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Biomedical subjects

T Saruta

Publications and source records attributed to T Saruta.

At least 559 records · Page 31Linked to original sources
PubMed1981

Effects of intracerebroventricular administration of dopamine and metoclopramide on blood pressure in rats.

The intracerebroventricular (i.c.v.) injection of dopamine (50--200 micrograms/kg) produced a dose-dependent decrease in arterial blood pressure in conscious rats. This depressor effect of dopamine was attenuated by the pretreatment with metoclopramide (16.5 micrograms/kg, i.c.v.), a dopamine receptor antagonist. Metoclopramide in higher doses (50 and 150 micrograms/kg), given i.c.v., produced an increase in blood pressure. The pretreatment with dopamine (50 micrograms/kg, i.c.v.) attenuated the pressor effect of metoclopramide. Furthermore, autonomic ganglion blockade with hexamethonium (25 mg/kg, i.v.) almost completely abolished the effects of dopamine and metoclopramide, indicating that these substances were exerting their effects within the central nervous system. These results suggest that the dopaminergic system in the brain is involved in regulation of systemic blood pressure in conscious rats.

Animals↗
PubMed1980

[Studies on the mechanism of secretion of adrenal steroid hormones from adenomas of primary aldosteronism and Cushing's syndrome (author's transl)].

The mechanism of secretion of adrenal steroid hormones from adenomas of primary aldosteronism and Cushing's syndrome was studied in 10 patients with primary aldosteronism and in 3 patients with Cushing's syndrome in in vivo and in vitro experiments. In all of the 10 patients with primary aldosteronism, ACTH stimulated aldosterone secretion from the adenomas more significantly than did angiotensin II and III. DOC and cortisol which were contained in the adenomas were also stimulated more significantly by ACTH than by angiotensin II and III. Responses of the adenomas of Cushing's syndrome to various stimulations were less than those of primary aldosteronism. Secretion of cortisol and aldosterone from the adenomas of Cushing's syndrome was stimulated by ACTH and angiotensin II to a similar degree. From these studies, it seems that secretion of adrenal steroid hormones from adenomas of primary aldosteronism is more sensitive to extradrenal stimulations than that of Cushing's syndrome, and ACTH is the main factor in the control of the secretion of adrenal steroid hormones from the adenomas.

Adenoma↗
PubMed1980

[Studies on angiotensin II receptors in the adrenal glands and in the aorta (author's transl)].

The angiotensin II receptor in the rabbit, rat and human adrenal gland and that in the rabbit and rat aorta were studied by using [3H]-angiotensin II ([3H]-AII). The adrenal glands and the aorta of each species were centrifuged at 20,000Xg for 30 min, and pellets which contained 95% of binding sites were collected and diluted by a buffer [20 mM Tris-HCl buffer (pH 7.4), 120 mM NaCl, 0.2% BSA, 1 mM EDTA] and used as a membrane fraction. The binding study was done by incubating the membrane fraction and [3H]-AII. After incubation at 25 degrees C for 30 min, the binding of the membrane fraction and [3H]-AII reached the equilibrium state, and free and bound angiotensin II were separated by 0.48 micrometer filters. Protein concentration was determined according to the method of Lowry. The binding sites fulfilled the criteria of the receptor which has organ and structure specificities, high affinity and reversibility. We could thus measure angiotensin II receptor in this study correctly and concisely. The properties of the angiotensin II receptor were analysed by Scatchard plot. The number of rabbit adrenal receptors (12833 +/- 2115 x 10(-15) mol/mg.protein) (M ++/- SD) was greater than that of the rat (1780 +/- 166 x 10(-15) mol/mg.protein) and that of the human (356 +/- 124 x 10(-15) mol/mg.protein). But the dissociation constant of all species was the same. The number of aorta binding sites was less than that of the adrenal in rabbits and rats. But the dissociation constant of rabbits and rats aorta binding sites was quite similar to that of adrenal glands.

Adrenal Glands↗
PubMed1980

Effects of prostaglandins E2, I2 and F2 alpha, arachidonic acid and indomethacin on pressor responses to norepinephrine in conscious rats.

The effects of prostaglandins E2 (PGE2), I2 (PGI2) and F2 alpha (PGF2 alpha), arachidonic acid and indomethacin on pressor responses to norepinephrine were examined in conscious rats. Intravenously infused PGE2, (0.3, 1.25 micrograms/kg/min), PGI2 (50, 100 ng/kg/min), PGF2 alpha (1.8, 5.4 micrograms/kg/min) and arachidonic acid (0.7, 1.4 mg/kg/min) did not change the basal blood pressure. Both PGE2 and PGI2 significantly attenuated pressor responses to norepinephrine, whereas PGF2 alpha significantly potentiated them. Arachidonic acid, a precursor of the prostaglandings (PGs), significantly attenuated pressor responses to norepinephrine. Since the attenuating effect of arachidonic acid was completely abolished by the pretreatment with indomethacin (5 mg/kg), arachidonic acid is thought to exert an effect through its conversion to PGs. On the contrary, intravenously injected indomethacin (0.2--5.0 mg/kg) facilitated pressor responses to norepinephrine in a dose-related manner without any direct effect on the basal blood pressure. These results suggest that endogenous PGs may participate in the regulation of blood pressure by modulating pressor responses to norepinephrine in conscious rats.

Animals↗
PubMed1980

The effects of prostaglandins E2 and I2, and arachidonic acid on vascular reactivity to norepinephrine in isolated rat mesenteric artery, hind limb and splenic artery.

The effects of prostaglandins E2 (PGE2) and I2 (PGI2), arachidonic acid, and indomethacin on the vascular reactivity to norepinephrine were tested in three different isolated rat vascular beds (mesenteric artery, hind limb and splenic artery) perfused with the Krebs bicarbonate solution. In these vascular beds PGE2 (0.25--16 ng/ml), PGI2 (0.1--100 ng/ml), arachidonic acid (0.1--10 micrograms/ml) or indomethacin (5--25 micrograms/ml) in the perfusate did not change the basal pressure. In the splenic artery, both PGE2 and PGI2 attenuated the vascular response to norepinephrine in a dose-related manner. In the mesenteric vascular bed and the hind limb, however, PGE2 potentiated the vascular response to norepinephrine, while PGI2 attenuated this response. Acahidonic acid, a prostaglandin precursor, potentiated the vasoconstrictor response to norepinephrine in the mesenteric artery and the hind limb, whereas in the splenic artery, attenuation of the response to norepinephrine occurred. In these three vascular beds, indomethacin, a prostaglandin synthetase inhibitor, attenutated the vascular response to norepinephrine. In the mesenteric artery and the hind limb, PGE2 and not PGI2 reversed the effect of indomethacin, while in the splenic artery, neither PGE2 nor PGI2 reversed the inhibitory effect of indomethacin. These results suggest that, at least in the rat mesenteric artery and the hind limb where the modulating effect of arachidonic acid is similar to that of PGE2, PGE2 and not PGI2 is a primary endogenous prostaglandin in determining the vascular reactivity to norepinephrine.

Animals↗
PubMed1980

A comparison of multiple forms of renin in rat renal perfusate with those in renal extract.

1. Physicochemical properties of renin secreted by isolated perfused rat kidney were examined and the results compared with those obtained for the renin in renal extract. 2. In renal extract, two high-molecular-weight renins (molecular weight 65 000 and 55 000) and one low-molecular-weight renin (molecular weight 39 000) were found. Their relative proportion varied depending on extraction conditions. By acidification, high-molecular-weight renins were converted into low-molecular-weight renin without marked changes in activity. 3. In renal perfusate only low-molecular-weight renin was found after renin stimulation by isoprenaline or anoxia. Inactive renin was not found. 4. Renin in renal extract and perfusate samples were both found to consist of at least four isoenzymes having different isoelectric points (pI). The pI patterns were identical in renal extract and perfusate samples: pI 5.7 (60-70%), 5.5 (15-25%), 5.3 (5-10%) and 5.0-5.2 (2-5%). 5. These results indicate that the native renin secreted by rat kidney consists entirely of the low-molecular-weight and active form comprising multiple isoenzymes with a stable pI pattern.

Animals↗
PubMed1980

Renin and aldosterone in hypothyroidism: relation to excretion of sodium and potassium.

Changes in plasma renin activity (PRA) and plasma aldosterone (PA) were studied together with the urinary excretion of sodium and potassium in patients with hypothyroidism. The basal levels of PRA and PA were significantly less than those in normal subjects. However, there was no significant relationship between PRA and PA. The response of PRA after administration of 40 mg of frusemide in patients with hypothyroidism was significantly less than that in normal subjects, although the excretion of sodium was slightly higher than that in normal subjects. On the other hand, the excretion of potassium in patients with hypothyroidism was significantly lower than that in normal subjects. The responses of PA to various stimulations, such as ACTH, angiotensin II, potassium and frusemide, were equally suppressed. These results suggest that PRA and PA may be suppressed independently in hypothyroidism ,probably due to dysfunction of juxtaglomerular cells and glomerulosa cells, respectively, and the possibility that suppression of PRA and PA in patients with hypothyroidism is related to exaggerated sodium excretion and a decrease in potassium excretion cannot be ruled out.

Adult↗
PubMed1980

Control of aldosterone in 17 alpha-hydroxylase deficiency.

The control mechanism of aldosterone in 3 patients with 17 alpha-hydroxylase deficiency was compared to that in a patient with a deoxycorticosterone-producing tumor. The basal levels of plasma renin activity (PRA) and plasma aldosterone (PAC) were decreased in 2 of the 3 patients with 17 alpha-hydroxylase deficiency and in the patient with a tumor. However, in the third patient with accelerated hypertension, those levels were normal. In the 3 patients with low PRA and PAC, PAC was stimulated by various procedures, although the responses were lower than those in control subjects. In the patient with accelerated hypertension, the responses were similar to those of the control subjects. After 6 months' treatment with dexamethasone, the low levels of PRA and PAC gradually returned to the lower limit of normal in 2 of the patients with 17 alpha-hydroxylase deficiency. These results suggest that the suppression of PAC in patients with 17 alpha-hydroxylase deficiency is probably due to a suppression of the renin-angiotensin system.

Adolescent↗
PubMed1980

Vascular action of high dose estrogen in rats.

Effects of estradiol hemisuccinate and diethylstilbestrol diphosphate on the cardiovascular system in male rats were examined in vivo and in vitro. In conscious rats, intravenously administered estradiol or diethylstilbestrol inhibited vascular responses to norepinephrine in a dose-dependent manner. Diethylstilbestrol in high doses significantly lowered the blood pressure of conscious rats. In the isolated mesenteric arteries perfused with Krebs bicarbonate solution, estradiol or diethylstilbestrol in the perfusate similarly inhibited vascular reactivity to norepinephrine in a dose-dependent manner. As in the in vivo experiments, a decrease in the basal pressure of the mesenteric vascular bed was observed when diethylstilbestrol was added to the perfusate at high concentrations. The results of these in vivo and in vitro studies strongly suggest that estradiol and diethylstilbestrol act directly on the vascular beds and attenuate vascular response to norepinephrine. It is also suggested that diethylstilbestrol by itself causes vasodilatation and a reduction in blood pressure when present at high concentrations.

Animals↗
PubMed1980

The effects of intracerebroventricular administration of tonin on water drinking and blood pressure in rats.

Intraventricular administration of tonin, an enzyme which forms angiotensin II directly from a natural protein substrate (angiotensinogen), stimulated water drinking and increased systemic blood pressure in rats. These responses were abolished by the simultaneous administration of an angiotensin II analogue, but unaffected by an angiotensin I- converting enzyme inhibitor. We confirmed, in vitro, that angiotensin II was generated when the brain homogenate was incubated with tonin in the presence of DFP and EDTA. These results indicate that the central effects of tonin on water drinking and systemic blood pressure are mediated via the direct formation of angiotensin II in the brain, and suggest the possibility that the tonin-angiotensin II system in the central nervous system might be important in controlling water balance and blood pressure.

Animals↗
PubMed1980

Mechanism of renin inhibition by beta adrenergic blocking agents. Effects of dl-, d-, l-propranolol and pindolol on renin release.

In order to reveal the mechanism of renin inhibition by beta adrenergic blocking agents, the effects of dl-, d-, l-propranolol and pindolol on renin release were studied. This was done by injecting them intraperitoneally or by using an in vitro system of rat kidney slices. In the in vivo study, dl-, d-, and l-propranolol inhibited plasma renin activity and renal renin content significantly in normal rats. Furthermore, in the in vitro study, the basal levels of renin in the media and that in the kidney were significantly inhibited by these agents. Pindolol also inhibited renin release, but its effects were significantly less than those of other agents. The finding that d-propranolol which has little beta adrenergic blocking action inhibited renin release, and that the effects of pindolol which displays strong beta adrenergic blocking action but little membrane stabilizing action, were less than those of other agents, may suggest that the inhibitory effects of beta adrenergic blocking agents on renin release are dependent mainly on the membrane stabilizing action rather than the beta adrenergic blocking action.

Adrenergic beta-Antagonists↗
PubMed1980

Effects of converting enzyme inhibitor (SQ 20881) on changes in blood pressure and plasma aldosterone induced by angiotensin I or acute hemorrhage in rabbits.

The effects of angiotensin converting enzyme inhibitor (CEI) upon blood pressure and plasma aldosterone (PA) were studied in rabbits with a simultaneous infusion of angiotensin I (ANG I) or with hemorrhagic hypotension. Pretreatment with CEI (SQ 20881), 1.0 mg/Kg, inhibited the effects of infused ANG I, 30 ng/Kg/min, upon PA and blood pressure at 30 min of the infusion, but the inhibition on PA was not significant at 60 min of the infusion. The same dose of CEI was ineffective in blocking the effect of 100 ng/Kg/min of ANG I on PA and blood pressure even at 30 min of the infusion. In rabbits with hemorrhagic hypotension, injection of CEI resulted in the decrement in blood pressure, whereas no decrement in blood pressure was observed in normal control rabbits. This study suggests that CEI exerts it's effect in part by inhibiting conversion of ANG I to angiotensin II (ANG II), but this can't exclude other mechanisms.

Aldosterone↗