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.

Upregulation of renin-angiotensin system and downregulation of kallikrein in obstructive nephropathy

1993 ◽  
Vol 264 (5) ◽  
pp. F874-F881 ◽  
Author(s):  
S. S. el-Dahr ◽  
J. Gee ◽  
S. Dipp ◽  
B. G. Hanss ◽  
R. C. Vari ◽  
...  
Keyword(s):  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Obstructive Nephropathy ◽  
Mrna Levels ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Kininase Ii ◽  
Plasma Angiotensin ◽  
Renin Mrna

The purpose of this study was to delineate the effects of prolonged (1 and 5 wk) unilateral ureteral obstruction (UUO) on the intrarenal renin-angiotensin and kallikrein-kinin systems in the rat. Systolic blood pressure (SBP) and plasma angiotensin (ANG) II levels were significantly higher at 1 and 5 wk of obstruction than in sham-operated groups. Also, plasma renin activity and ANG I levels were elevated at 1 wk (P < 0.05), and plasma angiotensin-converting enzyme (ACE)-kininase II activity was elevated at 5 wk (P < 0.05). Blockade of ANG II receptors with losartan (Dup 753) prevented the rise in SBP after UUO and normalized SBP in chronically hypertensive UUO rats. Renin mRNA levels and ANG II content were elevated in the obstructed kidneys at 1 and 5 wk compared with sham-operated kidneys (P < 0.05). ACE-kininase II activity was elevated in both the obstructed and contralateral kidneys at 5 wk compared with sham-operated kidneys (P < 0.05). In marked contrast to renin, total immunoreactive kallikrein contents and tissue kallikrein mRNA levels in the obstructed kidneys were reduced to 25% of sham-operated kidneys both at 1 and 5 wk (P < 0.001). The results indicate that urinary obstruction activates renin and suppresses kallikrein gene expression. Activation of ACE-kininase II by UUO also serves to enhance intrarenal ANG II generation and kinin degradation. The results implicate ANG II overproduction and kinin deficiency in the pathogenesis of UUO-induced hypertension and intrarenal vasoconstriction.

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.

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.

Studies on the Renin-Angiotensin System in a Kininogen-Deficient Individual

1983 ◽  
Vol 65 (2) ◽  
pp. 121-126 ◽  
Author(s):  
Patrick Y. Wong ◽  
Gordon H. Williams ◽  
Robert W. Colman
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Activity ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Normal Individuals

1. The physiological responses of the renin-angiotensin system were studied in an individual with kininogen deficiency (patient 1) with absent plasma bradykinin and markedly impaired prekallikrein conversion into kallikrein. After sodium depletion, patient 1 had a low plasma renin activity (1.4 pmol of ANG I h−1 ml−1) and a low angiotensin II concentration (36 pg/ml) compared with values in 11 normal individuals (4.0 ± 0.94 pmol of ANG I h−1 ml−1) and 63 ±6 pg/ml respectively). 2. Unlike normal individuals, in the kininogen-deficient subject there was no significant fall of renin activity or angiotensin II after dietary sodium repletion. Intravenous sodium repletion also failed to further decrease plasma renin activity or angiotensin II. 3. The usual two- to three-fold rise in plasma renin activity and angiotensin II observed in normal subjects on assumption of the upright posture after ingestion of 200 mg of sodium/day failed to occur in the kininogen-deficient individual. 4. These data in vivo are in agreement with observations in vitro that once plasma kallikrein forms it may be important in converting prorenin into renin. In the absence of kininogen, activation of prekallikrein to kallikrein is grossly defective, which may in part account for the diminished response of the renin-angiotensin system to changes in sodium balance and posture.

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.

What Stimulates the Renin—Angiotensin System in Rats with two-Kidney Renal Hypertension?

1983 ◽  
Vol 64 (5) ◽  
pp. 463-470
Author(s):  
Y. Takata ◽  
A. E. Doyle ◽  
M. Veroni ◽  
S. G. Duffy
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Activity ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Contralateral Kidney ◽  
The One ◽  
Renin Content

1. Blood pressure, the hypotensive effect of captopril, plasma renin activity, renal renin content and kidney weight were measured in the two-kidney—one-clip model, the one-kidney—one-clip model and the two-kidney—one-clip model with the ureter of the contralateral kidney ligated in rats. The ureteric ligation was performed to abolish urinary excretion from the contralateral kidney in the two-kidney—one-clip model. 2. The development of hypertension after renal artery constriction was earlier and greater in the one-kidney—one-clip model and the two-kidney—one-clip model with ureter of the contralateral kidney ligated than in the two-kidney—one-clip model. A single oral dose of captopril produced a greater fall in blood pressure in both the two-kidney models than in the one-kidney—one-clip group. 3. Plasma renin activity and renal renin content of the clipped kidney were higher in the two-kidney model rats, whether or not the ureter had been ligated, than in the one-kidney—one-clip model animals, although more than half the rats from the two-kidney model had normal values. There was a significant correlation between plasma renin activity and the response to captopril in all groups, whereas in none of the three groups was the correlation between plasma renin activity and blood pressure significant. 4. The clipped kidney had a higher renin content than did the contralateral kidney, and the weight of the ischaemic kidney was decreased compared with the contralateral kidney whether it was untouched or had its ureter ligated. The weight of the clipped kidney was in the order one-kidney—one-clip model > two-kidney—one-clip model with ureter of the contralateral kidney ligated > two-kidney—one-clip model. 5. It was concluded that the renin-angiotensin system was stimulated to the similar degree in some animals for the two-kidney—one-clip models, whether or not the ureter of the contralateral kidney had been ligated, compared with the one-kidney—one-clip animals. This finding suggests that the contralateral kidney can stimulate renin secretion and synthesis in the clipped kidney independently of Na+ excretion.

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.

Plasma renin activity and forearm blood flow in paraplegic humans

1985 ◽  
Vol 59 (3) ◽  
pp. 924-927 ◽  
Author(s):  
P. R. Freund ◽  
G. L. Brengelmann
Keyword(s):  
Blood Flow ◽  
Plasma Renin Activity ◽  
Forearm Blood Flow ◽  
Control Period ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
The Body ◽  
Renin Activity ◽  
Angiotensin System ◽  
Renin Angiotensin

We recently found that paraplegic humans respond to hyperthermia with subnormal increase in skin blood flow (SkBF), based on measurements of forearm blood flow (FBF). Is this inhibition of SkBF a defect in thermoregulation or a cardiovascular adjustment necessary for blood pressure control? Since high resting plasma renin activity (PRA) is found in unstressed individuals with spinal cord lesions and since PRA increases during hyperthermia in normal humans, we inquired whether the renin-angiotensin system is responsible for the attenuated FBF in hyperthermic resting paraplegics. Five subjects, 28–47 yr, with spinal transections (T1-T10), were heated in water-perfused suits. Blood samples for PRA determinations were collected during a control period and after internal temperature reached approximately 38 degrees C. Some subjects with markedly attenuated FBF had little or no elevation of PRA; those with the best-developed FBF response exhibited the highest PRA. Clearly, circulating angiotensin is not the agent that attenuates SkBF. Rather, increased activity of the renin-angiotensin system may be a favorable adaptation that counters the locally mediated SkBF increase in the lower body and thus allows controlled active vasodilation in the part of the body subject to centrally integrated sympathetic effector outflow.

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