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.

scholarly journals Local renin-angiotensin system contributes to hyperthyroidism-induced cardiac hypertrophy

1999 ◽  
Vol 160 (1) ◽  
pp. 43-47 ◽  
Author(s):  
H Kobori ◽  
A Ichihara ◽  
Y Miyashita ◽  
M Hayashi ◽  
T Saruta
Keyword(s):  
Angiotensin Ii ◽  
Thyroid Hormone ◽  
Cardiac Hypertrophy ◽  
Plasma Renin Activity ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Plasma Angiotensin ◽  
Renin Mrna

We have reported previously that thyroid hormone activates the circulating and tissue renin-angiotensin systems without involving the sympathetic nervous system, which contributes to cardiac hypertrophy in hyperthyroidism. This study examined whether the circulating or tissue renin-angiotensin system plays the principal role in hyperthyroidism-induced cardiac hypertrophy. The circulating renin-angiotensin system in Sprague-Dawley rats was fixed by chronic angiotensin II infusion (40 ng/min, 28 days) via mini-osmotic pumps. Daily i.p. injection of thyroxine (0.1 mg/kg per day, 28 days) was used to mimic hyperthyroidism. Serum free tri-iodothyronine, plasma renin activity, plasma angiotensin II, cardiac renin and cardiac angiotensin II were measured with RIAs. The cardiac expression of renin mRNA was evaluated by semiquantitative reverse transcriptase-polymerase chain reaction. Plasma renin activity and plasma angiotensin II were kept constant in the angiotensin II and angiotensin II+thyroxine groups (0.12+/-0.03 and 0.15+/-0.03 microgram/h per liter, 126+/-5 and 130+/-5 ng/l respectively) (means+/-s.e.m.). Despite stabilization of the circulating renin-angiotensin system, thyroid hormone induced cardiac hypertrophy (5.0+/-0.5 vs 3.5+/-0.1 mg/g) in conjunction with the increases in cardiac expression of renin mRNA, cardiac renin and cardiac angiotensin II (74+/-2 vs 48+/-2%, 6.5+/-0.8 vs 3.8+/-0.4 ng/h per g, 231+/-30 vs 149+/-2 pg/g respectively). These results indicate that the local renin-angiotensin system plays the primary role in the development of hyperthyroidism-induced cardiac hypertrophy.

Effect of methylprednisolone upon arterial pressure and the renin angiotensin system in the rat

1975 ◽  
Vol 228 (2) ◽  
pp. 613-617 ◽  
Author(s):  
LR Krakoff ◽  
R Selvadurai ◽  
E Sutter
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Substrate ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Significant Fall ◽  
Arterial Blood ◽  
Methylprednisolone Treatment

The effect of methylprednisolone or deoxycorticosterone upon systemic arterial blood pressure and components of the renin-angiotensin system was studied in the rat. Rats maintained on regular diets given methylprednisolone suspension 20 mg/kg body wt demonstrated a significant increase in arterial pressure of + 37 plus or minus 5 mmHg, mean plus or minus SE, over a 2-wk period, whereas those treated with DOC and untreated controls showed no significant change. On normal diets, plasma renin concentration (PRC) of methylprednisolone-treated rats was significantly higher than that of DOC-treated rats. Methylprednisolone treatment also resulted in a significant elevation of plasma renin substrate concentration (PRS). Calculated plasma renin activity (PRA) was highest in methylprednisolone-treated rats, significantly above that of the DOC and no-steroid groups. NaCl supplementation resulted in a significant fall in PRC and PRA in all three groups; however, PRS remained significantly above normal in the methylprednisolone-treated rats. The pressor effect of angiotensin II was slightly increased in methylprednisolone-treated rats. Infusion of [Sar1,Ala8]angiotensin II (P-113) in methylprednisolone-treated rats resulted in a significant fall in diastolic arterial pressure. The results imply that methylprednisolone hypertension in the rat may be in part angiotensin dependent.

ANG II prolongs splanchnic nerve-mediated inhibition of duodenal mucosal alkaline secretion in the rat

1997 ◽  
Vol 273 (3) ◽  
pp. R942-R946 ◽  
Author(s):  
B. Johansson ◽  
M. Holm ◽  
L. Chen ◽  
A. Pettersson ◽  
C. Jonson ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Control Level ◽  
Renin Angiotensin System ◽  
Splanchnic Nerve ◽  
Total Blood ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Alkaline Secretion

Hypovolemia inhibits duodenal mucosal alkaline (HCO-3) secretion by activation of sympathoadrenergic nerves. A possible involvement of the renin-angiotensin system was investigated. Experiments were performed on chloralose-anesthetized rats. The mucosal alkaline output by a duodenal segment was measured using in situ pH-stat titration equipment. A modest hypovolemia was induced by bleeding the animals approximately 10% of the total blood volume. This procedure decreased duodenal mucosal alkaline secretion to a sustained level of approximately 50% of baseline and reduced mean arterial pressure by approximately 20 mmHg. Intravenous pretreatment with the angiotensin-converting enzyme (ACE) inhibitor enalaprilate (0.7 mg/kg) or the angiotensin II-receptor antagonist losartan (10 mg/kg) altered the response to hypovolemia to a transient one, and alkaline secretion returned to the control level within 40-50 min. When exogenous angiotensin II was administered intravenously (0.25 and 0.75 microgram.kg-1.h-1), a hypovolemia-induced sustained depression of the secretion was observed even during ACE inhibition. Direct electrical stimulation (3 Hz, 5 V, 5 ms, bilaterally) of the peripheral splanchnic nerves decreased duodenal mucosal alkaline secretion to approximately 60% of the control level and increased mean arterial pressure by approximately 20 mmHg. However, in enalaprilate-pretreated animals, the inhibition of alkaline secretion due to splanchnic nerve stimulation was transient, a response that became sustained on angiotensin II substitution. These results suggest that the renin-angiotensin system prolongs the sympathoadrenergic inhibition of duodenal mucosal alkaline secretion and that angiotensin II, in this regard, acts mainly on the peripheral sympathetic efferents.

The response of the Renin-Angiotensin System in Rats to the Injection of Angiotensin II Antibodies

1974 ◽  
Vol 48 (s2) ◽  
pp. 27s-30s
Author(s):  
E. Hackenthal ◽  
H. Bauknecht ◽  
P. Oster
Keyword(s):  
Angiotensin Ii ◽  
Binding Capacity ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Distribution Volume ◽  
Antibody Concentration ◽  
Half Time ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Plasma Angiotensin

1. Antibodies against angiotensin II were purified by affinity chromatography. 2. When injected intravenously into rats, the antibody distributed in the extracellular space with a half-time of 11 h and a distribution volume of about 10 ml/100 g body weight. The antibody was eliminated with a half-time of 7 days. 3. Plasma angiotensin II concentrations increased about 100-fold the control values 7 min after antibody injection and declined in parallel with the antibody concentration. It was calculated that only about 1–4% of the binding capacity of the antibody was occupied by angiotensin throughout the experiment. 4. Since the plasma renin concentration was normal, except during the short initial phase of stimulation, it is concluded that upon antibody injection the renin-angiotensin system rapidly, reached an equilibrium, with concentrations of free angiotensin close to or identical with normal concentrations.

Investigation of the Mechanism of β2-Agonist-Induced Activation of the Renin—Angiotensin System

1995 ◽  
Vol 88 (4) ◽  
pp. 433-437 ◽  
Author(s):  
Evelyn A. Millar ◽  
Gordon T. McInnes ◽  
Neil C. Thomson
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Serum Potassium ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Serum Angiotensin Converting Enzyme ◽  
Renin Angiotensin ◽  
Plasma Angiotensin

1. We have previously described activation of the renin—angiotensin system in asthma, and also by high-dose nebulized β2-agonists. In this study we sought to determine the mechanism responsible. 2. The influence of the angiotensin-converting enzyme inhibitor, lisinopril, on the response of the renin—angiotensin system and serum potassium to nebulized salbutamol was investigated in a randomized, double-blind, crossover study in eight healthy volunteers using a factorial block design. On study days, subjects received lisinopril 20 mg orally or identical placebo tablets followed 3 h later by nebulized salbutamol or placebo inhalation; plasma renin, angiotensin II, serum angiotensin-converting enzyme and potassium were measured at intervals for 120 min after inhalation. 3. Following salbutamol, plasma renin and angiotensin II concentrations were increased significantly compared with placebo [mean (SEM) plasma renin of 61.7 (15.6) μ-units/ml and angiotensin II of 17.7 (5.4) pg/mol 15 min after salbutamol, P < 0.05 versus placebo]. Baseline plasma renin concentrations were increased [160.1 (20.6) μ-units/ml] and baseline plasma angiotensin II concentrations were reduced [1.4 (0.1) pg/ml] by lisinopril, P < 0.05 versus placebo in each case. Inhibition of angiotensin-converting enzyme completely inhibited this salbutamol-induced rise in plasma angiotensin II [mean (SEM) plasma angiotensin II of 1.5 (0.4) pg/ml 15 min after salbutamol, P < 0.05 versus placebo] but had no effect on the changes in plasma renin concentrations after the β2-agonist [mean (SEM) plasma renin of 198.4 (18.9) μ-units/ml 15 min after salbutamol]. 4. Serum angiotensin-converting enzyme concentrations tended to increase throughout the study period following salbutamol compared with placebo, although this difference was not statistically significant. Lisinopril caused complete suppression of serum angiotensin-converting enzyme. 5. Salbutamol significantly reduced serum potassium concentrations [mean (SEM) baseline serum potassium of 4.26 (0.16) mmol/l decreasing to 3.08 (0.2) mmol/l at 45 min, P < 0.05 versus placebo]. Although lisinopril had no significant effect on serum potassium, the hypokalaemic response to salbutamol was significantly reduced in the presence of the angiotensin-convering enzyme inhibitor [mean (SEM) decrease in serum potassium of −1.2 (0.2) mmol/l compared with −0.8 (0.2) mmol/l, P < 0.05 versus placebo]. 6. Mean blood pressure was unaffected by active therapy. One subject experienced dizziness and headache after lisinopril. 7. The results of this study confirm that nebulized salbutamol causes activation of plasma renin and angiotensin II. Pretreatment with an angiotensin-converting enzyme inhibitor prevented the salbutamol-induced increase in plasma angiotensin II but not renin concentration. 8. We conclude that elevation of plasma angiotensin II induced by high-dose nebulized β2-agonists involves the classical components of the renin—angiotensin system including angiotensin-converting enzyme.

Plasma renin and angiotensin in dehydrated and rehydrated rats

1986 ◽  
Vol 250 (5) ◽  
pp. R898-R901 ◽  
Author(s):  
R. Di Nicolantonio ◽  
F. A. Mendelsohn
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Plasma Angiotensin

The role of the renin-angiotensin system in the stimulation and termination of dehydration-induced drinking was examined in the rat. Rats dehydrated for 48 h had significantly elevated renin, angiotensin II, plasma Na+ concentration, osmolality, and hematocrit when compared with replete controls. Although plasma Na+ concentration, osmolality, and hematocrit of dehydrated rats had returned to control replete levels by 2-4 h after the return of water, the plasma renin and angiotensin II levels exhibited a further increase on rehydration and remained significantly above dehydration levels for 2-4 h after the return of water. The levels of renin and angiotensin II in rehydrated rats were maintained at levels in excess of the dipsogenic threshold for circulating angiotensin II during the 8-h period after rehydration, indicating that termination of the drinking is not dependent on a reduction of circulating angiotensin II. Finally, rehydrated rats did not drink significantly more than replete controls in the 1- to 8-h postrehydration period despite plasma angiotensin II levels in excess of that of the dipsogenic threshold for angiotensin II, indicating that mechanisms exist which override the dipsogenic action of circulating angiotensin II.

Role of renin-angiotensin system in response to hemorrhage in fetal sheep

1981 ◽  
Vol 240 (6) ◽  
pp. H848-H854 ◽  
Author(s):  
H. S. Iwamoto ◽  
A. M. Rudolph
Keyword(s):  
Venous Blood ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Fetal Life ◽  
Fetal Sheep ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Plasma Angiotensin ◽  
Blood Pressures ◽  
Placental Blood

During fetal life, the autonomic nervous system is not fully mature, and it is likely that hormonal mechanisms play an important role in controlling cardiovascular function. In chronically instrumented fetal sheep, hemorrhage increased plasma renin activity and plasma angiotensin concentration significantly from 6.7 +/- 2.5 to 15.2 +/- 3.1 ng.ml-1.h-1 and from 74 +/- 19 to 182 +/- 43 pg/ml, respectively. Both mean arterial and venous blood pressures decreased initially from 45 to 35 Torr and from 3.5 to 2.5 Torr, respectively; then both returned to control values. Fetal heart rate decreased initially from 174 beats/min and then increased to 186 beats/min. To determine whether angiotensin had a role in mediating these responses to hemorrhage, we hemorrhaged a second group of fetuses before and during infusion of saralasin, a competitive antagonist of angiotensin. Hemorrhage during infusion of saralasin decreased heart rat from 170 to 145 beats/min and further decreased mean arterial pressure to 30 Torr. Cardiac output decreased from 436 +/- 25 to 368 +/- 30 ml.min-1.kg-1, and umbilical-placental blood flow decreased from 205 +/- 20 to 145 +/- 10 ml.min-1.kg-1. We conclude that the renin-angiotensin system plays a major role in the response to hemorrhage in fetal sheep.

Splanchnic vasoconstriction in heat-stressed men: role of renin-angiotensin system

1982 ◽  
Vol 52 (6) ◽  
pp. 1438-1443 ◽  
Author(s):  
P. Escourrou ◽  
P. R. Freund ◽  
L. B. Rowell ◽  
D. G. Johnson
Keyword(s):  
Heat Stress ◽  
Arterial Pressure ◽  
Nervous Activity ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Sympathetic Nervous Activity ◽  
Plasma Norepinephrine ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Norepinephrine Concentration

We conducted a two-part study to determine whether the renin-angiotensin system contributes to the rise in splanchnic vascular resistance (SVR) during heat stress (rectal temperature was raised 1 degree C). In experiment 1 (control) seven men on a normal salt diet were directly heated (water-perfused suits) for 40–50 min. Arterial pressure (85 Torr) was unchanged; plasma renin activity (PRA) rose from 102 to 239 ng angiotensin I.100 ml-1.3 h-1; and SVR increased 73% (from 63 to 109 units). Experiment 2 was a repetition of experiment 1 on the same subjects, except that propranolol (10 mg iv) was given at the onset of heating to block renin release. Propranolol attenuated the rise in heart rate and reduced mean arterial pressure from 82 to 72 Torr; it blocked the rise in PRA with heating in two subjects, reduced it in three, but increased it in two. Although changes in SVR paralleled those in PRA in three subjects, SVR still rose 60% (from 58 to 99 units) after PRA rise was blocked. In both experiments, plasma norepinephrine concentration rose indicating increased sympathetic nervous activity. During mild heat stress, increased PRA is not a major factor in the increase of SVR.

scholarly journals Sustained Dysregulation of the Plasma Renin-angiotensin System in Acute COVID-19

2021 ◽  
Author(s):  
Kevin Burns ◽  
Matthew Cheng ◽  
Todd Lee ◽  
Allison McGeer ◽  
David Sweet ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Clinical Trial Registration ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin ◽  
Plasma Angiotensin

Abstract SARS-CoV-2 enters cells by binding to angiotensin-converting enzyme 2 (ACE2), and COVID-19 infection may therefore induce changes in the renin-angiotensin system (RAS). To determine the effects of COVID-19 on plasma RAS components, we measured plasma ACE, ACE2, and angiotensins I, (1-7), and II in 46 adults with COVID-19 at hospital admission and on days 2, 4, 7 and 14, compared to 50 blood donors (controls). We compared survivors vs. non-survivors, males vs. females, ventilated vs. not ventilated, and angiotensin receptor blocker (ARB) and angiotensin-converting enzyme (ACE) inhibitor-exposed vs. not exposed. At admission, COVID-19 patients had higher plasma levels of ACE (p=0.012), ACE2 (p=0.001) and angiotensin-(1-7) (p<0.001) than controls. Plasma ACE and ACE2 remained elevated for 14 days in COVID-19 patients, while plasma angiotensin-(1-7) decreased after 7 days. In adjusted analyses, plasma ACE was higher in males vs. females (p=0.042), and plasma angiotensin I was significantly lower in ventilated vs. non-ventilated patients (p=0.001). In summary, plasma ACE and ACE2 are increased for at least 14 days in patients with COVID-19 infection. Angiotensin-(1-7) levels are also elevated, but decline after 7 days. The results indicate dysregulation of the RAS with COVID-19, with increased circulating ACE2 throughout the course of infection.Clinical Trial Registration: https://clinicaltrials.gov/ Unique Identifier: NCT04510623

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