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Biomedical subjects

M Yamakado

Publications and source records attributed to M Yamakado.

At least 55 records · Page 3Linked to original sources
PubMed1985

The extrarenal effects of aldosterone on the distribution of extracellular fluid in conscious adrenalectomized-nephrectomized rats.

In order to examine the extrarenal roles of aldosterone in cardiovascular homeostasis, the present study compared blood pressure, extracellular fluid volume (ECFV) and plasma volume (PV) in the three following groups: 10 nephrectomized (NX) rats, 10 nephrectomized-adrenalectomized (NX-AX) rats, and 10 NX-AX and aldosterone-treated (NX-AX-A) rats. Two-hundred and fifty micrograms of aldosterone, mixed with sesame oil, was given subcutaneously in the NX-AX-A rats. Mean arterial pressure (MAP) was recorded through previously implanted carotid catheters. ECFV and PV were measured using 35S-Na2SO4 and 131I-RISA, respectively, 24 h after the operation. These measurements were performed in an unanesthetized and unrestricted condition. MAP gradually increased in the NX group, while a gradual decrease was observed in the other groups. However, MAP was significantly higher in the NX-AX-A group than in the NX-AX group 6 h after the operation and thereafter. Changes in body weight were comparable in the three groups 24 h after the operation. ECFV and PV were both reduced in the NX-AX and the NX-AX-A groups as compared to the NX group (P less than 0.001 NX-AX vs NX, and P less than 0.05 and P less than 0.025 NX-AX-A vs NX, respectively). Although ECFV was comparable in the NX-AX and the NX-AX-A groups, PV was significantly greater in the NX-AX-A group than in the NX-AX group (P less than 0.05). There was a significant positive correlation between MAP and PV in the rats as a whole (r = 0.68, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1985

Diffuse hepatic calcification as a sequela to shock liver.

A 31-yr-old Japanese woman who was on chronic hemodialysis for 3 yr died of intractable congestive heart failure. Three years before death, the patient was in a state of shock for 48 h due to ventricular tachycardia and gastrointestinal bleeding, which was followed by marked elevation of serum transaminase. Four months later, abdominal plain radiography demonstrated diffuse hepatic calcification. At autopsy, microscopic examination of the liver revealed parenchymal necrosis and tiny calcifications in the central to midzonal area of the lobule. Calcification in the degenerative area of the hepatic lobule occurred subsequent to parenchymal ischemia after overt shock that lasted for 2 days. Although a definitive explanation for the calcification was not obtained, it may be related to the disturbances of intracellular Ca2+ homeostasis as a result of ischemic liver injury or it may be related to an elevated calcium-phosphorus product in the uremic state.

Adult↗
PubMed1985

Sites of action of beta-melanocyte stimulating hormone in aldosterone biosynthesis in the rat.

The sites of action of beta-melanocyte stimulating hormone (beta-MSH) on aldosterone biosynthesis were studied using collagenase-dispersed adrenal glomerulosa cells from rats maintained on either normal or sodium-deficient diets for 2 weeks. Isolated cells were treated with a cyanoketone derivative (WIN 19,578) to isolate the early and late steps in aldosterone biosynthesis. WIN 19,578 (1 microM) completely blocked aldosterone production stimulated by sodium depletion, AII, ACTH, and beta-MSH. beta-MSH (1 microM) significantly stimulated pregnenolone production (early step) and the conversion of corticosterone to aldosterone (late step) in aldosterone biosynthesis. The effect of beta-MSH was similar to AII and ACTH. Sodium depletion enhanced the effect of beta-MSH only on the late step in aldosterone biosynthesis. In conclusion, beta-MSH stimulates both the early and late steps of aldosterone biosynthesis. These results suggest that beta-MSH or peptides containing beta-MSH may play a role in the regulation of aldosterone production.

Adrenal Glands↗
PubMed1985

[Postnatal development of barreloid neuropils in the ventrobasal complex of mouse thalamus: a histochemical study for cytochrome oxidase].

Postnatal development of barreloid neuropils was studied in the ventrobasal complex of mouse thalamus. A single barreloid neuropil which topographically represented a corresponding facial vibrissa on the contralateral side was demonstrated as a solid reaction mass with the method for cytochrome oxidase. This architectural unit was called a vibrissa compartment. On postnatal Day 0, the nuclear area of the ventrobasal complex showed higher activity for the enzyme than in regions around, but no barreloids were seen. Barreloid neuropils became detectable on postnatal Day 3 in the dorsomedial subnucleus of the ventrobasal complex and the septal delimitation of barreloids was established on postnatal Day 6. The arrangement of barreloids showed a distinct orderlines similar to that of facial vibrissae on a horizontal section. Barreloid neuropils contained synaptic glomeruli ensheathed with glial processes, in which dendritic processes and their excrescences of nerve cells received large terminal knobs in well-organized manner. On postnatal Day 10, immature glomerular forms were found in barreloid neuropils. The synaptic glomerulus of mature type, however, was not formed till postnatal Day 13. The number of synaptic junctions was examined in barreloid neuropils from postnatal Day 3 to 21. The result that the growth rate of synaptic junctions was the highest in a short period from postnatal Day 10 to 13 suggested rapid maturation of barreloid neuropils in this period. On postnatal Day 21, several types of synaptic contacts became remarkable in matured glomeruli. One of them, a filamentous type with association of clear synaptic vesicles at presynaptic sites was indicated. And non-synaptic junctional complex accompaning tubular structures beneath dense materials at dendritic sites was remarked between terminal knobs and dendritic processes. From results the following conclusions are remarked that at the level of mouse thalamus, septal delimitation of vibrissa compartments appeared on postnatal Day 3 and was established until postnatal Day 6. On the other hand, barreloid neuropils containing glomerular synaptic complexes became a maturing state on postnatal Day 13, that is, about one week later after architectural compartmentalization.

Animals↗
PubMed1984

[An extrarenal role of aldosterone on the regulation of blood pressure].

This study was designed to examine the effects of aldosterone on the distribution of extracellular fluid between the intra- and extra-vascular compartments, and to relate the changes in the fluid distribution to blood pressure in nephrectomized and nephrectomized-adrenalectomized male Wistar rats. Polyethylene catheters were inserted into the right common carotid artery and the right jugular vein, and bilateral nephrectomy with or without adrenalectomy was performed. The animals were divided into three groups: 10 nephrectomized rats (NX), 10 nephrectomized-adrenalectomized rats (NX-AX), and 10 nephrectomized-adrenalectomized and aldosterone treated rats (NX-AX-A). Aldosterone (250 micrograms/rat: Aldocorten, Ciba), mixed with sesame oil, was given subcutaneously in the NX-AX-A. After these procedures, food and water were withheld. Twenty four hours later, blood pressure and body fluid volumes were measured in the unanesthetized unrestricted condition. Mean arterial pressure (MAP) was directly recorded through the carotid catheter using electric manomater. Plasma volume (PV) and extracellular fluid volume (ECFV) were measured according to the dilution principle using 131I-RISA and 35S-Na2SO4, respectively. Interstitial fluid volume (IF) defined as ECFV minus PV and PV/IF ratio was also calculated. In NX, NX-AX and NX-AX-A, the transcapillary escape rate of albumin (TER) was determined after 6 hours. TER was obtained by measuring the disappearance of intravenously injected 131I-RISA for 2 hours after injection. The initial body weight and the changes in body weight were similar among the three groups. MAP was definitely higher in the NX than in the NX-AX and the NX-AX-A. Moreover, it was significantly higher in the NX-AX-A than in the NX-AX (p less than 0.001). Although ECFV and IF were equally and significantly reduced in the NX-AX-A and the NX-AX as compared to the NX, PV was significantly higher in the NX-AX-A than in the NX-AX (p less than 0.01), leading to a significantly lower PV/IF ratio in the latter than in the former (p less than 0.02). When a relationship between MAP and PV was examined in the rats as a whole, a significant positive correlation was found between the two parameters (r = 0.69, p less than 0.001). This relationship still held in the NX-AX and the NX-AX-A in combination (r = 0.69, p less than 0.001). TER was significantly higher in the NX-AX than in the others (p less than 0.001 vs NX, and p less than 0.02 vs NX-AX-A).(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenalectomy↗
PubMed1984

Effect of natrium ionophore on aldosterone production in the rat adrenal gland.

The effect of the natrium ionophore, monensin, on aldosterone production was studied using rat adrenal collagenase-dispersed capsular cells. Monensin inhibited aldosterone production in a dose-dependent fashion (10(-9)-10(-6)M). Although monensin inhibited both ACTH- and angiotensin II (AT-II)-stimulated aldosterone production, its inhibitory effect on ACTH-stimulated aldosterone production was greater than that on AT-II-stimulated aldosterone production. The inhibitory effect of monensin on aldosterone production was not accompanied by significant changes in cAMP production. Furthermore, (Bu)2cAMP-stimulated aldosterone production was inhibited by monensin. These results suggest that the inhibitory effect of monensin on aldosterone production is due to an increase in intracellular sodium ion concentration, and that monensin acts at step(s) distal to the generation of cAMP. The differences in the inhibitory effects of monensin on the steroidogenic action of AT-II and that of ACTH may be related to the presence of different steroidogenic mechanisms, including calcium ion dependency.

Adrenal Glands↗
PubMed1983

Effect of sodium deficiency on beta-melanocyte-stimulating hormone stimulation of aldosterone in isolated rat adrenal cells.

The effect of sodium deficiency on the adrenal sensitivity to beta MSH was studied using collagenase-dispersed rat adrenal cells from rats maintained on a normal sodium or a sodium-deficient diet for 2 weeks. In the cells prepared from adrenals of rats fed a normal sodium diet, angiotensin II (AII) and ACTH caused a dose-dependent increase in aldosterone production by glomerulosa cells at a threshold concentration of 10(-10) M and induced a maximal response at 10(-8) M. beta MSH also stimulated aldosterone production at a threshold of 10(-8) M and a maximum at 10(-6) M. However, in the cells from sodium-depleted rats, the threshold for AII was 10(-11) M and the maximum was 10(-8) M, while the threshold for ACTH and beta MSH was 10(-10) M. The shift to the left of the dose-response curve for beta MSH during sodium depletion was greater than that for AII or ACTH. The aldosterone levels obtained with maximal doses of beta MSH and AII were similar during sodium depletion. Sodium depletion did not affect the corticosterone response of decapsular cells to all three stimulators. In conclusion, sodium deficiency enhances the sensitivity of the adrenal glomerulosa cells to beta MSH, causing significant stimulation of aldosterone production by doses of beta MSH within the physiological range. These data suggest that beta MSH or peptides containing beta MSH may play a role in the regulation of aldosterone secretion during sodium deficiency in the rat.

Adrenal Glands↗
PubMed1983

Effects of chronic administration of captopril on blood pressure and the renin-angiotensin-aldosterone system in normotensive rats.

The chronic effects of oral administration of an angiotensin converting enzyme inhibitor (captopril, 63-80 mg/Kg/day) on blood pressure and the renin-angiotensin-aldosterone system were-studied in normotensive male Wistar rats. Blood pressure (BP), plasma renin activity (PRA), plasma renin concentration (PRC), plasma renin substrate concentration (PRS), plasma aldosterone concentration (PAC) and renal renin content (RRC) were measured after 2, 9, 19, 29 and 58 days of captopril administration. BP was determined in awake rats and blood samples were obtained by decapitation. In addition, BP responses to bolus injections of angiotensin I (AI, 80 ng/Kg), angiotensin II (AII, 80 ng/Kg) and bradykinin (BK, 10 micrograms/Kg) were examined in conscious rats which had received captopril for 20 days. The BP of the rats which had been given captopril for 9 days or longer was significantly lower than that of the control rats. PRA and PRC were markedly increased, and both PRS and PAC were decreased in the captopril-treated rats. RRC, which was reduced after 2 days of captopril administration, was substantially increased thereafter. Although the pressor responses to AII were similar in the captopril treated and the control rats, the responses to AI were reduced to 50% of those to AII in the former. The depressor responses to BK in the captopril-treated rats were 2.3 times as large as those in the control rats. Our results show that long-term use of captopril lowers BP in normotensive rats on a normal sodium intake.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1981

[The effects of the angiotensin converting enzyme inhibitor, captopril, on catecholamine concentrations in rat plasma, heart, brain and kidneys (author's transl)].

Two studies were designed to examine the effect of the angiotensin converting enzyme inhibitor, captopril, on the sympathetic nervous system. In the first study, blood pressure (BP), heart rate (HR), and norepinephrine (NE) concentrations in the heart were measured in rats which had been given the agent orally in tap water (0.5 mg/ml) for 2, 9, 19, 29, and 58 days. BP and HR were measured using a tail-microphone to which a tachometer to record HR was connected in the unanesthetized and unrestricted condition. Heart NE was extracted with perchrolic acid and measured with the THI method on a high pressure liquid chromatography. The same study was also done in the control rats. The BP of the rats which had been given captopril for 9 days or more was significantly lower than in the control rats, while HR was not different between the two groups of rats. The ratio of heart weight/body weight was significantly lower in the captopril rats than in the control rats 58 days after the captopril administration. The ratio was significantly correlated with BP in these captopril and control rats (r = 0.59, p less than 0.01). In contrast to the control rats, the NE concentrations in the heart gradually increased in the captopril rats, thus being significantly higher in the latter than in the former after 29 and 58 days of captopril administration (p less than 0.01 for both observations). In addition, the lower the BP was, the higher the NE concentrations in the heart was in all the rats (r = 0.52, p less than 0.001). In the second study, BP, HR, and NE concentrations in plasma, heart, brain and the left kidney were measured in rats which had been on captopril for 2 and 29 days. Renal renin content (RRC) was also measured in the right kidney. In this study, BP and HR were recorded through a carotid catheter which had been inserted 4 hrs previously under light ether anesthesia. BP was significantly lower and NE concentrations in the heart was higher in the captopril rats than in the control rats after 29 days of captopril administration. There was a significant negative correlation between BP and NE concentrations in the heart in the captopril and the control rats (r = -0.88, p less than 0.001). No difference in HR was found between the 2 groups. NE concentrations in plasma, brain and kidney showed no significant differences between the captopril and the control rats in either of the stages of sacrifice. RRC was markedly reduced in the rats with 2 days of captopril, while it increased in the rats with 29 days of captopril. However, the RRC had no definite relationship with the NE concentrations in plasma or that in the kidney. The results show that chronic administration of captopril reduces the heart weight in normotensive rats. This effect points on the one hand to a decrease in "cardiac after-load" and on the other to changes of humoral factors such as plasma angiotensin II induced by captopril...

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1979

Subdivision of mouse vibrissae on an embryological basis, with descriptions of variations in the number and arrangement of sinus hairs and cortical barrels in BALB/c (nu/+; nude, nu/nu) and hairless (hr/hr) strains.

Development of vibrissae was studied in dd/y mouse embryos by scanning electron microscopy. Arrangement of vibrissae and cortical barrels were also studied by light microscopy in adult dd/y, BALB/c(nu/+), nude (BALB/c, nu/nu) and hairless (hr/hr) mice to find genetic or epigenetic variations. Rudiments of vibrissae first appear on Day 12 of pregnancy as longitudinal ridges on the developing muzzle, and each hair rudiment is represented by a dome on the ridges. The dorsal two rows (A and B; Woolsey and Van der Loos, '70) of mystacial vibrissae are on the lateral nasal prominence, while the ventral three (C, D and E) are on the maxillary prominence. Smaller hairs of mystacial vibrissae appear at the labial part of the maxillary prominenceon Day 13. The rudiments of rhinal hairs also appear at this stage on the part of the muzzle derived from the medial nasal prominence. Thus the so-called mystacial vibrissae should be subdivided into three (or 4, including the rhinal) groups on an embryological basis. They are the lateral nasal, the maxillary and the labial. A supernumerary sinus hair and a corresponding barrel was observed between D and C rows uni-or bilaterally in one third of individuals of BALB/c, nude and hairless mice. It is suggested that supernumerary hairs tend to occur between the groups of hairs as defined above. In nude and hairless mice small barrels representing labial hairs are diminished in number. The number of hair follicles, however, is normal.

Animals↗
PubMed1977

Population and structure of nerve cells in mouse submandibular ganglion.

The anatomy of the mouse submandibular ganglion, and population and fine structure of nerve cells were studied by light and electron microscopy. The submandibular ganglion is a plexus containing up to forty ganglia along the main and the smaller excretory ducts of the submandibular gland. Measurements of the volume of nerve cell bodies display a pattern of distribution with two main peaks, suggesting the presence of large and small types of the intraganglionic neuron. The large neurons mainly have axo-dendritic synapses in which the postsynaptic element is a small spine-like process, while axo-somatic synapses are more common in the small neurons. In some small neurons nuclear chromatin is unusually conspicuous, and accumulations of vesicles of fairly uniform size occur within the cell body. Decentralized ganglia contain almost no synapses showing the absence of definite interneurons.

Animals↗