Diagnostic Value of Plasma Renin Activity and Plasma Angiotensin II in Renovascular Hypertension : Prognosis and Treatment of Renal Hypertension

1. The renin-angiotensin and kinin-kallikrein systems of Dahl salt-sensitive and salt-resistant rats fed diets with different salt contents were analysed using biochemical and immunocytochemical techniques. 2. Blood pressure increased by 45% in salt-sensitive rats only, after 4 weeks on a high-salt diet. The plasma renin activity and plasma angiotensin II concentration remained at the same levels in salt-sensitive rats on the high-salt diet as on the normal salt diet, whereas the plasma renin activity and plasma angiotensin II concentration of salt-resistant rats fed the high-salt diet were lower. The plasma renin activity and the plasma angiotensin II concentration were elevated in both salt-resistant and salt-sensitive rats fed the salt-deficient diet but were much more elevated in salt-resistant than in salt-sensitive rats. 3. The kidney immunocytochemical data paralleled the data on plasma parameters. Salt-sensitive rats had fewer renin positive juxtaglomerular apparatuses than salt-resistant rats on the normal diet, and the increase on the sodium-deficient diet was also smaller in salt-sensitive rats. Salt-sensitive rats fed the high-salt diet and the standard diet had almost no angiotensin II immunoreactivity compared with the salt-resistant rats on the same diets. 4. The total renal kallikrein content of salt-sensitive rats was lower than that of salt-resistant rats on all three diets, as was the amount of kallikrein excreted in the urine on the standard and the high-salt diets. The differences resulted from a reduction in active kallikrein. The increase in kallikrein in salt-sensitive and salt-resistant rats on the salt-deficient diet was not significantly different. 5. There were similar changes in immunopositive kallikrein in the kidneys of salt-sensitive and salt-resistant rats with diet, with a large increase in kallikrein biosynthesis on the low-salt diet. The plasma concentration of high-molecular-mass kininogen was not significantly different in salt-sensitive and salt-resistant rats, but there was a significant increase in T-kininogen in salt-sensitive rats fed the high-salt diet. 6. In conclusion, the absence of decreases in the plasma renin activity and the plasma angiotensin II concentration in salt-sensitive rats fed the high-salt diet might partially explain the increase in blood pressure.

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Measurement of Plasma Renin Activity as a Valid Estimation of Plasma Angiotensin Status

Annals of Clinical Biochemistry International Journal of Laboratory Medicine ◽

10.1177/000456327801500160 ◽

1978 ◽

Vol 15 (1-6) ◽

pp. 250-252 ◽

Cited By ~ 2

Author(s):

J. E. Roulston ◽

G. A. Macgregor ◽

Theresa Adam ◽

Nirmala D. Markandu

Keyword(s):

Angiotensin Ii ◽

Plasma Renin Activity ◽

Plasma Renin ◽

Renin Activity ◽

Activity Measurement ◽

Plasma Samples ◽

Angiotensin I ◽

Plasma Angiotensin ◽

Rate Limiting

Measurement of plasma renin activity is widely used as an indirect assessment of plasma angiotensin II concentration. There has been some controversy over the validity of this assay as an estimate of circulating angiotensin II levels because, during the in vitro generation of angiotensin I by renin, over a period of time, substrate concentration may diminish to such an extent that it becomes rate-limiting, giving an artificially low reflection of angiotensin II levels. In this paper the initial angiotensin I concentration, that is the concentration before in vitro angiotensin I generation, has been compared with the corresponding plasma renin activity for 2752 individual plasma samples. A linear relationship was found between the initial angiotensin I concentration and the plasma renin activity below 60 ng ml−1 h−1. This indicates that, under the conditions of this assay, substrate does not appear to become rate-limiting except at exceedingly high levels of plasma renin activity. These results appear to provide further validation for the use of plasma renin activity measurement as a reflection of the concentration of circulating angiotensin II levels.

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Effect of aldosterone on vascular angiotensin II receptors in the rat

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y85-250 ◽

1985 ◽

Vol 63 (12) ◽

pp. 1522-1527 ◽

Cited By ~ 85

Author(s):

Ernesto L. Schiffrin ◽

Douglas J. Franks ◽

Jolanta Gutkowska

Keyword(s):

Angiotensin Ii ◽

Plasma Renin Activity ◽

Binding Sites ◽

Mesenteric Artery ◽

Plasma Renin ◽

Renin Activity ◽

Angiotensin Ii Receptors ◽

Rat Mesenteric Artery ◽

Plasma Angiotensin ◽

Dose Dependent Fashion

The effect of aldosterone on the density and affinity of binding sites for 125I-labelled angiotensin II was investigated in a particulate fraction prepared from the rat mesenteric arteriolar arcades. The infusion of aldosterone 6.6 μg/h intraperitoneally via Alzet osmotic minipumps for 6 d produced an increase in the density of binding sites for 125I-labelled angiotensin II without change in affinity. After sodium depletion, mesenteric artery angiotensin II receptors were down-regulated as expected. An increase in the number of binding sites could be found when aldosterone was infused into sodium-depleted rats with no change in the elevated plasma renin activity. The intraperitoneal infusion of angiotensin II (200 ng ∙ kg−1 ∙ min−1 for 6 d) simultaneously with aldosterone resulted in down-regulation of vascular angiotensin II receptors, whereas after intravenous angiotensin II infusion (at 60 ng ∙ kg−1 ∙ min−1) the density of angiotensin II binding sites rose with aldosterone infusion. Plasma renin activity (PRA) was reduced and plasma angiotensin II increased in a dose-dependent fashion after angiotensin II infusion. An aldosterone concentration of 3 ng/mL for 18 h produced an increase in the number of angiotensin II binding sites in rat mesenteric artery smooth muscle cells in culture. We conclude that increased plasma aldosterone may result in up-regulation of vascular angiotensin II receptors independently of changes in plasma renin activity, and may in certain physiological states effectively antagonize the down-regulating action of angiotensin II.

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Plasma Renin Activity, Plasma Angiotensin and Plasma and Urinary Electrolytes in Normal and Toxaemic Pregnancy, Including a Prospective Study

Clinical Science ◽

10.1042/cs0450115 ◽

1973 ◽

Vol 45 (1) ◽

pp. 115-127 ◽

Cited By ~ 21

Author(s):

R. D. Gordon ◽

E. M. Symonds ◽

E. G. Wilmshurst ◽

C. G. K. Pawsey

Keyword(s):

Angiotensin Ii ◽

Plasma Renin Activity ◽

Prospective Study ◽

Plasma Renin ◽

Late Pregnancy ◽

Normal Pregnancy ◽

Renin Activity ◽

Creatinine Ratio ◽

Plasma Angiotensin ◽

A Prospective Study

1. In a prospective study involving fifty-six women, measurements of body weight, urinary creatinine, sodium and potassium and plasma sodium, potassium and renin activity were made in mid-pregnancy and at 36 weeks. The effect of sodium restriction and sodium loading on these measurements was assessed in mid-pregnancy. 2. Mean plasma renin activity was significantly higher throughout pregnancy than the normal non-pregnant mean level. It was lower at 36 weeks than in mid-pregnancy in those whose pregnancy was normal but not in those who developed toxaemia of pregnancy between 38 and 40 weeks. In mid-pregnancy in both groups sodium depletion was significantly elevated but sodium loading did not significantly depress plasma renin activity. 3. The urinary potassium/creatinine ratio in mid-pregnancy and urinary sodium/creatinine ratio at 36 weeks were lower in those who subsequently developed toxaemia, raising the possibility of a functional renal lesion which antedates the morphologically recognizable lesion of late pregnancy. 4. In a second study involving sixty-six different women plasma angiotensin II levels between 6 and 40 weeks of pregnancy were mostly above the normal range, and highest levels were observed between 21 and 30 weeks. The plasma angiotensin II levels in six women with established toxaemia of pregnancy were not significantly different from the levels in nine women with normal pregnancy of the same duration. 5. While the renal glomerular lesion is presumably the major determinant in the development of toxaemia, the heightened activity of the renin-angiotensin-aldosterone system which is appropriate to normal pregnancy is an aggravating factor in established toxaemia, and may predispose to its development in some patients by failing to decline in late pregnancy.

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Kidney renin gene expression after renin inhibition in the marmoset

Clinical Science ◽

10.1042/cs0810387 ◽

1991 ◽

Vol 81 (3) ◽

pp. 387-392 ◽

Cited By ~ 7

Author(s):

Yutaka Kitami ◽

Kunio Hiwada ◽

Eiki Murakami ◽

Takeru Iwata ◽

Shinjiro Muneta ◽

...

Keyword(s):

Angiotensin Ii ◽

Oral Administration ◽

Plasma Renin Activity ◽

Plasma Renin ◽

Renin Activity ◽

Renin Inhibitor ◽

Renin Synthesis ◽

Mrna Content ◽

Plasma Angiotensin ◽

Renin Mrna

1. The effects of renin inhibitor ES-8891 on renin synthesis and its secretion by the kidney were investigated in normotensive sodium-depleted marmosets. We measured plasma renin activity, plasma immunoreactive renin concentration, plasma angiotensin II concentration and kidney renin mRNA content after oral administration of ES-8891 (60 mg day−1 kg−1) for 1 week. 2. The mean blood pressure was significantly decreased (P< 0.01) on day 7 after oral administration of ES-8891. There was no significant change in heart rate during the administration. 3. Oral administration of ES-8891 for 1 week markedly decreased the plasma renin activity, the plasma immunoreactive renin concentration and the plasma angiotensin II concentration (to 18%, 41% and 24% of the corresponding control values; P < 0.05 for each, n = 5). 4. The kidney renin mRNA content in ES-8891-treated marmosets was significantly lower than that in normal controls (4.2 ± 3.5 versus 12.8 ± 5.5 pg/μg of total RNA, means ± sd, P < 0.05, n = 5). 5. Oral administration of the renin inhibitor ES-8891 for 1 week not only inhibited plasma renin activity but also decreased renin synthesis and its secretion by the kidney.

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Renin, Blood Volume and Response to Saralasin in Patients on Chronic Haemodialysis: Evidence against Volume- and Renin-‘Dependent’ Hypertension

Clinical Science ◽

10.1042/cs0540305 ◽

1978 ◽

Vol 54 (3) ◽

pp. 305-312

Author(s):

B. P. McGrath ◽

J. G. G. Ledingham

Keyword(s):

Blood Pressure ◽

Angiotensin Ii ◽

Plasma Renin Activity ◽

Blood Volume ◽

Plasma Renin ◽

Renin Activity ◽

Mean Blood Pressure ◽

Dietary Sodium ◽

Chronic Haemodialysis ◽

Plasma Angiotensin

1. No significant relationship was found between blood pressure and blood volume, sulphate space or plasma angiotensin II concentration in 59 non-nephrectomized haemodialysis patients, of whom 42 were hypertensive. Supine mean blood pressure was only weakly correlated with plasma renin activity and the correlation was not improved when blood pressure was related to expressions combining renin and volume. 2. Changes in supine mean blood pressure during saralasin infusion were related to pre-infusion plasma renin activity (P < 0·001) or plasma angiotensin II (P < 0·02) but also to blood volume (P < 0·001) or sulphate space (P < 0·001). A fall of more than 10% in mean blood pressure during saralasin infusion was observed in only 12 patients (one normotensive), in five of whom there was evidence of volume depletion. 3. Thirteen patients (nine hypertensive) were studied at two levels of dietary sodium: 100 mmol/day and < 20 mmol/day. Supine mean blood pressure in hypertensive patients was lower during the period of higher salt intake despite increased volumes. 4. Hypertension in haemodialysis patients cannot be adequately explained by abnormalities either in volume homeostasis and/or in the renin—angiotensin system.

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