scholarly journals Angiotensin (1–12) in Humans With Normal Blood Pressure and Primary Hypertension

Hypertension ◽  
2021 ◽  
Vol 77 (3) ◽  
pp. 882-890
Author(s):  
Carlos M. Ferrario ◽  
Seethalakshmi R. Iyer ◽  
John C. Burnett ◽  
Sarfaraz Ahmad ◽  
Kendra N. Wright ◽  
...  
Keyword(s):  
Plasma Concentrations ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Potential Contribution ◽  
Ang Ii ◽  
Women Patients ◽  
Normal Blood Pressure ◽  
Angiotensin Ii Receptor ◽  
Normotensive Subjects ◽  
First Time

The importance of canonical versus noncanonical mechanisms for the generation of angiotensins remains a major challenge that, in part, is heavily swayed by the relative efficacy of therapies designed to inhibit renin, ACE (angiotensin-converting enzyme), or the Ang II (Angiotensin II) receptor. Ang (1–12) (angiotensin [1-12]) is an Ang II forming substrate serving as a source for Ang II–mediated tissue actions. This study identifies for the first time the presence of Ang (1–12) in the blood of 52 normal (22 women) and 19 (13 women) patients with hypertension not receiving antihypertensive medication at the time of the study. Normal subjects of comparable ages and body habitus had similar circulating plasma Ang (1–12) concentrations (women: 2.02±0.62 [SD] ng/mL; men 2.05±0.55 [SD] ng/mL, P >0.05). The higher values of plasma Ang (1–12) concentrations in hypertensive men (2.51±0.49 ng/mL, n=6) and women (2.33±0.63 [SD] ng/mL, n=13) were statistically significant ( P <0.02) and correlated with elevated plasma renin activity, systolic and pulse pressure, and plasma concentrations of NT-proBNP (N-terminal prohormone BNP). The increased plasma Ang (1–12) in patients with hypertension was not mirrored by similar changes in plasma angiotensinogen and Ang II concentrations. The first identification of an age-independent presence of Ang (1–12) in the blood of normotensive subjects and patients with hypertension, irrespective of sex, implicates this non-renin dependent substrate as a source for Ang II production in the blood and its potential contribution to the hypertensive process.

Factors associated with vasopressin release in exercising swine

1994 ◽  
Vol 266 (1) ◽  
pp. R118-R124 ◽  
Author(s):  
C. L. Stebbins ◽  
J. D. Symons ◽  
M. D. McKirnan ◽  
F. F. Hwang
Keyword(s):  
Plasma Volume ◽  
Plasma Concentrations ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
Treadmill Running ◽  
Maximal Heart Rate ◽  
Ang Ii ◽  
Strong Correlations ◽  
Vasopressin Release ◽  
Lysine Vasopressin

This study examined the effect of dynamic exercise on vasopressin release in the miniswine and factors that may elicit this response (n = 15). Thus lysine vasopressin (LVP), the catecholamines epinephrine and norepinephrine (EPI and NE), plasma renin activity (PRA), and plasma volume, Na+, and osmolality were measured before and during treadmill running at work intensities of 60, 80, and 100% of each swine's maximal heart rate reserve (HRR). LVP increased in a progressive manner similar to that of humans, ranging from 5.9 +/- 0.4 pg/ml before exercise to 30.1 +/- 4.5 pg/ml during maximal exercise. EPI, NE, and PRA [an index of angiotensin II (ANG II) activity] demonstrated a pattern of response comparable to LVP. Although these hormones can influence the release of LVP, only PRA displayed a strong correlation with LVP (r = 0.84). When ANG II synthesis was blocked (captopril, 1-3 mg/kg, intra-atrial injection) during exercise (80% HRR), plasma LVP was reduced from 9.9 +/- 0.6 to 7.5 +/- 0.6 pg/ml (P < 0.05). In addition, moderate-to-strong correlations were found between plasma concentrations of LVP and plasma osmolality (r = 0.79) and body temperature (r = 0.78). Plasma LVP also correlated with decreases in plasma volume (r = 0.84). These data suggest that the miniswine model is a good one for studying vasopressin effects during exercise and that ANG II appears to be a particularly strong stimulus for the release of this hormone.

scholarly journals Analysis of free and protein-bound nitrotyrosine in human plasma by a gas chromatography/mass spectrometry method that avoids nitration artifacts

2000 ◽  
Vol 345 (3) ◽  
pp. 453-458 ◽  
Author(s):  
Matthew T. FROST ◽  
Barry HALLIWELL ◽  
Kevin P. MOORE
Keyword(s):  
Reactive Nitrogen Species ◽  
Plasma Proteins ◽  
Biological Fluids ◽  
Plasma Concentrations ◽  
Normal Subjects ◽  
Gas Chromatography Mass Spectrometry ◽  
Highly Sensitive ◽  
Acidic Conditions ◽  
First Time

Measurement of nitrotyrosine in biological fluids and tissues is increasingly being used to monitor the production of reactive nitrogen species in vivo. The detection of nitrotyrosine in vivo has been reported with the use of a variety of methods including immunoassay, HPLC and GLC/MS. The validity of HPLC and immunoassays have been questioned with regard to their selectivity and sensitivity limits. In principle, the measurement of nitrotyrosine by GLC/MS permits a highly specific, highly sensitive and fully quantitative assay. The nitration of tyrosine under acidic conditions in the presence of nitrite is well documented. Derivatization for the full quantification of nitrotyrosine by using GLC/MS can lead to the artifactual nitration of tyrosine if performed under acidic conditions in the presence of nitrite. We describe a novel alkaline method for the hydrolysis and derivatization of nitrotyrosine and tyrosine, and demonstrate its applicability to the measurement of plasma concentrations of both free and protein-bound nitrotyrosine and tyrosine. A detection limit of 1 pg for nitrotyrosine and 100 pg for tyrosine has been achieved. Our method allows, for the first time, the analysis of free and protein-bound nitrotyrosine and tyrosine in biological samples. The plasma concentrations (means±S.E.M.) of free tyrosine and nitrotyrosine in eight normal subjects were 12±0.6 μg/ml and 14±0.7 ng/ml respectively. Plasma proteins contained tyrosine and nitrotyrosine at 60.7±1.7 μg/mg and 2.7±0.4 ng/mg respectively.

scholarly journals Effects of truncated angiotensins in humans after double blockade of the renin system

2003 ◽  
Vol 285 (5) ◽  
pp. R981-R991 ◽  
Author(s):  
Ronni R. Plovsing ◽  
Christian Wamberg ◽  
Niels C. F. Sandgaard ◽  
Jane A. Simonsen ◽  
Niels-Henrik Holstein-Rathlou ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Biological Activities ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Urinary Concentration ◽  
Ang Ii ◽  
Ang Iv

Angiotensins different from ANG II exhibit biological activities, possibly mediated via receptors other than ANG II receptors. We studied the effects of 3-h infusions of ANG III, ANG-(1-7), and ANG IV in doses equimolar to physiological amounts of ANG II (3 pmol · kg-1 · min-1), in six men on low-sodium diet (30 mmol/day). The subjects were acutely pretreated with canrenoate and captopril to inhibit aldosterone actions and ANG II synthesis, respectively. ANG II infusion increased plasma angiotensin immunoreactivity to 53 ± 6 pg/ml (+490%), plasma aldosterone to 342 ± 38 pg/ml (+109%), and blood pressure by 27%. Glomerular filtration rate decreased by 16%. Concomitantly, clearance of endogenous lithium fell by 66%, and fractional proximal reabsorption of sodium increased from 77 to 92%; absolute proximal reabsorption rate of sodium remained constant. ANG II decreased sodium excretion by 70%, potassium excretion by 50%, and urine flow by 80%, whereas urine osmolality increased. ANG III also increased plasma aldosterone markedly (+45%), however, without measurable changes in angiotensin immunoreactivity, glomerular filtration rate, or renal excretion rates. During vehicle infusion, plasma renin activity decreased markedly (∼700 to ∼200 mIU/l); only ANG II enhanced this decrease. ANG-(1-7) and ANG IV did not change any of the measured variables persistently. It is concluded that 1) ANG III and ANG IV are cleared much faster from plasma than ANG II, 2) ANG II causes hypofiltration, urinary concentration, and sodium and potassium retention at constant plasma concentrations of vasopressin and atrial natriuretic peptide, and 3) a very small increase in the concentration of ANG III, undetectable by usual techniques, may increase aldosterone secretion substantially.

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.

Dietary chloride modifies renin release in normal humans

1981 ◽  
Vol 241 (4) ◽  
pp. F361-F363 ◽  
Author(s):  
R. J. Koletsky ◽  
R. G. Dluhy ◽  
R. G. Cheron ◽  
G. H. Williams
Keyword(s):  
Sodium Intake ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Renin Release ◽  
Upright Posture ◽  
Ang Ii ◽  
Low Salt ◽  
Normal Humans ◽  
The Mean ◽  
Induced Changes

The effect of high and low chloride diets on the responses of plasma renin activity (PRA), angiotensin II (ANG II), and aldosterone (Aldo) to upright posture was studied in the same normal subjects in balance on constant sodium intake. Diet 1 consisted of 10 meq Na/day (low Na) and either 50 or 150 meq Cl/day. Diet 2 consisted of 200 meq Na/day (high Na) and either 20 or 200 meq Cl/day. The mean recumbent PRA level on the high Na-high Cl diet tended to be lower than on the high Na-low Cl diet but was not significantly different. However, the absolute peak upright PRA levels, 8.8 +/- 1.0 vs. 4.4 +/- 0.8 ng . ml-1 . h-1, and the incremental difference (delta PRA) between recumbent and peak upright PRA levels, 5.5 +/- 0.8 vs. 2.2 +/- 0.5 ng . ml-1 . h-1, were significantly less on the high Na-high Cl diet compared with the high Na-low Cl diet. Similar significant changes were seen in ANG II and Aldo levels. However, there were no significant changes in PRA, ANG II, and Aldo responses to upright posture on the low Na diet when the dietary Cl was varied. It is concluded that dietary Cl is another factor modifying renin release. However, Cl is probably less important than Na because Cl-induced changes in PRA were not seen in the low salt state.

Intralymphocytic Sodium in Hypertensive Patients: A Significant Correlation

1979 ◽  
Vol 57 (s5) ◽  
pp. 325s-327s ◽  
Author(s):  
E. Ambrosioni ◽  
F. Tartagni ◽  
L. Montebugnoli ◽  
B. Magnani
Keyword(s):  
Blood Pressure ◽  
Normal Subjects ◽  
Sodium Concentration ◽  
The Other ◽  
Mean Blood Pressure ◽  
Normal Blood ◽  
Normal Blood Pressure ◽  
Hypertensive Patients ◽  
Normotensive Subjects

1. Intralymphocytic sodium concentration was measured in 50 patients with essential stable hypertension, 44 patients with labile hypertension and 40 subjects with normal blood pressure. 2. Intralymphocytic sodium concentration in normotensive subjects was significantly lower than in the other two groups. 3. The concentration was significantly correlated with mean blood pressure in the group as a whole and in the groups with stable and with labile hypertension. No correlation was found in normal subjects.

Reduced number of angiotensin II receptors on platelets in insulin-dependent diabetes

1986 ◽  
Vol 71 (2) ◽  
pp. 217-220 ◽  
Author(s):  
J. M. C. Connell ◽  
Yu-An Ding ◽  
B. M. Fisher ◽  
B. M. Frier ◽  
P. F. Semple
Keyword(s):  
Angiotensin Ii ◽  
Type I Diabetes ◽  
Plasma Concentrations ◽  
Normal Subjects ◽  
Insulin Dependent Diabetes ◽  
Angiotensin Ii Receptors ◽  
Diabetic Patients ◽  
Type I ◽  
Angiotensin Ii Receptor ◽  
Insulin Dependent

1. Angiotensin II receptors on platelets were studied in 13 patients with uncomplicated type I diabetes mellitus and in 15 age-matched normal subjects. 2. Receptor density on cells from the diabetic patients was 15% lower than the normal subjects (5.2 ± 0.8 sd sites/platelet in diabetic patients and 6.4 ± 0.8 in normals, P < 0.001), but there were no differences in receptor affinity as measured by Kd (4.9 ± 1.5 × 10−10 mol/l in diabetic patients and 5.4 ± 1.4 × 10−10 mol/l in normals). 3. Plasma concentrations of renin and angiotensin II were similar in both groups. 4. The reduced density of angiotensin II receptors on platelets from patients with insulin-dependent diabetes may reflect a generalized abnormality of angiotensin II receptor regulation.

Atrial natriuretic peptide: Evidence of action as a natriuretic hormone at physiological plasma concentrations in man

1987 ◽  
Vol 72 (3) ◽  
pp. 305-312 ◽  
Author(s):  
J. V. Anderson ◽  
J. Donckier ◽  
N. N. Payne ◽  
J. Beacham ◽  
J. D. H. Slater ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Natriuretic Hormone ◽  
Plasma Aldosterone Concentration ◽  
Water Excretion ◽  
Physiological Range ◽  
Atrial Natriuretic

1. The administration of exogenous atrial natriuretic peptide (ANP) causes a natriuresis and diuresis in man, but this has, to date, only been demonstrated at plasma ANP concentrations within the high pathological or pharmacological ranges. Evidence that ANP acts physiologically requires the demonstration of a natriuretic effect when it is infused to recreate plasma concentrations similar to those observed after physiological stimuli. 2. We infused human α-ANP (1–28) at a calculated rate of 1.2 pmol min−1 kg−1 for 3 h into seven water-loaded normal subjects, achieving plasma ANP concentrations within the upper part of the physiological range. The subjects' resting plasma ANP concentration increased from 3.8 ± 1.5 to 20.9 ± 1.9 pmol/l. 3. The infusion of ANP caused a 60% increase of mean urinary sodium excretion from 111 ± 18 to 182 ± 30 μmol/min (P < 0.001) and a 28% increase of mean water excretion from 10.8 ± 0.8 to 13.8 ± 1.6 ml/min (P < 0.01). 4. The infusion suppressed mean plasma renin activity from 1.55 ± 0.10 to 1.17 ± 0.06 pmol of ANG I h−1 ml−1 (P < 0.001). Mean plasma aldosterone concentration (242 ± 16 basally and 215 ± 15 pmol/l at the end of ANP infusion) did not change significantly. Pulse rate and blood pressure were unchanged throughout the study. 5. No significant change in any of the variables mentioned above occurred during the infusion of the vehicle alone on a separate study day. 6. The demonstration that recreation of plasma concentrations of ANP within the physiological range by intravenous infusion induces a natriuresis provides new evidence supporting the role of ANP as a natriuretic hormone.

Stimulation of the renin-angiotensin system by growth hormone in Lewis dwarf rats

1993 ◽  
Vol 265 (2) ◽  
pp. E332-E339 ◽  
Author(s):  
B. Wyse ◽  
M. Waters ◽  
C. Sernia
Keyword(s):  
Growth Hormone ◽  
Plasma Concentrations ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin Ii Receptor ◽  
Gh Treatment ◽  
Angiotensin System ◽  
Lewis Rats ◽  
Renin Angiotensin ◽  
Igf I

A genetically growth hormone (GH)-deficient strain of Lewis rats was used to test the hypothesis that the actions of GH on electrolyte and fluid homeostasis are mediated by the renin-angiotensin-aldosterone system (RAAS). Dwarf rats injected with recombinant bGH (2 mg.kg-1 x day-1) for 7 days (group GH1+) and 28 days (group GH4+), respectively, were compared with saline-injected dwarf (group GH-) and normal (group N) Lewis rats. GH decreased Na+ excretion and increased renal glomerular filtration rate in dwarf rats. The dietary intake and plasma concentrations of Na+ and K+ remained unchanged. GH increased plasma insulin-like growth factor I (IGF-I) concentrations in dwarf rats (GH - = 109 +/- 9, GH1+ = 184 +/- 5, GH4+ = 189 +/- 28, N = 477 +/- 29 ng/ml plasma). Plasma angiotensinogen increased towards the levels found in normal Lewis rats (GH- = 859 +/- 38, GH1+ = 906 +/- 18, GH4+ = 1,027 +/- 19, N = 1497 +/- 80 ng angiotensin I/ml plasma); plasma renin activity increased above that of the normal Lewis (GH- = 10.2 +/- 0.6, GH1+ = 11.7 +/- 0.7, GH4+ = 16.7 +/- 2.4, N = 10.6 +/- 0.8 ng angiotensin I.ml plasma-1 x h-1). Plasma aldosterone, corticosterone, and triodothyronine concentrations were unchanged by GH treatment. Angiotensin II receptor densities in GH- rats (liver = 356 +/- 23, kidney = 228 +/- 28, adrenal = 478 +/- 58 fmol/mg protein) were upregulated by GH (GH4+ rats; liver = 573 +/- 27, kidney = 360 +/- 86, adrenal = 721 +/- 78 fmol/mg protein).(ABSTRACT TRUNCATED AT 250 WORDS)

Biochemical Correlates of the Increase in Blood Pressure with Age

1978 ◽  
Vol 55 (s4) ◽  
pp. 377s-379s ◽  
Author(s):  
C. E. Grim ◽  
M. H. Weinberger ◽  
D. P. Henry ◽  
F. C. Luft ◽  
N. S. Fineberg
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Renin Activity ◽  
Multiple Correlation Analysis ◽  
Normotensive Subjects ◽  
Relationship Of ◽  
The Relationship

1. Blood pressure, plasma renin activity, plasma aldosterone, urinary noradrenaline during sleep (UNA-S) and several estimates of sodium intake were determined in 379 normotensive subjects (age 13–70) to investigate the relationship of these variables to blood pressure. 2. Blood pressure was correlated with age, weight, plasma renin activity UNA-S, and estimates of sodium intake. These variables were frequently intercorrelated. 3. Multiple-correlation analysis revealed that after removal of the effects of age, blood pressure was related to weight, plasma renin activity, UNA-S and estimates of sodium intake. 4. However, multiple-regression analysis failed to demonstrate an effect of plasma renin activity, UNA-S, or estimates of sodium intake on blood pressure when the effects of age, weight, race and sex were removed. 5. Careful matching of subjects by age, weight, race and sex in studies of blood pressure and biochemical factors in normal subjects is crucial to proper interpretation of such data.

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