BIOLOGICAL ACTIVITY OF DES-ASP<sup>1</sup>-ANGIOTENSIN II (ANGIOTENSIN III) IN MAN

Kono, Tsuyoshi; Oseko, Fumimaro; Shimpo, S; Nanno, Masataka; Endo, Jiro

doi:10.1210/jcem-41-6-1174

Cited by 39 publications

(17 citation statements)

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“…This encouraged us to undertake the present experiments. The doses of AII, AIII and NE administered in the present study were known to be tolerable and sufficient enough to cause a significant rise in BP (Kono et al, 1975;Kono et al, 1976;Kono et al, 1978). In the present experiments AII-, AIII-and NE-induced BP rises were all inhibited by the combined infusion of DTZ, whereas DTZ alone snowed no hypotensive effect in 5 normal men.…”

Section: Methodssupporting

confidence: 45%

“…Increases in P1 Aldo after AII and AIII are thought to be caused exclusively by direct stimulation of adrenal zona gromerulosa cells by the angiotensins and not by ACTH stimulation, because in our previous studies PC did not increase after infusion of the same doses of AII and AIII in normal men (Kono et al, 1975;Kono et al, 1978). In Experiments 2 and 3, the addition of DTZ did not inhibit further increase in P1 Aldo.…”

Section: Methodsmentioning

confidence: 64%

“…The radioimmunoassay methods for PRA, P1 Aldo and PC were described previously (Kono et al, 1975;Kono et al, 1980).…”

Section: Endocrinolmentioning

confidence: 99%

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

et al. 1980

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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 not alter AII-, or AIIIinduced 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.

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Section: Methodssupporting

confidence: 45%

Section: Methodsmentioning

confidence: 64%

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

et al. 1980

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“…Before, during and after the infusions of these peptides and/or the administration of SQ 14225 BP was measured every2or3min, and plasma AI, (Kono et al, 1975).…”

Section: Methodsmentioning

confidence: 99%

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

et al. 1979

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SynposisEffects of an orally active angiotensin I-converting enzyme inhibitor, SQ14225, on the actions of angiotensin I (AI) infused intravenously for120to390min were studied in5normal men. When20ng/kg/min of AI infusion was started immediately after a single oral administration of100mg of SQ14225, a significant rise in blood pressure (BP) was observed for the first15min, but BP began to fall from 17min and returned to the pretreatment level at45min.This BP level continued at least to120min and in one subject to180min. In this subject BP began to rise again from185minand reached the level of15min at390min. Plasma Al level increased gradually from45min.At15min plasma renin activity (PRA) decreased and plasma aldosterone (PA) increased, but then PRA began to increase and PA began to decrease. At120min 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 after120or180min.On the other hand, in the5men sole AI infusion caused a continued BP rise, PRA decrease and PA increase, and sole SQ14225 administration caused increases in plasma AI and PRA and a decrease in PA b ut no BP change. From these results it was concluded that complete blockade and partial inhibition of AI conversion by100mg of oral SQ14225lasted for about2.5and 6.5hr, 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.

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“…On the other hand, deletion of N-terminal aspartic acid of Ile5-ANG II considerably lowered pressor activity, slightly weakened steroidogenic activity and hastened the speed of catabolism of the original peptide (Kono et al, 1975;Kono et al, 1985). However, the effect of the removal of N-terminal aspartic acid from C-terminal deleted ANG II has never been studied.…”

mentioning

confidence: 99%