor phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1984

Peroneal flap for reconstruction in the extremity: preliminary report.

The peroneal flap has many advantages, such as thin subcutaneous tissue, availability of a large-diameter artery and vein for anastomosis, a long pedicle, and freely designed size and shape. This technique is introduced because it has many outstanding features that allow it to be used to meet a variety of specific needs, such as a free peroneal flap, a peroneal island flap, a free vascularized fibular graft with skin, and a monitoring flap in free vascularized fibular grafts. We have found the peroneal flap to be especially useful.

Child↗
PubMed1984

The actions of noradrenaline on neurones of the rat substantia gelatinosa in vitro.

Intracellular recordings were made from substantia gelatinosa (s.g.) neurones in slices cut from adult rat spinal cord and maintained in vitro. Noradrenaline applied by superfusion (1-50 microM), or by brief pressure ejection from a micropipette, reversibly hyperpolarized 80% of the s.g. cells. The noradrenaline induced hyperpolarization was associated with an increase in conductance and it reversed in polarity at -88 mV. The reversal potential changed when the external potassium concentration was changed, as predicted by the Nernst equation. The noradrenaline hyperpolarization was antagonized by phentolamine and yohimbine but not by propranolol and prazosin. The hyperpolarization was probably a direct action on the impaled cell and not due to release or block of release of other transmitters, because the effects persisted during a perfusion with a low calcium/high magnesium solution or in a solution containing cobalt and high magnesium. In 35 of 148 cells, noradrenaline caused a dose-related increase of spontaneous excitatory post-synaptic potentials (e.p.s.p.s). This effect was blocked by tetrodotoxin. The noradrenaline induced increase in e.p.s.p.s was blocked by phentolamine and prazosin but not by the alpha 2-blockers yohimbine and RX 781094. A few cells were depolarized by noradrenaline, and this was blocked by prazosin but not by yohimbine. It is suggested that noradrenaline may inhibit nociceptive input to the spinal cord by increasing the potassium conductance of s.g. neurones.

Adrenergic alpha-Antagonists↗
PubMed1984

Centrally-induced vasopressor responses to sodium-potassium adenosine triphosphatase inhibitor, ouabain, may be mediated via angiotensin II in the anteroventral third ventricle in the brain.

Central cardiovascular effects of the sodium-potassium adenosine triphosphatase (Na+, K+-ATPase) inhibitor, ouabain, were investigated by injecting it intracerebroventricularly (ICV) using conscious Wistar rats. Ouabain, 0.1-10 micrograms injected ICV, produced dose-related pressor responses attaining peak elevations after about 5 min. To investigate the underlying mechanisms of these central pressor responses, angiotensin II blockers were injected ICV before the injections of ouabain. 1-Sar, 8-Ile angiotensin II (ang IIa), 50 micrograms, given 3 min before the ouabain, abolished the pressor responses to ouabain, 5 micrograms. Angiotensin I converting enzyme inhibitor (CEI, captopril), 100 micrograms, also significantly attenuated the pressor responses to ouabain. Since previous results with ICV injections of ouabain suggested that the pressor responses are mediated via a release of brain angiotension II, and the site of action of brain angiotensin II is believed to be the anteroventral third ventricle (AV3V) area of the brain, ICV injections of ouabain were repeated using rats whose AV3V areas had been destroyed electrically. The pressor responses were smaller in the AV3V lesioned rats than in sham-operated rats. The abdominal sympathetic nerve activity was recorded using three conscious, normotensive Wistar rats. ICV injections of ouabain, 5 micrograms, elicited pressor responses as described above and these were accompanied by a corresponding increase in the nerve firing, lasting for 5-7 min. These responses were again abolished by pretreatment with an angiotensin II antagonist. These results suggest that centrally administered ouabain elicits vasopressor responses which increase peripheral sympathetic nerve activity.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1984

KCl inhibits hypothalamic activity to attenuate hypertension in DOCA-salt rats.

Potassium supplementation attenuated the development of hypertension in DOCA-salt rats but did not affect blood pressure in control rats. However, it caused a decrease in body weight in both groups of rats. Sympathetic nerve and pressor responses either to electrical stimulation of the hypothalamus or to intracisternal injections of hypertonic NaCl were enhanced in DOCA-salt rats but were normalized by KCl supplementation. Since the pressor responses to injected norepinephrine or tyramine remained unaltered by KCl treatment, a peripheral inhibition of cardiovascular reactivity was considered unlikely. Pretreatment with methyclothiazide also attenuated the elevation in blood pressure but did not affect the responsiveness to hypothalamic stimulation; hence increased natriuresis or diuresis alone could not account for the effects induced by KCl. These findings are consistent with the conclusion that KCl supplementation attenuates the development of DOCA-salt hypertension in rats by acting on the central nervous system to reduce sympathetic output.

Anesthesia↗
PubMed1984

Centrally induced vasopressor and sympathetic nerve responses to carbachol in rats.

Blood pressure rose when carbachol was injected into the cerebral ventricles in conscious rats, but the heart rate fell. When rats were later anesthetized with urethane to allow recording of abdominal sympathetic nerve activity, carbachol injected similarly produced the following biphasic responses: initial vasodepression followed by a sustained pressor phase accompanied by corresponding changes in peripheral sympathetic nerve activity. The heart rate was transiently suppressed following the injection. Spinal section abolished the initial hypotensive phase and accompanying bradycardia and made the response purely pressor. By contrast, intravenous injections elicited purely vasodepressor responses. Thus, carbachol administered centrally caused vasopressor responses possibly via both activation of sympathetic vasomotor centers and a release of pituitary hormones. Since anesthesia attenuated the pressor responses and made them biphasic, these results indicate that central cholinergic mechanisms are inhibited during anesthesia and that a sympatho-inhibitory mechanism of cholinergic receptors exists behind the pressor responses, as disclosed during anesthesia.

Anesthesia↗
PubMed1984

The role of prostaglandins in the regulation of blood pressure with special reference to vascular reactivity.

The role of prostaglandins (PGs) in the regulation of blood pressure was analysed from the point of view of vascular reactivity to PGs and also of PG-induced modulation of pressor response. The vasodepressor effect of PGE1 was more sensitive in the patients with essential hypertension than in the normotensive subjects. In the normotensive subjects or in rats, pressor response to norepinephrine was modulated by PGE1, enhanced under treatment with indomethacin, an inhibitor of PG biosynthesis, and suppressed under an infusion of PGE1. These results indicate that pressor response to norepinephrine is modulated by exogenous and endogenous PGs. The PG-induced modulation disappeared after chemical sympathectomy, suggesting that the PG-induced modulation of pressor response is regulated by the sympathetic nervous system. In sympathetic neurotransmission, PGs could play an important role in the regulation of norepinephrine release. Renal content of norepinephrine was reduced under treatment with indomethacin, indicating an enhanced release of norepinephrine and an enhanced turnover of norepinephrine in the kidneys under treatment with indomethacin. These results suggest that a deficient state of PG may enhance the pressor response and norepinephrine release. As there is much evidence indicating that the reduction of PG synthesis in patients and animals with hypertension, vascular reactivity to PGs and PG-induced modulation of pressor response may play significant roles in the regulation of blood pressure and could be causal factors of hypertension.

Adult↗
PubMed1984

Retardation of the development of hypertension in DOCA-salt rats by renal denervation.

To determine the importance of the renal nerves in DOCA-salt hypertension, either renal denervation or a sham-operation was carried out on both DOCA-salt-treated and non-DOCA-treated rats. The systolic blood pressure of the non-DOCA rats remained within normotensive levels, in which the difference in blood pressure levels between the renal denervated and the sham-operated groups was not significant. On the other hand, the blood pressure of the rats treated with DOCA, and having intact renal nerves, began to rise by the end of the first week and rose consistently thereafter, whereas, in the renal denervated DOCA-salt rats, the blood pressure started to rise by the second week and then proceeded to increase gradually. The differences between the sham and the denervated rat groups were significant throughout the four weeks. The mean arterial pressure, directly measured from the caudal artery of conscious rats during the fourth week of this study, was 166 +/- 7 mmHg in the sham-operated and 129 +/- 4 mmHg in the renal-denervated rats (the data having an 1% significant difference). To test the effects of renal denervation on the natriuresis, pentobarbital-anesthetized rats were infused intravenously with physiological saline. The renal denervated rats which had received DOCA excreted more sodium than did the sham-operated rats. When the rats were later anesthetized with urethane to allow intracisternal injections of hypertonic saline, the mean blood pressure in renal denervated rat groups was again lower than that of the sham-denervated rat groups. However, subsequent intracisternal injections of 5% saline produced similar pressor responses as well as tachycardia in both DOCA groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1984

Augmented central cholinergic mechanisms in spontaneously hypertensive rats. Involvement of deranged noradrenergic mechanisms in the brain.

Intracerebroventricular (ICV) injections of carbachol produced biphasic blood pressure responses consisting of initial vasodepression of short duration followed by a sustained pressor phase, which were accompanied by corresponding changes in sympathetic nerve activity in normotensive outbred-Wistar rats (NT) under urethane-anesthesia. In both normotensive Kyoto Wistar rats (WKY) and spontaneously hypertensive rats (SHR), on the other hand, carbachol elicited purely pressor responses, and accompanying sympathetic nerve activity was little affected. The magnitude of the pressor responses was larger in SHR than in WKY or NT rats. Spinal sectioning did not affect the magnitude of the pressor responses. Vasopressor responses to intravenous injections of arginine-vasopressin were not significantly different between WKY and SHR. These results indicate that carbachol injected intracerebroventricularly produces vasopressor effects mainly by releasing pituitary hormones, probably vasopressin, and that augmented pressor responses in SHR may be due to excessive release of vasopressin. When central noradrenergic neurons had been destroyed with ICV injections of 6-hydroxydopamine in both NT and WKY rats, carbachol-induced vasopressor responses were markedly augmented and resulted in responses similar to those of SHR. These findings indicate that central noradrenergic vasodepressive neurons are deficient and that the augmented vasopressor responses to carbachol resulted from deranged central noradrenergic mechanisms in SHR.

Animals↗