INHIBITION OF ANGIOTENSIN III ACTION BY DES-ASP1-,ILEU8-ANGIOTENSIN II IN MAN

1978 ◽  
Vol 87 (2) ◽  
pp. 359-366
Author(s):  
Tsuyoshi Kono ◽  
Fumitake Ikeda ◽  
Fumimaro Oseko ◽  
Masataka Nanno ◽  
Hiroo Imura ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Adrenal Cortex ◽  
Intravenous Infusion ◽  
Inhibitory Effect ◽  
Plasma Aldosterone ◽  
Angiotensin Iii ◽  
Normal Men

ABSTRACT 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 (All) in the same 5 normal men demonstrate that this dose of AIIIA antagonizes AIII and All 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 All in man.

Biological Activity of Angiotensin II-(4-8)-Pentapeptide in Man

1982 ◽  
Vol 63 (s8) ◽  
pp. 195s-197s ◽  
Author(s):  
T. Kono ◽  
F. Oseko ◽  
F. Ikeda ◽  
H. Imura ◽  
M. C. Khosla ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Bartter's Syndrome ◽  
Pressure Plasma ◽  
Significant Change ◽  
Normal Men

1. When the angiotensin II-(4-8)-pentapeptide was infused intravenously at rates of 0.31-5.55 nmol min−1 kg−1 for 10–120 min into five normal men or two patients with Bartter's syndrome, no significant change was observed in blood pressure, plasma renin activity and plasma aldosterone, and the lowest dose did not inhibit the captopril-induced increase in plasma renin activity in the normal men. 2. An intravenous infusion of the pentapeptide at 9–0 nmol min−1 kg−1 for 15 min significantly raised blood pressure in the five normal men but not in patients with Bartter's syndrome. Blood pressure returned to the pre-treatment level 60 min after the cessation of the infusion in the normal men. 3. At the same dose level none of the seven subjects examined showed any significant change in plasma renin activity and plasma aldosterone. 4. Angiotensin II-(5-8)-tetrapeptide was infused intravenously into one of the normal men at a rate of 41.5 nmol min−1 kg−1 for 15 min, but it caused no significant change in blood pressure, plasma renin activity and plasma aldosterone. 5. These results suggest that the pentapeptide and probably the tetrapeptide do not possess renin-suppressing and steroidogenic actions in man but that the former peptide does elicit a modest pressor action with a prolonged duration.

ROLE OF ANGIOTENSIN III IN THE REGULATION OF BLOOD PRESSURE, PLASMA ALDOSTERONE AND PLASMA RENIN ACTIVITY IN RABBIT

1978 ◽  
Vol 89 (1) ◽  
pp. 132-141 ◽  
Author(s):  
Ikuo Saito ◽  
Takao Saruta ◽  
Toyohisa Eguchi ◽  
Kazuoki Kondo ◽  
Ryuichi Nakamura ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Pressure Plasma ◽  
Angiotensin Iii ◽  
Pre Treatment

ABSTRACT To evaluate the role of angiotensin III in the control of blood pressure, plasma aldosterone and plasma renin activity (PRA), the pressor, steroidogenic and PRA-suppressing effect of angiotensin III was studied in rabbits with or without simultaneous constant infusion of Ile7-angiotensin III, an analogue of angiotensin III, or Sar1Ala8-angiotensin II, an analogue of angiotensin II, and compared with the effect of angiotensin II. Infusion of 30 ng/kg/min of angiotensin III or angiotensin II produced a twofold increase in plasma aldosterone. Pressor response to angiotensin III was approximately one tenth of that of angiotensin II. Infusion of angiotensin II suppressed the PRA significantly, while infusion of angiotensin III did not suppress it. Angiotensin II or angiotensin III induced-increase in plasma aldosterone was attenuated by the pretreatment with either Ile7-angiotensin III or Sar1Ala8-angiotensin II. Pressor or PRA-suppressing action of angiotensin II was unaffected by the pre-treatment with Ile7-angiotensin III, while it was significantly inhibited by pre-treatment with Sar1Ala8-angiotensin II. This study indicates that angiotensin III or angiotensin III analogues affect the adrenal glands selectively and suggests that there are differences between the receptor sites for angiotensins in vascular smooth muscle, kidney and those in the adrenal cortex.

Responses of patients with Bartter's syndrome to angiotensin III and angiotensin II-(3–8)-hexapeptide

1985 ◽  
Vol 109 (2) ◽  
pp. 249-253 ◽  
Author(s):  
Tsuyoshi Kono ◽  
Fumitake Ikeda ◽  
Ataru Taniguchi ◽  
Hiroo Imura ◽  
Fumimaro Oseko ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Binding Sites ◽  
Bartter’S Syndrome ◽  
Bartter's Syndrome ◽  
Pressor Responses ◽  
Angiotensin Iii ◽  
Before And After ◽  
Normal Men ◽  
Indomethacin Treatment

Abstract. Studies were conducted to determine whether or not angiotensin III [AIII] and angiotensin II-(3-8)-hexapeptide [ANG-(3–8)] have their own specific arteriolar binding sites different from angiotensin II [AII] binding site(s) in man. Four patients with Bartter's syndrome were given asn1-,val5-AII by iv infusion at rates of 10, 20, 50 and 100 pmol/kg · min, each for 7 min. One hour later AIII was infused iv in the same 4 patients at rates of 50, 100, 250 and 500 pmol/kg · min, each for 7 min. After 100 or 150 mg/day of indomethacin treatment for 7 days, the same All and AIII infusions were repeated. All patients showed blunted pressor responses to both All and AIII before indomethacin and the responses were improved after indomethacin. Moreover, increment curves of blood pressure for AII were almost identical with those for AIII in individual patients both before and after indomethacin. ANG-(3–8) was infused iv in 3 normal men and 3 of the 4 patients with Bartter's syndrome at a rate of 3.500 pmol (2.838 ng)/kg·min for 15 min. Blood pressure rose in the normal men (12/12 mmHg on the average) but did not rise in the patients. These results suggest that All, AIII and ANG-(3–8) have the same arteriolar binding sites in man.

Biological activity of des-asp-,des-arg-angiotensin II in man

1982 ◽  
Vol 99 (4) ◽  
pp. 577-584 ◽  
Author(s):  
Tsuyoshi Kono ◽  
Fumitake Ikeda ◽  
Fumimaro Oseko ◽  
Yoshiaki Ohmori ◽  
Ryuichi Nakano ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Biological Activity ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Renin Release ◽  
Direct Inhibition ◽  
Normal Men

Abstract. The biololgical activity of des-asp1-,des-arg2-angiotensin II (3-8AII) was studied in man. When 3-8AII was infused iv at rates of 22 and 308 pmol (17.5 and 250 ng)/kg · min separately into 5 normal men each for 120 min, blood pressure showed no change, plasma renin activity (PRA) decreased gradually and plasma aldosterone showed a gradual slight increase. The lower dose of 3-8AII partially inhibited captopril-induced PRA increase and plasma aldosterone decrease in the same 5 normal men and the higher dose of the hexapeptide completely abolished them. In one of the 5 normal men blood pressure rose in response to doses of 3-8AII greater than 2220 pmol (1750 ng)/kg · min. When 3-8AII was infused iv at 308 pmol/kg · min into 2 patients with Bartter's syndrome for 60 min, it caused marked decreases in PRA and plasma aldosterone but no change in blood pressure. This decrease in plasma aldosterone is thought to be secondary to the decrease in PRA. From these results it is evident that 3-8AII has a minimal pressor action, a weak aldosterone-stimulating action and a significant renin-suppressing action in man and this PRA-lowering action is thought to be due to direct inhibition of renin release by its whole molecule or a smaller part of the molecule.

BIOLOGICAL ACTIVITY OF HIGH DOSE OF DES-ASP1-,ILEU8-ANGIOTENSIN II IN MAN

1977 ◽  
Vol 86 (1) ◽  
pp. 156-161 ◽  
Author(s):  
Tsuyoshi Kono ◽  
Fumimaro Oseko ◽  
Fumitake Ikeda ◽  
Masataka Nanno ◽  
Jiro Endo
Keyword(s):  
Blood Pressure ◽  
Biological Activity ◽  
Angiotensin Ii ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
High Dose ◽  
Agonist And Antagonist ◽  
High Doses ◽  
Slight Rise ◽  
Normal Men

ABSTRACT The biological activity of high doses of des-asp1-,ileu8-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.

The Effect of Insulin on the Rise in Blood Pressure and Plasma Aldosterone after Angiotensin II in Normal Man

1983 ◽  
Vol 64 (4) ◽  
pp. 383-386 ◽  
Author(s):  
H. Vierhapper ◽  
W. Waldhäusl ◽  
P. Nowotny
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Surface Area ◽  
Body Surface Area ◽  
Body Surface ◽  
Serum Potassium ◽  
Intravenous Infusion ◽  
Serum Insulin ◽  
Plasma Aldosterone ◽  
Normal Man

1. The effect of an intravenous infusion of insulin [2.5 units h−1 (m2 of body surface area)−1] on the rise in blood pressure and plasma aldosterone after intravenous angiotensin II (5, 10, and 20 ng min−1 kg−1) was investigated in six healthy, sodium-loaded men. 2. Serum insulin reached 96.8 ± 18.1 μ-units/ml (control: 7.0 ± 1.5 μ-units/ml) and serum potassium fell from 4.2 ± 0.2 mmol/l to 3.6 ± 0.2 mmol/l (P < 0.005). 3. Hyperinsulinaemia increased (P < 0.05) the secretion of aldosterone during the largest dose of angiotensin II (20 ng min−1 kg−1), but had no effect on the rise in blood pressure after angiotensin II.

Abstract 39: Adrenal ßArrestin1 Raises Serum Aldosterone Levels And Blood Pressure, Both Significant Stroke Risk Factors, In Experimental Rats And Mice

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Anastasios Lymperopoulos ◽  
Ashley Bathgate ◽  
Norma C Salazar
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Gene Delivery ◽  
Adrenal Cortex ◽  
Stroke Risk ◽  
Fluorescent Protein ◽  
Serum Aldosterone ◽  
Increased Risk ◽  
In Vivo Gene Delivery

Introduction: It is widely accepted nowadays that elevation of serum levels of aldosterone, a mineralocorticoid hormone with toxic effects in several cardiovascular tissues, including the heart and cerebral blood vessels, can significantly raise stroke risk. The success of mineralocorticoid receptor blockers, such as eplerenone, at preventing stroke attacks attests to this. Aldosterone is normally produced and secreted by the adrenal cortex in response to angiotensin II. We recently reported that adrenal βarrestin1 (βarr1) plays a crucial role in the physiological angiotensin II-stimulated aldosterone production in the adrenal cortex, leading to marked elevation of circulating serum aldosterone levels in vivo (Lymperopoulos A. et al., Proc. Natl. Acad. Sci. USA. 2009;106:5825-5830). Hypothesis: Herein, we examined the potential impact of this adrenal βarr1-dependent aldosterone elevation on stroke risk in experimental animals in vivo. Methods: We used the βarr1 knockout (βarr1KO) mouse model, studying it alongside wild type (WT) control mice, and also adult male Sprague-Dawley rats, in which adrenal βarr1 was overexpressed in vivo via adrenal-targeted adenoviral-mediated βarr1 gene transfer. Serum aldosterone was measured by ELISA and blood pressure via telemetry. Results: Serum aldosterone at 7 days post-in vivo gene delivery was markedly elevated in adrenal βarr1-overexpressing rats (536+50 pg/ml), compared to control rats receiving the green fluorescent protein (GFP) adenoviral transgene (235+40 pg/ml, p<0.05, n=5). This translated to a significant increase in mean arterial pressure of the βarr1-overexpressing rats (155+5 mmHg) compared to control GFP-expressing rats (137+8 mmHg, p<0.05, n=5), again at 7 days post-in vivo gene delivery, which was prevented by concurrent eplerenone treatment. In contrast, βarr1KO mice had significantly lower serum aldosterone levels (270+20 pg/ml) compared to WT controls (498+35 pg/ml, p<0.05, n=5), at 4 weeks post-experimental myocardial infarction. Conclusions: Adrenal βarr1 up-regulation can dramatically increase circulating aldosterone levels and systemic blood pressure, thus conferring increased risk for stroke in experimental rodents.

Effect of intravenous angiotensin II on Fos distribution and drinking behavior in rabbits

1997 ◽  
Vol 272 (5) ◽  
pp. R1515-R1524 ◽  
Author(s):  
E. Badoer ◽  
D. McKinlay
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Intravenous Infusion ◽  
Drinking Behavior ◽  
Ventrolateral Medulla ◽  
Lamina Terminalis ◽  
Ang Ii ◽  
Solitary Tract ◽  
Cell Nuclei ◽  
Drinking Response

We investigated the effect of intravenous infusion of angiotensin II (ANG II, 40 ng.kg-1.min-1) on the distribution of Fos in the subfornical organ (SFO), organum vasculosum of the lamina terminalis (OVLT), and the medulla of the conscious rabbit. ANG II elicited significant increases in the number of Fos-positive cell nuclei in the SFO and OVLT (15- and 10-fold, respectively). Raising blood pressure with phenylephrine did not elicit Fos in these nuclei. These nuclei are believed to be responsible for the dipsogenic actions of ANG II; however, ANG II was not dipsogenic. When blood pressure was held at preinfusion levels by the coadministration of sodium nitroprus-side and ANG II, the rabbits did not drink but Fos production in the lamina terminalis was elevated. In the medulla, ANG II did not significantly increase Fos production in the nucleus of the solitary tract (NTS) or ventrolateral medulla (VLM). However, with the coadministration of sodium nitroprusside, there were marked increases in the NTS and VLM. The results suggest that neurons in the SFO and OVLT are either not involved in the dipsogenic pathways or there is disruption further downstream in the central pathways that would normally mediate a drinking response to ANG II.

scholarly journals Deficiency of T-type Ca2+ channels Cav3.1 and Cav3.2 has no effect on angiotensin II-induced hypertension but differential effect on plasma aldosterone in mice

2019 ◽  
Vol 317 (2) ◽  
pp. F254-F263
Author(s):  
Anne D. Thuesen ◽  
Stine H. Finsen ◽  
Louise L. Rasmussen ◽  
Ditte C. Andersen ◽  
Boye L. Jensen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Natriuretic Peptide ◽  
Mineralocorticoid Receptor ◽  
Plasma Aldosterone ◽  
Receptor Blocker ◽  
Ang Ii ◽  
Induced Hypertension

T-type Ca2+ channel Cav3.1 promotes microvessel contraction ex vivo. It was hypothesized that in vivo, functional deletion of Cav3.1, but not Cav3.2, protects mice against angiotensin II (ANG II)-induced hypertension. Mean arterial blood pressure (MAP) and heart rate were measured continuously with chronically indwelling catheters during infusion of ANG II (30 ng·kg−1·min−1, 7 days) in wild-type (WT), Cav3.1−/−, and Cav3.2−/− mice. Plasma aldosterone and renin concentrations were measured by radioimmunoassays. In a separate series, WT mice were infused with ANG II (100 ng·kg−1·min−1) with and without the mineralocorticoid receptor blocker canrenoate. Cav3.1−/− and Cav3.2−/− mice exhibited no baseline difference in MAP compared with WT mice, but day-night variation was blunted in both Cav3.1 and Cav3.2−/− mice. ANG II increased significantly MAP in WT, Cav3.1−/−, and Cav3.2−/− mice with no differences between genotypes. Heart rate was significantly lower in Cav3.1−/− and Cav3.2−/− mice compared with control mice. After ANG II infusion, plasma aldosterone concentration was significantly lower in Cav3.1−/− compared with Cav3.2−/− mice. In response to ANG II, fibrosis was observed in heart sections from both WT and Cav3.1−/− mice and while cardiac atrial natriuretic peptide mRNA was similar, the brain natriuretic peptide mRNA increase was mitigated in Cav3.1−/− mice ANG II at 100 ng/kg yielded elevated pressure and an increased heart weight-to-body weight ratio in WT mice. Cardiac hypertrophy, but not hypertension, was prevented by the mineralocorticoid receptor blocker canrenoate. In conclusion, T-type channels Cav3.1and Cav3.2 do not contribute to baseline blood pressure levels and ANG II-induced hypertension. Cav3.1, but not Cav3.2, contributes to aldosterone secretion. Aldosterone promotes cardiac hypertrophy during hypertension.

Angiotensin II infusion increases vasopressin, ACTH, and 11-hydroxycorticosteroid secretion

1978 ◽  
Vol 234 (1) ◽  
pp. R66-R71 ◽  
Author(s):  
D. J. Ramsay ◽  
L. C. Keil ◽  
M. C. Sharpe ◽  
J. Shinsako
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Concentration ◽  
Plasma Renin Activity ◽  
Plasma Levels ◽  
Intravenous Infusion ◽  
Plasma Renin ◽  
Acth Secretion ◽  
Plasma Vasopressin ◽  
Bilateral Carotid

The effects of intravenous infusion of Asp1. Ile5-angiotensin II on blood pressure, plasma vasopressin, ACTH and 11-hydroxycorticosteroid levels and on plasma renin activity were studied in five trained, conscious dogs. The dogs were prepared with bilateral carotid loops. Infusion of angiotensin II at rates of 5, 10, and 20 ng/kg.min raised its plasma concentration from 23 +/- 7 to 48 +/- 8, 125 +/- 8, and 187 +/- 21 pg/ml, respectively. The lowest rate of infusion was mildly pressor, the two higher rates more so. All rates of infusion promptly increased vasopressin levels and depressed renin levels. The two higher rates also stimulated ACTH, although with a latency of 30-45 min. Since the rates of infusion of angiotensin II employed produced plasma levels within the physiological range, it is suggested that peripherally generated angiotensin II may play an important role in the regulation of vasopressin, and ACTH secretion.

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