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Biomedical subjects

J Endo

Publications and source records attributed to J Endo.

At least 109 records · Page 6Linked to original sources
PubMed1981

Stimulating effect of alpha-adrenoceptor agonists on isoproterenol-induced amylase release in rat parotid tissue.

Isoproterenol (ISO)-induced amylase release from rat parotid slices was increased by the addition of methoxamine to either a normal or a calcium (Ca)-free medium. The potentiating effect of methoxamine was completely blocked by the addition of phentolamine, irrespective of whether the slices were incubated in the normal or the Ca-free medium; and the effect also disappeared after prolonged preincubation (60 min) of the slices in the Ca-free medium. Both verapamil and procaine reduced methoxamine-induced amylase release, but only verapamil blocked the stimulating effect of methoxamine in the normal medium. ISO-induced accumulation of cyclic AMP in the slices was unaffected by methoxamine or phenylephrine. The results suggest a possibility that the potentiating effect of methoxamine on ISO-induced amylase release may be independent of the presence of extracellular Ca and the increased accumulation of cyclic AMP in the tissue is unnecessary.

Adrenergic alpha-Agonists↗
PubMed1980

Application of immobilized enzymes to clinical analyses : use of co-immobilized glucose oxidase and peroxidase in column form.

Glucose oxidase from Aspergillus niger and peroxidase from horseradish were simultaneously immobilized onto alkylamine glass beads which were then packed into a 1.5 x 20 mm column and integrated in the flow system of an AutoAnalyzer I. Glucose in serum, up to 5.0 g/l, was continuously determined at a rate of 60 samples per hour. The co-immobilized enzyme column gave better sensitivity as compared with an enzyme column which contained a mixture of two kinds of individually immobilized enzymes. The enzyme column was sufficiently stable while in use for two months. The results correlated satisfactorily well with those obtained by other well established methods for glucose assay.

Blood Glucose↗
PubMed1980

Biological activity of des-Asp1-angiotensin I in man.

The biological activity of des-Asp1-angiotensin I (des-Asp1-AI) was studied in five normal men. An iv infusion of 300 ng (258 pmol)/kg.min des-Asp1-AI caused a remarkable rise in blood pressure, a decrease in PRA, and an increase in plasma aldosterone concentration. The pressor and steroidogenic actions of this dose of des-Asp1-AI were slightly less than those of 100 ng (111 pmol)/kg.min des-Asp1-angiotensin II [Angotensin III (AIII)] which we reported previously and were abolished by a single oral administration of 100 mg of a converting enzyme inhibitor, SQ 14225. These results indicate that in man, as in animals, a rise in blood pressure and an increase in plasma aldosterone concentration after an infusion of des-Asp1-AI are entirely due to the actions of AIII converted from this nonapeptide, and that the conversion rate of des-Asp1-AI to AIII in normal men is less than 43%. This is much less than the conversion rate of angiotensin I to angiotensin II. It seems unlikely that des-Asp1-AI has physiological significance in the human renin-angiotensin-aldosterone system.

Aldosterone↗
PubMed1980

Effects of diltiazem hydrochloride on pressor and steroidogenic actions of angiotensins and norepinephrine in man.

The effect of diltiazem hydrochloride (DTZ), a calcium-antagonist, on pressor and steroidogenic action of angiotensin II (AII), angiotensin III (AIII) and norepinephrine (NE) was studied in 5 normal men. AII, AIII and NE were infused intravenously for 50 min from 0900 hr at a rate of 20 ng/kg/min, 100 ng/kg/min and 200 ng/kg/min, respectively. DTZ was infused intravenously alone or in combination with each of these pressor substances at a rate of 1 mg/min from 0910 hr to 0930 hr. DTZ alone did not cause significant changes in blood pressure (BP) and plasma aldosterone concentration (P1 Aldo). On the other hand, DTZ combined with AII, AIII or NE significantly inhibited the rise in BP induced by these pressor substances. DTZ also inhibited the NE-induced increase in P1 Aldo, whereas it did dot alter AII-, or AIII-induced increase in P1 Aldo. These results indicate that in normal men pressor actions of AII, AIII and NE are calcium-dependent and calcium ions are also involved in NE-induced increase in P1 Aldo.

Adult↗
PubMed1979

Use of immobilized enzymes in automated clinical analysis: determination of uric acid and glucose using immobilized enzymes in column form.

We studied the use of immobilized enzymes, covalently bound to alkylaminosilane derivative of porous glass, to automated clinical analysis on uric acid and glucose in blood, serum and urine. A microcolumn with an immobilized enzyme was prepared and used in an AutoAnalyzer I continuous flow system. Uricase (EC 1.7.3.3) from Candida utilis and glucose oxidase (EC 1.1.3.4) from Aspergillus niger were immobilized for the determination of uric acid and glucose, respectively. Hydrogen peroxide produced by these oxidases was colorimetrically determined using horse-radish peroxidase (EC 1.11.1.7) and a hydrogen acceptor in solution. Sensitivity and wash charactertistics of a column with immobilized enzyme, 1.5 mm of inner diameter and up to 40 mm in length, were satisfactory at an assay speed of 50 samples per hour. The results correlated well with those obtained by other well established methods utilizing the AutoAnalyzer system. The immobilized enzymes were sufficiently stable for at least two months of 2000 tests when used repeatedly. Clinical trials proved that this method is capable of replacing the soluble enzyme method, giving reliable and reproducible results at lower cost.

Autoanalysis↗
PubMed1979

Effects of angiotensin I-converting enzyme inhibitor, SQ 14225, in nomal men.

Effects of an orally active angiotensin I-converting enzyme inhibitor, SQ 14225, on the actions of angiotensin I (AI) infused intravenously for 120 to 390 min were studied in 5 normal men. When 20 ng/kg/min of AI infusion was started immediately after a single oral administration of 100 mg of SQ 14225, a significant rise in blood pressure (BP) was observed for the first 15 min, but BP began to fall from 17 min and returned to the pretreatment level at 45 min. This BP level continued at least to 120 min and in one subject to 180 min. In this subject BP began to rise again from 185 min and reached the level of 15 min at 390 min. Plasma AI level increased gradually from 45 min. At 15 min plasma renin activity (PRA) decreased and plasma aldosterone (PA) increased, but then PRA began to increase and PA began to decrease. At 120 min the values of PRA and PA were similar to the pretreatment values. In one subject plasma AI and PRA began to decrease and PA began to increase after 120 or 180 min. On the other hand, in the 5 men sole AI infusion caused a continued BP rise, PRA decrease and PA increase, and sole SQ 14225 administration caused increases in plasma AI and PRA and a decrease in PA but no BP change. From these results it was concluded that complete blockade and partial inhibition of AI conversion by 100 mg of oral SQ 14225 lasted for about 2.5 and 6.5 hr, respectively and that BP rise, PRA suppression and aldosterone stimulation after AI infusion were entirely due to the actions of angiotensin II converted from AI.

Adult↗
PubMed1979

Lack of inhibition of ACTH-induced aldosterone stimulation by des-asp1-,ileu8-angiotensin II in man.

In 5 normal men an intravenous injection of 0.5 mg of synthetic 1-24 ACTH caused a significant increase in plasma aldosterone and a simultaneous intravenous infusion of 600 ng/kg/min of des-asp1-, ileu8-angiotensin II (AIIIA) did not inhibit this increase. Since this dose of AIIIA is known to inhibit an angiotensin II-induced increase in plasma aldosterone in normal men, the present results suggest that the ACTH-induced aldosterone stimulation is mediated by an adrenocortical receptor which is different from angiotensin II receptors.

Adrenocorticotropic Hormone↗
PubMed1978

Inhibition of angiotensin III action by DES-ASP1-,ILEU8-angiotensin II in man.

In 5 normal men intravenous infusion of 600 ng/kg/min of des-asp1-ileu8-angiotensin II (AIIIA) inhibited a rise in blood pressure as well as increase in plasma aldosterone caused by an intravenous infusion of 20 or 100 ng/kg/min of des-asp1-angiotensin II (angiotensin III, AIII). This result and our previous study on simultaneous infusions of 600 ng/kg/min of AIIIA and 20 ng/kg/min of angiotensin II (AII) in the same 5 normal men demonstrate that this dose of AIIIA antagonizes AIII and AII on the adrenal cortex as well as peripheral arterioles and that AIIIA has the same degree of inhibitory effect on the aldosterone-stimulating action of AIII and on that of AII in man.

Adult↗
PubMed1977

Biological activity of high dose of des-asp 1-, ileu 8-angiotensin II in man.

The biological activity of high doses of des-asp 1-, ileu 8-angiotensin II (AIIIA) was studied in man. In 5 normal men an intravenous infusion of 600 ng/kg/min of AIIIA for 30 min caused a slight rise in blood pressure, a decrease in plasma renin activity and an increase in plasma aldosterone. This dose inhibited pressor and steroidogenic actions of angiotensin II infused into the same 5 normal men at a rate of 20 ng/kg/min for 30 min. These results are considerably different from our previous report using lower dose (200 ng/kg/min) of AIIIA and indicate that in man AIIIA has both agonist and antagonist activities on the peripheral arterioles as well as on the adrenal cortex.

Aldosterone↗