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M Kumada

Publications and source records attributed to M Kumada.

At least 73 records · Page 4Linked to original sources
PubMed1991

Endothelin-sensitive areas in the ventral surface of the rat medulla.

In urethane-anesthetized rats, subregions of the ventral surface of the medulla (VSM) in which endothelin (ET) caused cardiorespiratory effects were mapped by topically applying 1 pmol of ET-1. Two distinct subregions, termed the rostral and caudal ET-sensitive areas, were identified. The rostral area was also sensitive to L-glutamate and glycine. It extended between the caudal end of the trapezoid body and the rootlet of the XIIth nerve partly overlying the pyramidal tract. In this position ET-1 caused the type I response consisting of an initial increase (excitatory component) in arterial pressure (AP), renal sympathetic nerve activity (RSNA), heart rate (HR), phrenic nerve activity (PNA) and the number of bursts of PNA (burst rate) followed by a sustained decrease (inhibitory component) in them. The caudal ET-sensitive area was located near the rootlet of the XIIth nerve. In this position ET-1 caused the type II response consisting of a decrease in PNA and an increase in burst rate. Part of this area responded to nicotine but not to glutamate or glycine. ET-3 (10 pmol) applied to the two ET-sensitive areas produced responses similar to those elicited by ET-1. The dose-response relationship was investigated by delivering ETs to the rostral area. The excitatory component of most of the variables was elicited at a dose of 1 fmol of ET-1 or 1 pmol of ET-3, whereas the inhibitory component was produced at 10 fmol of ET-1 or 10 pmol of ET-3. These results suggest that subregions of the rat's VSM may participate in the central cardiorespiratory control by ET.

Administration, Topical↗
PubMed1991

Cardiorespiratory effects of topical application of endothelin-1 to the ventral surface of the rat medulla.

In urethane-anesthetized and vagotomized rats, we examined the cardiorespiratory effects of a topical application of endothelin-1 (ET-1) to the ventral surface of the medulla (VSM) and surveyed subregions of the VSM influenced by these effects. ET-1 (0.1 fmol) delivered to the S area of the VSM via a needle (i.d. of approximately 100 microns) gently pressed on the VSM had no effect on mean arterial pressure (MAP), heart rate (HR), renal sympathetic nerve activity (RSNA), phrenic nerve activity (PNA), or the burst rate of PNA. However, a dose of 1 fmol of ET-1 induced transient but significant increases in MAP, HR, RSNA, and burst rate while at a dose of 10 fmol or more, PNA also increased and simultaneously longer-lasting decreases in MAP, RSNA, and PNA followed the initial increase. The subregion of the VSM in which ET-1 most prominently elicited these effects was the S and caudal part of the M area, where topical application of 50 nmol of L-glutamate caused cardiorespiratory changes. Additionally, there was a restricted region within the caudal VSM in which ET-1 caused a decrease in PNA with an increase in burst rate. These results support our hypothesis that the VSM is crucially involved in the cardiorespiratory changes induced by centrally administered ET-1.

Administration, Topical↗
PubMed1990

Activity of barosensitive neurons in the caudal ventrolateral medulla that send axonal projections to the rostral ventrolateral medulla in rabbits.

In urethane-anesthetized rabbits, we successfully recorded unit activity of four neurons in the caudal ventrolateral medulla (CVLM) that were excited by orthodromic stimulation of the aortic nerve and by antidromic stimulation of the rostral ventrolateral medulla (RVLM). The sum of mean onset latency of excitation to stimulation of the aortic nerve (37.5 ms) and mean conduction time of antidromic spikes (10.5 ms) was close to the mean onset latency of inhibition of reticulospinal neurons in the RVLM to stimulation of the aortic nerve (47.1 ms) as previously reported by us. Three of 4 neurons received excitatory input from carotid sinus baroreceptors as well. Our results provide strong evidence for the hypothesis that neurons in the CVLM subserve the arterial baroreceptor-sympathetic vasomotor reflex.

Animals↗
PubMed1990

Stimulation of calcium mobilization but not proliferation by bombesin and tachykinin neuropeptides in human small cell lung cancer cells.

The tachykinin family of neuropeptides, including substance P and neurokinins A and B, induce a transient increase in intracellular free calcium concentration in human small cell lung carcinoma (SCLC) cells, as measured with a calcium indicator fura-2. The effects are dose dependent and even greater than that of bombesin at equimolar concentrations in these cells. The tachykinins, like bombesin, induce calcium mobilization mainly from intracellular store(s). None of the peptides, however, shows a stimulatory effect on DNA synthesis. In addition, exogenously applied bombesin does not stimulate DNA synthesis at any concentration tested. We also examined the effects of a recently reported bombesin antagonist [D-Arg1, D-Phe5, D-Trp7,9, Leu11]substance P in SCLC cells, and compared them to those in Swiss 3T3 fibroblasts in which the mitogenic effect of bombesin is well characterized. The antagonist at 10(-5) M completely abolishes the Ca2+-mobilizing effect of 10(-7) M bombesin in SCLC cells, and that of 10(-9) M but not 10(-7) M bombesin in Swiss 3T3 cells. The antagonist at this concentration effectively inhibits the mitogenic action of bombesin (10(-9) M) in Swiss 3T3 cells; however, much higher doses (approximately 10(-4) M) are needed to inhibit DNA synthesis in SCLC cells. Moreover, the antagonist inhibits DNA synthesis in bombesin/gastrin-releasing peptide-nonproducing cells with a similar dose dependency as in producing cells. These results indicate that bombesin/gastrin-releasing peptide and other calcium mobilizing peptides do not always act as a growth factor in SCLC cells, and that the bombesin antagonist could inhibit growth of SCLC cells through a mechanism other than bombesin antagonism.

Bombesin↗
PubMed1990

Modulatory effects of endothelin-1 on central cardiovascular control in rats.

In urethane-anesthetized and immobilized rats, modulatory effects of endothelin-1 (ET-1) on central cardiovascular control were examined. An injection of 0.1 pmol of ET-1 into the cisterna magna caused immediate increases in arterial pressure (AP), renal sympathetic nerve activity (RSNA), and heart rate (HR) that lasted for 5-45 min. At doses of 1 and 10 pmol, intracisternal ET-1 elicited initial increases (phase I) followed by decreases in these variables below the pre-injection level (phase II). At the dose of 1 or 10 pmol, the arterial baroreceptor reflex was suppressed during the latter part of phase I and during phase II. The three variables subsequently returned to, or often exceeded, pre-injection levels in 30 to 60 min and reflex activity recovered (phase III). However, AP often remained below control throughout the 2-h observation period. Essentially identical responses to intracisternal ET-1 were observed in unanesthetized precollicular decerebrated or urethane-anesthetized rats. Application of a piece of filter paper soaked with 1 pmol of ET-1 to the ventral surface of the medulla (VSM) caused the pattern of changes similar to the following intracisternal injection. A microinjection of 4 pmol of ET-1 into the nucleus tractus solitarius (NTS) caused a moderate increase in RSNA with a minute fall in AP. Intrathecal administration of ET-1 resulted in moderate changes in AP and RSNA at the dose as high as 100 pmol. We conclude that intracisternally administered ET-1 modulates tonic and reflex control of AP and sympathetic vasomotor activity and that the VSM appears to be involved critically in this modulation.

Animals↗
PubMed1990

Modulatory effects of rat endothelin on central cardiovascular control in rats.

To characterize the modulatory action of rat endothelin (endothelin-3 or ET-3) on the cardiovascular control by the central nervous system (CNS), ET-3 was injected into the cisterna magna of urethane-anesthetized and immobilized rats. An injection of 100 pmol of ET-3 caused immediate rises in arterial pressure (AP), renal nerve activity (RNA), and heart rate (HR). These variables subsequently decreased and, in 5-20 min, fell below the pre-injection level. Simultaneously, the arterial baroreceptor reflex was almost totally suppressed. Although RNA and HR subsequently returned to, or often exceeded, pre-injection levels in 20 to 60 min and reflex activity recovered, AP sometimes remained below control for at least 2 h. A similar pattern of changes was elicited in unanesthetized precollicular decerebrated rats. The responses to ET-3 were abolished by hexamethonium chloride, but were not conspicuously altered by arginine vasopressin antagonist or angiotensin II antagonist. The CNS sites responsible for ET-induced changes were subsequently searched. Topical application of ET-3 to the ventral surface of the medulla (VSM) caused the pattern of changes in AP, RNA, and HR similar to that following intracisternal injection. Microinjection of ET-3 into the nucl. tractus solitarius (NTS) increased AP and RNA, whereas intrathecal administration of it decreased them. We conclude that intracisternally administered ET-3 centrally modulates both tonic and reflex control of AP by the sympathetic nervous system and that the VSM appears to be primarily responsible for the modulation, although NTS and spinal cord may also be involved in it.

Angiotensin II↗
PubMed1990

[An aged case of orthostatic hypotension possibly due to parasympathetic neurodysfunction].

94-year-old male patient, with orthostatic hypotension, possibly due to impairment of vasoconstriction and parasympathetic nervous system dysfunction was reported. This patient experienced faintness and lower muscle weakness on standing. The blood pressure was 180/90 mmHg in a supine position, while it significantly decreased to 100/58 mmHg in an upright position. There was no evidence indicating the presence of organic brain diseases, cardiovascular diseases, and endocrine diseases, plasma catecholamine, renin, aldosterone, and vasopressin levels at rest were within normal range. Thus, the cause of orthostatic hypotension of this patient was unknown. His systolic blood pressure decreased by 70 mmHg, and his diastolic blood pressure also decreased by 25 mmHg in response to a 70 degrees head-up tilting test (170/71-100/46 mmHg). Plasma vasopressin level significantly increased in response to this test (0.62-67.2 pg/ml). Plasma catecholamine levels also increased (Adr 0.01-0.10 ng/ml, Ndr 0.05-0.22 ng/ml). Other autonomic nervous system examinations revealed normal responses to mental arithmetic test, hyperventilation test, cold pressure test, and adrenalin test. However, the results of the carotid occlusion test, acetylcholine test, atropine test, phenylephrine test were considered to be abnormal. From these findings, we concluded that the functions of sympathetic nervous system were almost intact, while the parasympathetic functions were impared in this case. The orthostatic hypotension of the patient as effectively treated with fludrocortisone. This report suggests that impairment of vasoconstriction and parasympathetic neurodysfunction might be involved in the development of orthostatic hypotension in the elderly.

Acetylcholine↗
PubMed1990

Prevalence of Cryptosporidium infection among domestic cats in the Tokyo Metropolitan District, Japan.

From February, 1988 to February, 1989, an epidemiological survey for feline cryptosporidiosis was carried out on domestic cats that had been committed to the Tokyo Metropolitan Animal Protection Center by owners residing in the Tokyo Metropolitan District. Of a total of 608 cats, 23 (3.8%) were found to have Cryptosporidium oocysts. The percentage of cats positive for the infection ranged from 0 to 13.6% by month. The infection was found to be more common in "baby" and "young" cats than in "middle" and "old" ones. No significant difference in incidence was shown between the sexes. In each positive cat, no apparent clinical symptom such as diarrhea was found, and the size of the oocysts measured from 4.3 to 4.7 microns in diameter (small type).

Age Factors↗
PubMed1988

Physiological characterization of the renal-sympathetic reflex in rabbits.

In urethane-anesthetized and vagotomized rabbits, electrical stimulation of the afferent renal nerve (RN) elicited reflex changes in renal nerve activity (RNA) and arterial pressure (AP). The responses were attributable mostly to excitation of nonmyelinated afferent fibers, although, in about 30% of the animals, they were contributed slightly by myelinated afferents. In about 70% of rabbits, the peristimulus time histogram (PTH) of RNA following stimulation of the RN consisted of a long-lasting inhibitory (I) component occasionally accompanied, during its recovery phase, by a transient excitatory (E) component. In these animals, tetanic stimulation of the RN resulted in a depressor response, either alone or, if an E component was present in the PTH, followed by a slight pressor response. In the remaining rabbits, the PTH was composed exclusively of an E component and tetanic stimulation caused a pressor response. Stimulation of the RN evoked reflex changes in cardiac sympathetic discharges comparable to that of RNA, whereas the change in cervical sympathetic discharges was much smaller. The sympathetic response remained intact after a total transection of the rostral medulla near the ponto-medullary junction; the I component was even augmented. However, it usually disappeared following a transection at the high cervical cord. Bilateral lesions of the nucl. tractus solitarius (NTS) near the obex failed to appreciably affect the response. Among chemical and mechanical stimuli examined, nociceptive stimulation of the kidney elicited a sympathetic response comparable to that following nerve stimulation. In conclusion, the renal-sympathetic reflex in rabbits (1) originates predominantly from nonmyelinated afferent renal fibers activated effectively by nociceptive stimulation applied to the kidney; (2) depends critically on medullary structures other than the NTS; and (3) evokes changes of the same temporal pattern but of nonuniform magnitude in sympathetic discharges to different organs.

Animals↗
PubMed1988

Participation of ventrolateral medullary neurons in the renal-sympathetic reflex in rabbits.

In an effort to locate medullary structures that mediate the renal-sympathetic reflex, the effect, on the excitatory (E) and inhibitory (I) components of that reflex, of certain drugs applied to the ventral surface of the medulla was investigated in urethane-anesthetized and vagotomized rabbits. Application of bicuculline, a GABA receptor antagonist, selectively abolished the I component of the renal-sympathetic reflex as well as the sympathoinhibition elicited by stimulation of the aortic nerve. The E component, on the other hand, was specifically eliminated by kynurenic acid, a glutamate receptor antagonist. Strychnine or atropine sulfate did not affect either reflex appreciably. Subsequently, within the region of the ventrolateral medulla (VLM) subjacent to the site of drug applications, we searched for neurons which responded to stimulation of the renal nerve and/or the aortic nerve. Of 68 responsive VLM neurons found, 50 (73.5%) responded to stimulation of both nerves. Of the 50 neurons, 40 were tested for their antidromic activation to stimulation of the spinal cord. Twenty-four neurons (60%) were antidromically activated. Responses of these reticulospinal neurons to stimulation of the renal nerve preceded that of renal nerve activity (RNA) by about 100 ms. All the antidromically activated, VLM neurons which responded to stimulation of the renal nerve also responded to stimulation of the aortic nerve. In conclusion, the renal-sympathetic reflex appears to be mediated by the same pool of bulbospinal neurons in the ventrolateral medulla that mediates the arterial baroreceptor reflex, and the E and I components of that reflex can be selectively abolished by pharmacological intervention of the subjacent ventral surface of the medulla.

Animals↗
PubMed1988

Barosensory neurons in the rostral ventrolateral medulla mediate the renal-sympathetic reflex in rabbits.

In urethane-anesthetized and vagotomized rabbits, activation of C-fibers of renal afferents resulted in a reflex change in multifiber renal nerve activity (RNA) which consisted of inhibitory (I) and excitatory (E) components, either alone or in combination. The I and E components were individually and reversibly blocked by bilateral application of bicuculline and kynurenic acid, respectively, to the ventral surface of medulla. Bicuculline further eliminated the sympathoinhibiton produced by stimulation of the aortic nerve. Within the subjacent rostral ventrolateral medulla (RVLM), we recorded 23 spontaneously active single units that responded to electrical stimulation of renal afferents and were antidromically activated by stimulation of the dorsolateral funiculus at the C2 level. Usually, the neuronal response preceded that of the RNA by about 100 ms. These bulbospinal RVLM neurons were barosensory, since they responded to stimulation of the aortic nerve. We conclude that barosensory neurons in the RVLM mediate the renal-sympathetic reflex in rabbits.

Administration, Topical↗
PubMed1988

A simple staining method for cryptosporidian oocysts and sporozoites.

A useful staining method for detection of cryptosporidian oocysts and sporozoites was developed and described. The modified Kohn's one-step staining technique with an additional modification, i.e., longer staining time and higher staining temperature than those originally described, was tested on fecal smears from cats infected with Cryptosporidium sp. By this improved staining procedure, the oocyst appeared as a slightly oval body containing four internal sporozoites colored blue to blue-gray. The oocyst wall was stained dark green to black. The morphological feature of the oocyst was recognized much more clearly by this staining technique than by such currently used techniques as acid-fast and Giemsa staining. This staining procedure proved to be simple and less costly and to secure a good preservation.

Animals↗
PubMed1987

Confluence of barosensory and nonbarosensory inputs at neurons in the ventrolateral medulla in rabbits.

In urethane-anesthetized rabbits, 209 spontaneously active neurons that responded to stimulation of aortic nerve A fibers were found within the ventrolateral medulla (VLM). The neurons, termed barosensory VLM neurons, were inhibited, except for three instances, by stimulation of A fibers. Forty-seven percent of barosensory VLM neurons tested (74 of 159) were activated antidromically by electrical stimulation of the dorsolateral funiculus at the C2 level. Activity of barosensory VLM neurons was enhanced by stimulation of carotid body chemoreceptors or the posterior hypothalamic area, whereas it was diminished by increases in arterial pressure elicited by injection of phenylephrine. Barosensory VLM neurons responded variously to stimulation, with two to three pulses at 40 or 100 Hz, of spinal afferents of cutaneous and muscle origins and the spinal trigeminal complex. Although stimulation of one group of somatosensory fibers could evoke different patterns of neuronal responses consisting of excitatory and inhibitory components, the following responses were most often encountered. Group II cutaneous afferents caused an inhibition. Recruitment of group III afferents brought about a brief excitatory component preceding it. Activation of group IV cutaneous fibers added a long latency excitatory component. Excitation of groups III and IV muscle afferents most often resulted in an inhibition, whereas stimulation of the spinal trigeminal complex elicited various combinations of excitatory and inhibitory components. These results are consistent with the view that neurons in the ventrolateral medulla receive barosensory and nonbarosensory inputs from various peripheral and central sources and participate in the control of sympathetic vasomotor activity and arterial pressure.

Afferent Pathways↗
PubMed1987

Recovery from immunesuppression in mice infected with Schistosoma japonicum by treatment of praziquantel.

To learn the possible alteration of immune response, hemolytic plaque-forming cells (PFC) produced in the spleen of Schistosoma japonicum infected mice treated with Praziquantel and untreated group were counted. There was no significant difference in the immunesuppression percentage between the treated and untreated groups 1 and 3 weeks after treatment. In 5 weeks after treatment, however, the immunesuppression percentage in the treated mice was markedly reduced in comparison with that of the untreated group. Recovery from immunesuppression appears to be associated with elimination or impairment of adult worms.

Animals↗
PubMed1986

A1 noradrenergic neurons tonically inhibit sympathoexcitatory neurons of C1 area in rat brainstem.

In rats anesthetized with urethane and paralyzed, bilateral microinjections of kainic acid (KA) into the region of caudal ventrolateral medulla (CVL) containing noradrenergic neurons of the A1 group (A1 area) elicited a decrease followed by an increase in arterial pressure (AP), heart rate (HR) and sympathetic renal nerve activity (RNA). The sympathoinhibitory and sympathoexcitatory effects of KA were prevented by bilateral microinjection of tetrodotoxin into an area of the rostral ventrolateral medulla (RVL) containing C1 adrenergic neurons (the C1 area). In contrast, the autonomic responses were not altered by interruption of the two other principal projections of A1 area neurons, namely to the hypothalamus or to the nucleus tractus solitarii. Bilateral microinjections of tyramine, clonidine, alpha-methylnoradrenaline or histamine into the C1 area elicited a dose-dependent, anatomically specific and reversible decrease in AP, HR and RNA. The effect of tyramine was blocked by previous microinjection of reserpine, 6-hydroxydopamine (6-OHDA), or phentolamine into the C1 area. Pretreatment with phentolamine unveiled a hypertensive effect of alpha-methylnoradrenaline. All effects of alpha-methylnoradrenaline were blocked by pretreatment of the C1 area with phentolamine plus DL-propranolol, whereas those elicited by histamine prevailed. Pretreatment of the C1 area with 6-OHDA abolished all changes in AP and HR elicited by microinjections of KA into the A1 area. We conclude that (1) neurons of the CVL tonically inhibit sympathetic activity, (2) this effect is mediated by an action upon vasomotor neurons of the C1 area of RVL, (3) the inhibition is mediated by noradrenergic projections from A1 neurons into the C1 area, and (4) this tonic sympathoinhibitory effect is independent of the baroreceptor reflex.

Adrenergic Fibers↗
PubMed1986

Absence of sustained hypertension in sinoaortic-denervated rabbits.

In 21 conscious unrestrained rabbits, arterial pressure was continuously recorded up to 11 wk by an indwelling catheter placed in the thoracic aorta. The average and standard deviation of the 24-h mean arterial pressure (MAP) were calculated and compared before and after sinoaortic denervation, sham operation, or cervical sympathectomy. At the time of sinoaortic denervation, the cervical sympathetic nerve was always disrupted bilaterally to remove possible arterial barosensory afferents contained in it. Subsequent to sinoaortic denervation performed on 12 rabbits, the average 24-h MAP was initially elevated but invariably returned to the predenervation level in 5-36 days (average 14 days). Meanwhile, the standard deviation remained elevated in all but one animal. In five sham-operated or four cervical-sympathectomized animals, neither the average 24-h MAP nor the standard deviation was significantly altered from that of controls. Our results are consistent with the view that the arterial baroreceptor reflex by itself does not play a critical role in determining the long-term level of arterial pressure.

Animals↗