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Biomedical subjects

S Saeki

Publications and source records attributed to S Saeki.

At least 181 records · Page 10Linked to original sources
PubMed1983

Decreased serum 19-nor-deoxycorticosterone (21-hydroxy-19-nor-4-pregnene-3, 20-dione) level in adrenal regeneration hypertensive rats.

An enzyme immunoassay of 19-nor-deoxycorticosterone in rat serum was established. The normal value of 19-nor-DOC in rat serum obtained from 9:00 am to 10:00 am was 148 +/- 30 ng/dl (mean +/- SE,n = 10). Serum levels of this steroid decreased in rats with adrenal regeneration hypertension during the course of the experiment up to 8 weeks, while systolic blood pressure rose progressively. We concluded that this mineralocorticoid is not involved at least as a circulating hormone in the pathogenesis of adrenal regeneration hypertension in rats.

Adrenal Glands↗
PubMed1983

alpha-Adrenergic blocking action of 1-O-hexadecyl-2-O-acetyl-sn-glycero-3-phosphocholine in rats.

The effect of 1-O-hexadecyl-2-O-acetyl-sn-glycero-3-phosphocholine (HAGPC), a major component of antihypertensive polar renomedullary lipid, on the pressor responses to norepinephrine and angiotensin II was investigated in normal Wistar rats. The pressor activity of norepinephrine (1 microgram/kg of body weight (BW)) and angiotensin II (40 ng/kg BW) were markedly suppressed when these substances were injected immediately after intravenous administration of 80 nmol/kg BW of HAGPC. When HAGPC was infused continuously at a rate of 20 nmol/kg BW/min, pressor responses to bolus injection of graded doses (0.5 to 10 micrograms/kg BW) of norepinephrine were significantly lowered, but pressor responses to 10 to 200 ng/kg BW of angiotensin II were not affected. These observations suggest that HAGPC has alpha-adrenergic blocking activity and does not influence angiotensin II receptors.

Adrenergic alpha-Antagonists↗
PubMed1982

Effect of prostacyclin infusion on active and inactive renin release in the isolated perfused kidney.

The effect of prostacyclin infusion into the renal artery of the isolated perfused hog kidney on the release of active and inactive renin was investigated. Infusion of prostacyclin at a rate of 0.1 microgram/min resulted in a significant increase (p less than 0.01) in active renin and a significant fall (p less than 0.01) in inactive renin. Prostacyclin also increased urinary kallikrein excretion (p less than 0.05). The results indicate that the kidney secretes not only active renin but also inactive renin, and suggest that prostacyclin stimulates the conversion of inactive renin to the active form through the activation of the renal kallikrein system.

Animals↗
PubMed1982

Effect of three angiotensin II antagonists, [Sar1, Thr8]-, [Sar1, Ile8]- and [Sar1, Ala8]angiotensin II on blood pressure and endocrine factors in normal subjects.

The biological effects of 1-Sarcosine, 8-Threonine angiotensin II ([Sar1, Thr8]ANG II) on blood pressure, plasma aldosterone concentration (PAC) and plasma renin activity (PRA) were investigated in six normal subjects on an unrestricted diet, and compared with those of 1-Sarcosine, 8-Isoleucine ANG II ([Sar1, Ile8]ANG II) and 1-Sarcosine, 8-Alanine ANG II ([Sar1, Ala8]ANG II). All three ANG II analogues (AIIA) showed agonistic pressor activity, that of [Sar1, Ile8]ANG II being greater than that of [Sar1, Thr8]ANG II or [Sar1, Ala8]ANG II. The antagonistic effect of [Sar1, Thr8]ANG II on blood pressure was less than [Sar1, I1e8]ANG II or [Sar1, Ala8]ANG II. Both [Sar1, Ile8]ANG II and [Sar1, Ala8]ANG II increased PAC and blocked the steroidogenic action of ANG II, while [Sar1, Thr8]ANG II showed little effect on PAC. All three AIIA caused similar suppression of PRA and showed no inhibitory effect on the decrease in PRA produced by ANG II. These results indicate that [Sar1, Thr8]ANG II is an AIIA with weak agonistic pressor action and that it has vascular selective properties. It is also suggested that ANG II receptors in a variety of target organs are heterogeneous.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1982

Salivary-type hyperamylasemia in primary lung cancer: observation of a possible precursor of the salivary-type isoamylase.

Although recent studies by column chromatography and electrophoresis showed that elevated amylase activity in the body fluids and tumor extracts in patients with primary lung cancer was mainly in the salivary-type isoamylase, neither mechanism nor mature of elevation of amylase have been clarified yet. This study was undertaken in order to make clear the nature of amylase elevated in the body fluids and tumor extracts of patients with primary lung cancer. In addition, amylase contained in the extracts of normal lungs and diseased lungs of patients who had died of various diseases was also studied. Our results revealed that amylase elevated in the body fluids and tumor extracts in patients with primary lung cancer was the salivary-type isoamylase and, moreover, that small amounts of salivary-type isoamylase in normal lung tissues and large amounts in diseased lung tissues were also contained. These facts suggested that salivary-type isoamylase was physiologically contained in normal lung tissues and large amounts in diseased lung tissues were also contained. These facts suggested that salivary-type isoamylase was physiologically contained in normal lung tissues and might be activated through pathological processes, such as inflammation, circulatory disturbance or tumor formation. Two peculiar isoamylases with cathodic mobility on polyacrylamide gel electrophoresis were found. One of them was so unstable that it was converted to the stable salivary-type isoamylase, suggesting the precursor of human salivary isoamylase.

Adenocarcinoma↗
PubMed1982

Release of prostaglandin I2 from hog kidney by propranolol.

Prostaglandin I2 (PGI2) decreases blood pressure. Perfusion of isolated hog kidney by propranolol in modified Krebs-Ringer solution resulted in a significant increase in 6-keto-prostaglandin F1 alpha, the major metabolite of PGI2. Prostaglandin E2 and renin activity remained unchanged. Because the concentration of PGI2-like substance in the renal vein has been shown to be greater than in the renal artery after bradykinin infusion, a contribution of PGI2 to the regulation of blood pressure was proposed. Isoproterenol has been shown to augment urinary kallikrein, but the effect of urinary kallikrein on propranolol is unclear. With a modified Krebs-Ringer solution free of plasma kininogen, a renin substrate, it was concluded that propranolol (1) induces PGI2 release from the kidney, which may contribute to a direct antihypertensive action of this beta-adrenergic blocking agent, and (2) decreases urinary kallikrein.

Animals↗