Evidence for the Local Occurrence of Angiotensin II in Rat Kidney and its Modulation by Dietary Sodium Intake and Converting Enzyme Blockade

1979 ◽  
Vol 57 (2) ◽  
pp. 173-179 ◽  
Author(s):  
F. A. O. Mendelsohn
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Enzyme Inhibitor ◽  
Sodium Intake ◽  
Rat Kidney ◽  
Plasma Renin ◽  
Renin Activity ◽  
Dietary Sodium ◽  
Ang Ii ◽  
Converting Enzyme

1. Angiotensin II (ANG II) was measured in acid-ethanol homogenates of rapidly frozen rat kidneys by a method involving ion-exchange and immunoadsorbent purification of peptides before radioimmunoassay. 2. Concentrations of ANG II found in kidney were 10–20 times that in plasma. 3. Perfusion of the kidneys via the renal artery with isotonic sodium chloride solution or with disodium EDTA solution did not alter the concentrations of intrarenal ANG II. 4. Animals fed on a sodium-deficient diet for 8 days had markedly higher concentrations of intrarenal ANG II, plasma renin activity and kidney renin concentration than sodium-replete animals. 5. After oral sodium loading for 3 weeks, rats had suppressed plasma renin activity and kidney renin concentration but unchanged intrarenal ANG II when compared with animals on a normal sodium intake. 6. One hour after the administration of a converting enzyme inhibitor (SQ 20881) plasma renin activity was elevated, kidney renin concentration unchanged and intrarenal ANG II was depressed. 7. These results demonstrate the presence of ANG II in the extravascular compartment of the kidney. They further suggest that its quantity is influenced by sodium intake and that angiotensin I converting enzyme is essential for its formation.

Effect of Angiotensin II and Converting Enzyme Inhibitor (Captopril) on Blood Pressure, Plasma Renin Activity and Aldosterone in Primary Aldosteronism

1981 ◽  
Vol 61 (s7) ◽  
pp. 289s-293s ◽  
Author(s):  
F. Mantero ◽  
F. Fallo ◽  
G. Opocher ◽  
D. Armanini ◽  
M. Boscaro ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Primary Aldosteronism ◽  
Enzyme Inhibitor ◽  
Plasma Renin ◽  
Renin Activity ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitor ◽  
Idiopathic Hyperaldosteronism

1. Patients with idiopathic hyperaldosteronism (IHA) show a response of aldosterone to posture which is not present in patients with aldosterone-producing adenoma (APA). We have determined whether this could be explained by a different sensitivity to angiotensin II. 2. Angiotensin II was infused in gradually increasing doses in six patients with APA and in seven patients with IHA. No changes in aldosterone concentration were found at the end of each period in APA, whereas there was a significant increase in IHA; blood pressure rose by a similar extent in both groups. 3. In order to evaluate the role of endogenous angiotensin II, captopril, a converting enzyme inhibitor, was administered to six patients with APA and five patients with IHA at a dose of 75 mg/day for 1 week. There was a significant fall of mean blood pressure in IHA and only minimal changes in APA. Plasma renin activity and plasma and urinary aldosterone were unchanged in APA. In IHA there was a small increase in upright plasma renin activity and a slight decrease in both plasma and urinary aldosterone, but these changes were not significant. 4. These findings further support the idea that idiopathic hyperaldosteronism is a clinical state different from that occurring in primary aldosteronism due to adenoma, and may be more closely related to essential hypertension.

Effect of enalapril (MK-421), an orally active angiotensin I converting enzyme inhibitor, on blood pressure, active and inactive plasma renin, urinary prostaglandin E2, and kallikrein excretion in conscious rats

1984 ◽  
Vol 62 (1) ◽  
pp. 116-123 ◽  
Author(s):  
Ernesto L. Schiffrin ◽  
Jolanta Gutkowska ◽  
Gaétan Thibault ◽  
Jacques Genest
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Ace Inhibition ◽  
Renin Activity ◽  
Prostaglandin E ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Angiotensin I Converting Enzyme

The angiotensin I converting enzyme (ACE) inhibitor enalapril (MK-421), at a dose of 1 mg/kg or more by gavage twice daily, effectively inhibited the pressor response to angiotensin I for more than 12 h and less than 24 h. Plasma renin activity (PRA) did not change after 2 or 4 days of treatment at 1 mg/kg twice daily despite effective ACE inhibition, whereas it rose significantly at 10 mg/kg twice daily. Blood pressure fell significantly and heart rate increased in rats treated with 10 mg/kg of enalapril twice daily, a response which was abolished by concomitant angiotensin II infusion. However, infusion of angiotensin II did not prevent the rise in plasma renin. Enalapril treatment did not change urinary immunorcactive prostaglandin E2 (PGE2) excretion and indomethacin did not modify plasma renin activity of enalapril-treated rats. Propranolol significantly reduced the rise in plasma renin in rats receiving enalapril. None of these findings could be explained by changes in the ratio of active and inactive renin. Water diuresis, without natriuresis and with a decrease in potassium urinary excretion, occurred with the higher dose of enalapril. Enalapril did not potentiate the elevation of PRA in two-kidney one-clip Goldblatt hypertensive rats. In conclusion, enalapril produced renin secretion, which was in part β-adrenergically mediated. The negative short feedback loop of angiotensin II and prostaglandins did not appear to be involved. A vasodilator effect, apparently independent of ACE inhibition, was found in intact conscious sodium-replete rats.

Failure of angiotensin II to suppress plasma renin activity in normotensive subjects with a positive family history of hypertension

2005 ◽  
Vol 109 (3) ◽  
pp. 311-317 ◽  
Author(s):  
Hans Herlitz ◽  
Eva Palmgren ◽  
Bengt Widgren ◽  
Mattias Aurell
Keyword(s):  
Angiotensin Ii ◽  
Family History ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Urinary Sodium ◽  
Renin Activity ◽  
Ang Ii ◽  
History Of ◽  
Family History Of Hypertension ◽  
Normotensive Subjects

The renin–angiotensin system is implicated in the pathophysiology of hypertension. Renin release is regulated by a number of factors, including circulating Ang II (angiotensin II), the so-called short feedback loop. The aim of the present study was to investigate the responsiveness of circulating Ang II on PRA (plasma renin activity) in normotensive subjects with a PFH or NFH (positive or negative family history of hypertension respectively). PRA, renal haemodynamics and urinary sodium excretion were measured during infusion of Ang II without and with pretreatment with the AT1 (Ang II type 1) receptor blocker irbesartan. Normotensive men with a PFH (n=13) and NFH (n=10), with a mean age of 38 years, were given on different occasions intravenous Ang II infusions of 0.1, 0.5 and 1.0 ng·kg−1 of body weight·min−1 before and after pretreatment with 150 mg of irbesartan once a day for 5 consecutive days. RPF (renal plasma flow) and GFR (glomerular filtration rate) were also measured. Before Ang II infusion, the PFH and NFH groups did not differ with respect to BP (blood pressure), body mass index, PRA, RBF (renal blood flow) or urinary sodium. There was no difference in BP or renal haemodynamic response to the highest Ang II dose between the groups. PRA declined with the highest Ang II dose (P<0.01) in subjects with a NFH, but not in subjects with a PFH. After treatment with irbesartan when Ang II had no effect on BP in either group, Ang II also suppressed PRA in subjects with a PFH (P<0.01), and the difference between the groups at baseline was thus eliminated. In conclusion, these findings indicate that subjects with a PFH have a defective Ang II suppression of PRA, which is corrected by AT1 receptor blockade.

Angiotensin II Blockade before and after Marked Sodium Depletion in Patients with Hypertension

1978 ◽  
Vol 54 (1) ◽  
pp. 75-83 ◽  
Author(s):  
P. Van Hoogdalem ◽  
A. J. M. Donker ◽  
F. H. H. Leenen
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Hypotensive Effect ◽  
Renin Activity ◽  
Mean Blood Pressure ◽  
Sodium Depletion ◽  
Before And After

1. Angiotensin II blockade before and after marked sodium depletion in patients with hypertension [unilateral renovascular (eight), bilateral renovascular (four) and essential (four)] was performed by intravenous administration of the angiotensin II antagonist Sar1-Ala8-angiotensin II (saralasin). 2. On normal sodium intake, saralasin decreased mean blood pressure by 8 mmHg in the unilateral renovascular group, by 6 mmHg in the bilateral renovascular group and increased it by 3 mmHg in the essential hypertensive group. After sodium depletion saralasin decreased mean blood pressure by 33 mmHg, 35 mmHg and 18 mmHg respectively. The saralasin-induced decrease in blood pressure significantly correlated with the log of the initial plasma renin activity. 3. Saralasin infusion decreased effective renal plasma flow (ERPF) in all three hypertension subgroups, both on normal sodium intake and after sodium depletion. Glomerular filtration rate decreased in direct relation to the hypotensive effect of saralasin but ERPF showed this relationship only after sodium depletion. On normal sodium intake saralasin increased filtration fraction by 17%, but decreased it by 7% after sodium depletion. 4. It is concluded that the hypotensive action of saralasin closely correlates with the value of circulating plasma renin activity, apparently independent of the aetiology of the hypertension. The decrease in ERPF during saralasin infusion in the patients on normal sodium intake seems mainly related to the agonistic activity of saralasin, but that after sodium depletion to the hypotensive effect of saralasin.

Effect of age on plasma aldosterone response to exogenous angiotensin II in normotensive subjects

1980 ◽  
Vol 94 (4) ◽  
pp. 552-558 ◽  
Author(s):  
Ryoyu Takeda ◽  
Shinpei Morimoto ◽  
Kenzo Uchida ◽  
Isamu Miyamori ◽  
Tetsuji Hashiba
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Sodium Intake ◽  
Plasma Renin ◽  
The Elderly ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Middle Aged ◽  
Basal Plasma ◽  
Normotensive Subjects

Abstract. The plasma aldosterone response to angiotensin II (10 ng/kg/min for 30 min, iv) under conditions of varied sodium intake was studied in 10 young subjects (20 to 35 years), 9 middle-aged (41 to 56 years) and 11 elderly (66 to 73 years) normotensive subjects. Basal plasma renin activity, basal plasma level and urinary excretion of aldosterone were significantly lower in the elderly than in the young and middle-aged groups on both 130 and 25 mEq sodium intakes. When sodium intake was reduced to 25 mEq for 3 days, the weight loss was significantly greater in the elderly than in the young and middle-aged groups. No significant differences in blood pressure and serum electrolytes were found between the three groups. Angiotensin II infusion caused significant increases in the mean blood pressure in all the three groups, but to a greater extent in the elderly group. Plasma aldosterone level and its absolute increment, but not its per cent increment, after angiotensin II infusion were significantly lower in the elderly than in the young and middle-aged groups. In combined young, middleaged and elderly subjects, the absolute plasma aldosterone increment correlated positively with basal plasma aldosterone and plasma renin activity levels on a 25 mEq sodium intake, and with plasma renin response to sodium restriction. These results suggest that ageing may cause a lesser plasma aldosterone response to angiotensin II with a decrease in basal plasma aldosterone, in parallel with a decrease in plasma renin activity, under condition of low sodium diet.

Hormonal and renal responses to converting enzyme inhibition during maximal exercise

1987 ◽  
Vol 63 (5) ◽  
pp. 1796-1800 ◽  
Author(s):  
C. E. Wade ◽  
S. R. Ramee ◽  
M. M. Hunt ◽  
C. J. White
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Maximal Exercise ◽  
Plasma Renin ◽  
Renin Activity ◽  
Converting Enzyme ◽  
Renal Handling ◽  
Renal Responses ◽  
Captopril Treatment

The role of angiotensin II in the hormonal and renal responses to maximal exercise was investigated by using the angiotensin-converting enzyme inhibitor captopril. Nine male subjects performed a standardized maximal treadmill test with and without acute captopril treatment (25 mg orally). At rest, captopril elevated plasma renin activity and lowered aldosterone levels. With maximal exercise, captopril treatment reduced the increase in mean arterial blood pressure by 8 mmHg and the increase in plasma renin activity by 3.0 ng ANG I.ml-1.h-1. The responses of adrenocorticotropin (ACTH), cortisol, and vasopressin to maximal exercise were not altered by captopril treatment. Although aldosterone levels were reduced at rest with captopril, during maximal exercise no difference was noted between treatments. Captopril treatment had no effects on the renal handling of salts or water during exercise. In conclusion, angiotensin II plays a role in the increase in mean blood pressure during maximal exercise in normal subjects but has no effect on the exercise responses of ACTH, vasopressin, and aldosterone or on the renal handling of salts and water.

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