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.

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 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.

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.

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.

Studies on the Effect of Angiotensin II and of Des1-angiotensin II on Blood Pressure, Plasma Renin Activity and Plasma Aldosterone in the Dog

1976 ◽  
Vol 51 (s3) ◽  
pp. 147s-150s
Author(s):  
R. Beckerhoff ◽  
G. Uhlschmid ◽  
W. Vetter ◽  
W. Siegenthaler
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Aldosterone Secretion ◽  
Pressure Plasma ◽  
Moderate Effect

1. The effects of infusions of equimolar doses of angiotensin II (AII) and of Des1-angiotensin II (heptapeptide) on plasma renin activity, blood pressure and plasma aldosterone were compared in normal anaesthetized dexamethasone-suppressed dogs. 2. Plasma renin activity was equally suppressed by both compounds. The increase in blood pressure induced by the heptapeptide averaged 43–62% of the increase during AII infusions. No significant differences in aldosterone increase were observed between AII and the heptapeptide. Plasma aldosterone, however, dropped significantly faster in heptapeptide-treated dogs after the end of the infusions. 3. Sar1-Ala8-angiotensin II (saralasin, 400 pmol min—1 kg—1) suppressed plasma aldosterone that was stimulated by heptapeptide (20 pmol min—1 kg—1) completely. The same angiotensin antagonist had only a moderate effect on plasma aldosterone stimulated by AII. After stopping the antagonist infusion, plasma aldosterone rose significantly higher in dogs infused with AII than in those receiving the heptapeptide. 4. The results demonstrate differences between the effects of AII and the heptapeptide both on blood pressure and on plasma aldosterone. They do not support the hypothesis that the heptapeptide may be the main mediator of aldosterone secretion.

The Hypotensive Effect of Propranolol in Captopril-Treated Patients Does Not Involve the Plasma Renin—Angiotensin—Aldosterone System

1981 ◽  
Vol 61 (s7) ◽  
pp. 441s-444s ◽  
Author(s):  
J. Staessen ◽  
R. Fagard ◽  
P. Lijnen ◽  
L. J. Verschueren ◽  
A. Amery
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Serum Potassium ◽  
Plasma Renin ◽  
Hypotensive Effect ◽  
Placebo Treatment ◽  
Plasma Aldosterone ◽  
Double Blind ◽  
Plasma Aldosterone Concentration ◽  
Plasma Angiotensin

1. With a double-blind cross-over protocol, 20 hypertensive captopril-treated patients were studied by adding in a variable sequence a placebo and propranolol (80 mg three times a day) to their captopril regimen (200 mg three times a day), during periods each lasting 1 month. During captopril—placebo treatment their diastolic blood pressure remained elevated between 90 and 114 mmHg. 2. The additional administration of propranolol produced a significant hypotensive effect, but no alterations of the plasma angiotensin II and aldosterone concentrations and of the urinary aldosterone excretion occurred. The present data indicate that in captopril-treated patients the hypotensive effect of propranolol is achieved independently of changes in the plasma angiotensin II and aldosterone concentration. 3. The additional administration of propranolol also produced an increase in the serum potassium levels in the absence of any change in the plasma aldosterone concentration or in the urinary aldosterone excretion.

Effect of angiotensin II and of an Angiotensin II Analogue (Sar1-Ile8-Angiotensin II) on Blood Pressure, Plasma Aldosterone and Plasma Renin Activity in the Dog

1974 ◽  
Vol 48 (s2) ◽  
pp. 41s-44s
Author(s):  
R. Beckerhoff ◽  
G. Uhlschmid ◽  
W. Vetter ◽  
H. Armbruster ◽  
J. Nussberger ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Arterial Blood Pressure ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Angiotensin Receptors ◽  
Pressure Plasma ◽  
Arterial Blood

1. The effect of infusions of equimolar doses of angiotensin II (AII) and of the angiotensin analogue Sar1-Ile8-angiotensin II on arterial blood pressure, plasma aldosterone and plasma renin activity were compared in normal anaesthetized dexamethasone suppressed dogs. 2. Angiotensin II induced a significant increase of blood pressure and of plasma aldosterone whereas plasma renin activity decreased. The blood pressure was only slightly affected by large doses of the analogue. Plasma aldosterone, however, increased and plasma renin activity decreased. These changes were significant but less pronounced than after the infusions of angiotensin II. Plasma aldosterone remained high and renin activity low for 40 min after the infusions of the analogue. 3. The results suggest a strong agonistic potency of Sar1-Ile8-angiotensin II at the adrenal and renal angiotensin receptors, and that it is almost ineffective at the vascular receptors. The inhibition of renin secretion by angiotensin seems not to be related to its vasoconstrictive activity.

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