INTER-RELATIONSHIPS BETWEEN PLASMA ANGIOTENSIN II, ARTERIAL PRESSURE, ALDOSTERONE AND EXCHANGEABLE SODIUM IN NORMOTENSIVE AND HYPERTENSIVE MAN

1976 ◽  
pp. 779-784
Author(s):  
D.G. BEEVERS ◽  
J.J. BROWN ◽  
V. CUESTA ◽  
D.L. DAVIES ◽  
R. FRASER ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Exchangeable Sodium ◽  
Plasma Angiotensin

Effect of baroreceptor denervation on stimulation of drinking by angiotensin II in conscious dogs

1991 ◽  
Vol 260 (3) ◽  
pp. E333-E337 ◽  
Author(s):  
C. K. Klingbeil ◽  
V. L. Brooks ◽  
E. W. Quillen ◽  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Drinking Water ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Plasma Osmolality ◽  
Plasma Angiotensin ◽  
High Doses ◽  
Stimulation Of

Angiotensin II causes marked stimulation of drinking when it is injected centrally but is a relatively weak dipsogen when administered intravenously. However, it has been proposed that the dipsogenic action of systemically administered angiotensin II may be counteracted by the pressor action of the peptide. To test this hypothesis, the dipsogenic action of angiotensin II was investigated in dogs, in which low and high baroreceptor influences had been eliminated by denervation of the carotid sinus, aortic arch, and heart. In five sham-operated dogs, infusion of angiotensin II at 10 and 20 ng.kg-1.min-1 increased plasma angiotensin II concentration to 109.2 +/- 6.9 and 219.2 +/- 38.5 pg/ml and mean arterial pressure by 20 and 29 mmHg, respectively, but did not induce drinking. In four baroreceptor-denervated dogs, the angiotensin II infusions produced similar increases in plasma angiotensin II concentration and mean arterial pressure but, in contrast to the results in the sham-operated dogs, produced a dose-related stimulation of drinking. Water intake with the low and high doses of angiotensin II was 111 +/- 44 and 255 +/- 36 ml, respectively. The drinking responses to an increase in plasma osmolality produced by infusion of hypertonic sodium chloride were not different in the sham-operated and baroreceptor-denervated dogs. These results demonstrate that baroreceptor denervation increases the dipsogenic potency of intravenous angiotensin II and provides further support for the hypothesis that the dipsogenic action of intravenous angiotensin II is counteracted by the rise in blood pressure.

Renin–Angiotensin System in Mild Essential Hypertension. the Functional Significance of Angiotensin II in Untreated and Thiazide-Treated Hypertensive Patients

1978 ◽  
Vol 55 (s4) ◽  
pp. 319s-321s ◽  
Author(s):  
H. Ibsen ◽  
A. Leth ◽  
H. Hollnagel ◽  
A. M. Kappelgaard ◽  
M. Damkjaer Nielsen ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Functional Significance ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Plasma Angiotensin

1. Twenty-five patients with mild essential hypertension, identified during a survey of a population born in 1936, were investigated. 2. Basal and post-frusemide values for plasma renin concentration and plasma angiotensin II concentration did not differ markedly from reference values in 25 40-year-old control subjects. In the untreated, sodium replete state saralasin infusion (5·4 nmol min−1 kg−1) produced an increase in mean arterial pressure in the patient group as a whole. 3. Twenty-one patients were treated with hydrochlorothiazide, mean dose 75 mg/day for 3 months. Pre-treatment, frusemide-stimulated plasma renin concentration and plasma angiotensin II, and values during thiazide treatment were higher in ‘non-responders’ (n = 10) to hydrochlorothiazide treatment than in ‘thiazide-responders’ (n = 11). During thiazide therapy, angiotensin II blockade induced a clear-cut decrease in mean arterial pressure in all ‘thiazide-nonresponders’ whereas only four out of 11 ‘thiazide-responders’ showed a borderline decline in mean arterial pressure. 4. The functional significance of the renin—angiotensin system in mild essential hypertension emerges only after thiazide treatment. Thiazide-induced stimulation of the renin—angiotensin system counter-balanced the hypotensive effect of thiazide in some 40% of the treated patients. Thus the responsiveness of the renin—angiotensin system determined the blood pressure response to thiazide treatment.

Effects of the angiotensin II receptor antagonist Losartan (DuP 753/MK 954) on arterial blood pressure, heart rate, plasma concentrations of angiotensin II and renin and the pressor response to infused angiotensin II in the salt-deplete dog

1992 ◽  
Vol 83 (5) ◽  
pp. 549-556 ◽  
Author(s):  
R. J. MacFadyen ◽  
M. Tree ◽  
A. F. Lever ◽  
J. L. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Pressor Response ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Plasma Angiotensin

1. The blood pressure, heart rate, hormonal and pressor responses to constant rate infusion of various doses of the angiotensin (type 1) receptor antagonist Losartan (DuP 753/MK 954) were studied in the conscious salt-deplete dog. 2. Doses in the range 0.1–3 μmin−1 kg−1 caused no change in blood pressure, heart rate or pressor response to angiotensin II (54 ng min−1kg−1), and a dose of 10 μgmin−1 kg−1 had no effect on blood pressure, but caused a small fall in the pressor response to angiotensin II. Infusion of Losartan at 30 μmin−1 kg−1 for 3 h caused a fall in mean blood arterial pressure from baseline (110.9 ± 11.2 to 95.0 ± 12.8 mmHg) and a rise in heart rate (from 84.6 ± 15.1 to 103 ± 15.2 beats/min). Baseline plasma angiotensin II (42.5 ± 11.8 pg/ml) and renin (64.5 ± 92.7 μ-units/ml) concentrations were already elevated in response to salt depletion and rose significantly after Losartan infusion to reach a plateau by 70 min. The rise in mean arterial blood pressure after a test infusion of angiotensin II (35.3 ± 11.6 mmHg) was reduced at 15 min (11.8 ± 6.8 mmHg) by Losartan and fell progressively with continued infusion (3 h, 4.3 ± 3.3 mmHg). The peak plasma angiotensin II concentration during infusion of angiotensin II was unaffected by Losartan, but the rise in plasma angiotensin II concentration during infusion was reduced because of the elevated background concentration. Noradrenaline infusion caused a dose-related rise in mean blood arterial pressure (1000 ngmin−1kg−1, +19.9 ± 8 mmHg; 2000ngmin−1 kg−1, +52.8 ± 13.9 mmHg) with a fall in heart rate (1000 ng min−1 kg−1, −27.9 ± 11.5 beats/min; 2000 ng min−1 kg−1, −31.2 ± 17.3 beats/min). During Losartan infusion the 1000 but not the 2000 ng min−1 kg−1 noradrenaline infusion caused a greater rise in mean arterial blood pressure and a greater fall in heart rate. The fall in heart rate tended to decrease with continued infusion of Losartan. Plasma catecholamine concentrations were unaffected by Losartan. In a further study, higher doses of Losartan (100, 300 and 1000 μg min−1 kg−1; 30 min) produced greater falls in mean arterial blood pressure also with a rise in heart rate and complete blockade of the pressor effect of infused angiotensin II. Some animals became disturbed at the highest dose. 3. Losartan produces rapid dose-related falls in blood pressure and a rise in heart rate and renin release with elevation of plasma angiotensin II. Pressor responses to angiotensin II are reduced at intermediate doses and are eliminated at high doses. Losartan does not appear to inhibit angiotensin II clearance from the plasma and may in some way increase it.

Interaction between CRF and angiotensin II in control of ACTH and adrenal steroids

1986 ◽  
Vol 250 (3) ◽  
pp. R396-R402 ◽  
Author(s):  
M. Keller-Wood ◽  
B. Kimura ◽  
J. Shinsako ◽  
M. I. Phillips
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Arteries ◽  
Corticotropin Releasing Factor ◽  
Adrenal Steroids ◽  
Ang Ii ◽  
Plasma Angiotensin ◽  
Acth Release

These experiments were designed to test for interactions between plasma angiotensin II (ANG II) and corticotropin-releasing factor (CRF) in the control of plasma adrenocorticotropin (ACTH), aldosterone, and corticosteroids, mean arterial pressure (MAP), and heart rate (HR) in conscious dogs. Five trained dogs with exteriorized carotid arteries were studied. Each dog was infused with saline and with CRF at three rates (2.5, 5, and 10 ng X kg-1 X min-1) and ANG II at three rates (5, 10, and 20 ng X kg-1 X min-1) for 60 min. The same animals were also coinfused with 10 ng X kg-1 X min-1 ANG II at each rate of CRF infusion and with 10 ng CRF X kg-1 X min-1 at each rate of ANG II infusion. Infusion of ANG II alone caused dose-related increases in aldosterone, corticosteroids, and MAP but did not alter ACTH or HR. Infusion of CRF alone increased ACTH, aldosterone, and corticosteroids but not MAP or HR. Coinfusion of CRF and ANG II caused ANG II dose-related ACTH responses but did not alter the sensitivity of the ACTH responses to CRF. Thus it appears that ANG II alone does not stimulate ACTH release but requires increased CRF concentrations to effect ACTH release.

An Altered Relation between Arterial Pressure and Plasma Angiotensin II Concentration Resulting from Prolonged Infusion of Angiotensin II

1978 ◽  
Vol 55 (s4) ◽  
pp. 217s-220s ◽  
Author(s):  
B. L. Bean ◽  
J. J. Brown ◽  
J. Casals-Stenzel ◽  
R. Fraser ◽  
A. F. Lever ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Concentration ◽  
Arterial Pressure ◽  
Dose Response ◽  
Pressure Curve ◽  
Prolonged Infusion ◽  
Prolonged Administration ◽  
Plasma Angiotensin ◽  
Constant Dose

1. Infusion of angiotensin II into dogs at constant dose over 2 weeks caused a progressive rise in arterial pressure. 2. When the infusion was stopped the pressure dropped slowly from hypertensive levels over 48 h. 3. Dose—response studies at weekly intervals showed progressive elevation, without steepening, of the plasma angiotensin II—blood pressure curve. 4. Thus, during prolonged administration of angiotensin II, a given plasma concentration of the peptide can sustain a higher arterial pressure than it can during acute infusions.

Captopril in Hypertension with Renal Artery Stenosis and in Intractable Hypertension; Acute and Chronic Changes in Circulating Concentrations of Renin, Angiotensins I and II and Aldosterone, and in Body Composition

1979 ◽  
Vol 57 (s5) ◽  
pp. 139s-143s ◽  
Author(s):  
A. B. Atkinson ◽  
J. J. Brown ◽  
R. Fraser ◽  
B. Leckie ◽  
A. F. Lever ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Artery Stenosis ◽  
Term Therapy ◽  
Exchangeable Sodium ◽  
Angiotensin I ◽  
Plasma Angiotensin ◽  
Sodium And Potassium

1. The converting-enzyme inhibitor captopril has been given in doses up to 450 mg daily to hypertensive patients with renal artery stenosis and to patients resistant to other therapy. 2. Captopril alone was effective in controlling hypertension in renal artery stenosis, irrespective of whether pretreatment plasma angiotensin II was raised or normal, except in one man with overall renal impairment. 3. In one woman with the hyponatraemic hypertensive syndrome secondary to renal artery thrombosis, captopril restored depleted exchangeable sodium and potassium to normal. In the other cases of renal artery stenosis with normal renal function, exchangeable sodium and total body potassium were not significantly altered, and there were no marked changes in plasma sodium and potassium. 4. The combination of captopril with a diuretic controlled blood pressure long-term in every case of previously resistant hypertension. 5. Within 2 h, captopril induced highly significant falls in arterial pressure, in plasma angiotensin II and aldosterone, with converse increases in plasma active and total renin and blood angiotensin I. 6. The initial fall in plasma angiotensin II was closely related to the concomitant fall in diastolic pressure. 7. The pattern of change in circulating renin, angiotensins I and II and aldosterone was maintained during long-term therapy, whether or not a diuretic was added. There was no tendency for plasma angiotensin II to increase despite sustained elevation of active renin and angiotensin I.

Angiotensin II and Sodium as Determinants of the Agonistic-Antagonistic Balance of Saralasin's Actions

1981 ◽  
Vol 60 (4) ◽  
pp. 377-385 ◽  
Author(s):  
R. Fagard ◽  
A. Amery ◽  
P. Lijnen
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Sodium Restriction ◽  
Plasma Angiotensin ◽  
Group 3 ◽  
Group 2 ◽  
Group 1

1. To study which factors determine the balance between the antagonistic and agonistic effects of the angiotensin II analogue [Sar1,Ala8]angiotensin II (saralasin) in man, saralasin was infused in subjects on a ‘normal’ sodium intake (group 1) and during sodium restriction with appropriately elevated plasma angiotensin II levels (group 2), and in sodium-restricted subjects in whom plasma angiotensin II was suppressed by converting-enzyme inhibition with captopril (group 3). 2. The saralasin-induced increase of plasma aldosterone concentration in group 1 was different (P<0.005) from the decrease in group 2, whereas saralasin produced a significant increase of plasma aldosterone in group 3. For the three groups combined the changes of plasma aldosterone were significantly related to control angiotensin II levels, but not to the 24 h urinary sodium excretion. The data suggest that it is the rise of angiotensin II in response to the sodium restriction and not the sodium restriction per se that is associated with the antagonistic action of saralasin on the adrenal receptors. 3. On average mean intra-arterial pressure at 30 min was not affected by saralasin in group 1, had decreased in group 2 and increased (P<0.001) by 4.4 mmHg in group 3. Overall the changes of arterial pressure were significantly related to control angiotensin II, but not to the 24 h sodium excretion, suggesting that the angiotensin II levels predominantly determine the agonistic-antagonistic balance of saralasin's actions on arterial pressure. 4. Although saralasin did not affect plasma renin activity in group 1, plasma renin rose in group 2 and was reduced by 40% (P<0.001) in group 3. For the three groups together the changes of plasma renin activity were significantly related to the changes of mean arterial pressure both on single and multiple regression analyses. The changes of pressure ‘explain’, however, only a fraction of the changes of plasma renin; it is suggested that saralasin has an agonistic effect on the renal receptors involved in the direct suppression of renin by angiotensin II in low-sodium, low-angiotensin conditions and that an antagonistic effect may contribute to the saralasin-induced rise of renin during sodium restriction with appropriate angiotensin II levels.

Sign in / Sign up

Export Citation Format

Share Document