Search PubMed⌕ Search

Biomedical subjects

S Satoh

Publications and source records attributed to S Satoh.

At least 865 records · Page 48Linked to original sources
PubMed1981

Converting enzyme inhibition and modulation of plasma renin activity with captopril in anesthetized rats.

We examined the effects of an orally active inhibitor of converting enzyme, captopril (D-3-mercapto-2-methylpropanoyl-L-proline), in pentobarbital-anesthetized rats. Intravenous (i.v.) administration of captopril (0.1, 0.3, 1.0, 3.0 mg/kg) resulted in a dose-dependent inhibition of the pressor responses to angiotensin I (1.0 micrograms/kg, i.v.); at 1.0 mg/kg, captopril markedly potentiated the magnitude and duration of vasodepressor responses elicited by bradykinin (0.3 micrograms/kg, i.v.). Captopril effected a marked elevation of plasma renin activity by its blocking action on the angiotensin II-mediated negative feedback of renin release without markedly altering systemic blood pressure and heart rate. Propranolol (1.5 mg/kg, i.v.), at a dose which almost completely inhibited isoproterenol (0.15 micrograms/kg/min, i.a.)-induced renin release, tended to suppress the captopril-induced renin release. However, indomethacin (5.0 mg/kg, i.v.) failed to change the captopril-induced renin release. These findings suggest that captopril specifically inhibits converting enzyme and kininase II, and that captopril-induced renin release is partially associated with the beta-adrenergic system without dedication by prostaglandins.

Acetylcholine↗
PubMed1981

A comparison of the vasoconstrictor effects of angiotensin II and angiotensin III in the canine renal vasculature.

The effects of angiotensin II and angiotensin III on systemic blood pressure and renal blood flow were studied in pentobarbital anesthetized dogs pretreated with phenoxybenzamine. Angiotensin II was more potent than angiotensin III in increasing systemic blood pressure when given intravenously. When angiotensin II and angiotensin III were administered directly into the renal artery, angiotensin II was also more potent than angiotensin III as a renal vasoconstrictor. Indomethacin potentiated the responses to angiotensin II and angiotensin III to the same extent. The results indicate that differential vasoconstrictor effects of the two peptides in renal vasculature contribute to the difference in potency of intravenously administered peptides on systemic blood pressure, and also suggest that vasodilator prostaglandins are involved in the vasoconstrictor properties of the two peptides in the renal vasculature of the dog.

Angiotensin II↗
PubMed1981

Effects of renal nerve stimulation, norepinephrine and angiotensin II on renal blood flow in relation to release of PG-like substances in anesthetized dogs.

The effects of vasoconstrictor stimulation, renal nerve stimulation or infusion of norepinephrine or angiotensin II into the renal artery, on renal blood flow were determined before and after the administration of indomethacin in pentobarbital-anesthetized dogs. When the renal blood flow was allowed to vary, in control responses, an initial rapid reduction was followed by a return to the control level, despite the continued application of vasoconstrictor stimulation. After the intravenous administration of indomethacin, a prostaglandin synthetase inhibitor, the recovery response was markedly diminished. Prostaglandin-like substances in renal venous blood were determined by bioassay of blood extracts, using rat fundus strips. Indomethacin suppressed the increase in the level of these substances during the application of vasoconstrictor stimulators. Our results indicate that renal prostaglandin-like substances are released during vasoconstrictor stimulation; under the present experimental conditions, this release blunts the effect of the stimuli.

Angiotensin II↗
PubMed1980

The effect of graded coronary flow reduction in the left anterior descending and septal arteries on left ventricular function in the canine heart.

WE quantitatively analyzed the effect of graded left anterior descending and septal coronary flow (LAD + septal flow) reduction on left ventricular function with a left ventricular end-diastolic pressure (LVEDP) of 6 mm Hg and 12 mm Hg. We used an isolated, ejecting, canine heart preparation ( n = 8), the coronary flow of which could be controlled independently of the aortic pressure. We kept the other hemodynamic variables - heart rate, left circumflex coronary flow, right coronary flow and aortic input impendance - constant within their normal physiologic range. We considered this reduction in LAD + septal flow to be analogous to that of the most frequent lesion in ischemic heart disease. There was no plateau in the left ventricular work caused by this reduction of the regional coronary flow. Therefore, the plateau commonly reported in previous studies may be partially a result of the compensatory elevation of LVEDP, which is necessary to maintain the left ventricular work.

Animals↗
PubMed1980

Hypotensive effect of captopril in relation to plasma renin activity in anesthetized rats.

the effect of captopril (D-3-mercapto-2-methylpropanoyl-L-proline), a converting enzyme inhibitor, on the systemic blood pressure in pentobarbital anesthetized rats was investigated. Experiments were performed in four groups of rats: untreated, Na-restricted, furosemide treated and bilaterally nephrectomized, respectively. Intravenous injection of 1 mg/kg of captopril caused a significant hypotensive effect in the three groups of rats but not in the nephrectomized group. Individual values for the hypotensive effect produced by captopril and plasma renin activity obtained just before injection of captopril showed a highly significant correlation.

Anesthesia↗
PubMed1980

Effect of captopril, a converting enzyme inhibitor on renal vascular resistance in pentobarbital anesthetized dogs.

The effects of captopril administered intravenously in a dose of 1 mg/kg on systemic blood pressure (SBP), renal blood flow (RBF) and renal vascular resistance (RVR) were examined in pentobarbital anesthetized dogs. Untreated dogs were used in experiments in which the renal artery remained intact and others in which the renal artery was partially occluded (RAO). Captopril significantly decreased SBP, increased RBF and decreased RVR in untreated dogs. RAO induced an increase in arterial plasma renin activity and this increase was accompanied by an increase in RVR in the contralateral kidney and rise in SBP. During RAO, captopril induced qualitatively similar, but greater decreases in SBP and RVR of the contralateral kidney compared with those in the untreated dogs. These results suggest the vasodilator effect of captopril depends on the background level of angiotensin II and the enhanced effect would be expected under conditions such as RAO where circulating angiotensin II contributes to vascular tone.

Anesthesia↗
PubMed1979

Protective effect of PSK, a protein-bound polysaccharide preparation against candidiasis in tumor-bearing mice.

In an experimental Candidiasis of tumor-bearing mice, the administration of PSK resulted in a prolongation of lifespan when mice were treated with PSK before infection or before and after infection. The viable fungal counts in kidneys 3 weeks after infection was found to be less in PSK-treated mice than the control mice without PSK administration. The delayed-type hypersensitivity reaction in infected tumor-bearing mice against Candida dead cells were stimulated to some extent by PSK administration. The fungal proliferation in kidneys of tumor-bearing mice at the early stage of infection was prevented by PSK administration. The experimental results involving chemotaxis and phagocytosis suggest that PSK administration restores or enhances the depressed protection of tumor-bearing mice against Candida infection, mostly due to potentiating the phagocytic activity of macrophages.

Adjuvants, Immunologic↗
PubMed1979

Possible Involvement of the Alternative Respiration System in the Ethylene-stimulated Germination of Cocklebur Seeds.

Respiration of nondormant upper cocklebur (Xanthium pensylvanicum Wallr.) seeds was enhanced by exogenous C(2)H(4), proportionally to the concentration of C(2)H(4) and the duration of presoaking of the seeds. Benzohydroxamic acid (BHM) and salicylhydroxamic acid (SHM), inhibitors of alternative respiration, inhibited both the germination of nondormant lower cocklebur seeds and the respiration of the upper seeds presoaked for periods of 12 to 30 hours. Both the growth and respiration of axial and cotyledonary tissues were also inhibited by BHM. Moreover, BHM inhibited both the C(2)H(4)-induced germination of the upper seeds and their C(2)H(4)-stimulated respiration; the inhibition occurred only with concomitant addition of C(2)H(4) and BHM. The respiration of seeds with a secondary dormancy induced by presoaking for prolonged periods was markedly stimulated by C(2)H(4) but not suppressed by BHM. It was suggested that the alternative respiration system may be involved in the normal germination process of cocklebur seeds, secondary dormancy may result from its inactivation, and C(2)H(4) may exert its germination-promoting action by stimulating the alternative respiration. The effects of BHM and SHM can suggest but not prove the involvement of the alternative respiration in seed germination.

Journal Article↗