Biomedical subjects
Publications and source records attributed to A Goto.
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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)
The inhibition of renin release by angiotensin II (AII) is well documented. However, the interaction of this short loop feedback mechanism of AII with the sympathetic nervous system is still unclear. This study was designed to investigate the possible functional relationship between AII and the beta-adrenergic receptors with respect to renin release in vivo. First, the effect of propranolol on captopril-induced renin release was examined in conscious rats. Secondly, the effect of AII on isoproterenol-induced renin release was determined. Captopril (1 mg/Kg) increased plasma renin activity (PRA) from 1.6 +/- 0.3 ng/ml/hr to 4.5 +/- 0.6 ng/ml/hr (p less than 0.01). In contrast, there was no significant change in PRA in rats which received both captopril and propranolol (before 0.9 +/- 0.2 ng/ml/hr, after 1.3 +/- 0.3 ng/ml/hr). Thus, propranolol attenuated the increase in PRA caused by captopril. Isoproterenol infusion (0.1 micrograms/Kg/min) provoked a significant increase in PRA (before 1.3 +/- 0.4 ng/ml/hr, after 6.6 +/- 1.7 ng/ml/hr, p less than 0.01). AII infusion in combination with isoproterenol also increased PRA from 1.6 +/- 0.4 ng/ml/hr to 5.2 +/- 0.3 ng/ml/hr (p less than 0.01). AII in this dose did not suppress isoproterenol-induced renin release. These results suggest that the beta-adrenergic receptor mediating renin release is functionally located distal to the AII receptor in the short loop mechanism controlling renin release.
Bee venom specific IgG antibodies for honeybee and common wasp were measured in normal control group, slightly bee injury group, heavy bee injury group and honeybee keeper's group. Relation among bee venom specific IgG antibody, bee venom specific IgE antibody and total IgE was analyzed. Normal control level of bee venom specific IgG antibody was measured under 60 U/ml. Bee venom specific IgG antibody in slightly bee injury group was higher than that in heavy bee injury group. Bee venom specific IgE antibody in slightly bee injury group was lower than that in heavy bee injury group. Bee venom specific IgE antibody in bee keeper's group was very high but bee venom specific IgG antibody was also high. From this results it seems that bee venom hypersensitivity can be prevented by high titer of bee venom specific IgG antibody even if bee venom specific IgE antibody is high titer.
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An anteroventral third ventricle (AV3V) lesion in the brain prevents several forms of experimental hypertension. The present experiment was designed to determine whether the AV3V lesion prevents NaCl-induced hypertension in Dahl salt-sensitive (S) rats and whether attenuation of vasopressin release reported in lesioned rats contributes to the protective effect of the AV3V lesion against hypertension. After the AV3V lesion Dahl S rats received daily injections of either vasopressin (pitressin tannate, 500 mU/kg) or vehicle during 10 wk of 8% high-NaCl diet. Sham-lesioned rats served as controls. The blood pressure in sham-lesioned rats receiving vehicle was 189 mmHg after 10 wk of high-NaCl diet. Lesioned rats given vehicle showed a significantly smaller increase in blood pressure than sham-lesioned rats (P less than 0.001), the blood pressure averaging 161 mmHg at 10 wk. Lesioned rats given vasopressin also showed a smaller increase in blood pressure than sham-lesioned rats (P less than 0.05), but the final blood pressure averaged 176 mmHg and was significantly higher than that of lesioned rats given vehicle (P less than 0.025). Vasopressin injections corrected the hypernatremia in lesioned rats. In another experiment the effect of the AV3V lesion on the renal papillary plasma flow (RPPF) in Dahl S rats was studied. Dahl S rats have a lower RPPF than Dahl salt-resistant (R) rats even on a low-NaCl intake. The AV3V lesion increased the RPPF by 14% in S rats (P less than 0.025). These findings suggest that NaCl-induced hypertension in Dahl S rats requires the integrity of the AV3V region for its full expression, and the ability of the AV3V lesion to attenuate the NaCl-induced hypertension in Dahl S rats is partly related to the attenuation of vasopressin release. Moreover, the AV3V lesion partly corrected one of the characteristic features of Dahl S rats, the reduction in RPPF, when compared with Dahl R rats, with both strains on a low-NaCl intake.
Effect of 4-aminopyridine (4-AP) on the isolated superior cervical ganglion of the rat was investigated by means of the sucrose-gap-method. 4-AP initiated discharges of postganglionic neurons and simultaneously increased the amplitude of the compound action potential evoked by supramaximal preganglionic nerve stimulation at concentrations higher than 0.1 mM. Ganglionic discharges induced by 4-AP were characterized by low frequency and high amplitude. These 4-AP-induced discharges were unaffected by removal of the preganglionic nerve trunk. These discharges were suppressed by d-tubocurarine, Ca removal from saline, or preganglionic denervation, whereas discharges of high frequency and low amplitude were observed after 4-AP in Ca-free solution or in denervated preparations. During perfusion with 4-AP, antidromic action potentials were recorded from the preganglionic nerve. When 4-AP was applied to the preganglionic nerve trunk, however, postganglionic responses were unaffected. It is suggested that discharges of postganglionic neurons were induced by 4-AP, possibly as a result of an initiation of action potentials in preganglionic terminal fibres running in the ganglion.
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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...
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1. The rise in blood pressure in Dahl salt-sensitive rats that received intracerebroventricular 6-hydroxydopamine was almost half that of the control rats throughout 20 weeks of high (8%) NaCl feeding. 2. The rise in blood pressure in Dahl salt-sensitive rats with bilateral complete electrolytic lesions of the paraventricular nuclei was almost half that of the control rats during 12 weeks of high (8%) NaCl feeding. 3. The bilateral complete electrolytic lesions of the suprachiasmatic nuclei enhanced the development of NaCl hypertension in Dahl salt-sensitive rats. 4. These results show that NaCl-induced hypertension in Dahl salt-sensitive rats requires the integrity of the central nervous system catecholaminergic neurones and the paraventricular nuclei for its full expression.
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This study deals with the nonsteroid antiinflammatory drug indomethacin, a prostaglandin synthesis inhibitor, in the treatment of carcinogen-induced colonic tumors in rats. CD-Fischer rats were given an intrarectal instillation of methylnitrosourea (2 mg, three times a week for the first to the fifth week) in order to produce colonic tumors. Thereafter, a long-term treatment with an i.p. injection of indomethacin (2.5 mg/kg body weight, three times a week) was started at the 11th week, before the tumors developed. At autopsy, after the 15-week treatment with indomethacin, the colonic tumor incidence was significantly lower in treated rats than in vehicle-treated or untreated control rats. However, the 10-week cessation of treatment following this effective dosage led to a rapid development of tumors. In another experimental group of rats in which tumors were detected endoscopically, when treatment was initiated late, at the 26th week, for 10 weeks, tumor incidence and number were not altered. The data suggested that indomethacin inhibited the development of colonic tumors but did not reject or kill the growing tumors. It is postulated that indomethacin treatment may effectively prevent the development of colonic cancer in patients at high risk of colonic adenomatosis and carcinomatosis.
A total of 73,897 cases of women above 30 years old were screened for their cervical cancer by Pap smear in Niigata prefecture in 1978 and 1979. From them 37 cases of invasive cancer (0.05%) including a case of endometrial adenocarcinoma, stage II, 30 cases of carcinoma in situ (0.04%), and 52 cases of dysplasia (0.07%) were detected. From the correlation between the check up frequency of these patients and the cervical malignancy detected, the following were pointed out: 1) No invasive cancer but carcinoma in situ were detected from those patients who were cytoscreened by successive annual visits. 2) Stage Ia but not more advanced cervical cancer were detected from those patients who were screened at 2 years interval. 3) Stage Ib or farther advanced cervical cancer were detected from those patients who visited at 3 years or more years interval just like from those patients who visited for the first time. To detect cervical cancer in its preinvasive stage, annual Pap smear of adult women over 30 years old should be continued.