Plasma atriopeptin during exercise in dogs under beta-blockade

1989 ◽  
Vol 256 (5) ◽  
pp. R1098-R1102
Author(s):  
F. Peronnet ◽  
S. A. Adjoa ◽  
L. Beliveau ◽  
D. Bichet ◽  
R. Nadeau ◽  
...  
Keyword(s):  
Heart Rate ◽  
Plasma Renin Activity ◽  
Treadmill Exercise ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
Vasopressin Release ◽  
Angiotensin System ◽  
H 26

The purpose of this study was to describe plasma atriopeptin concentrations at rest and in response to moderate treadmill exercise (10 min, 4 km/h, 26% slope) performed with or without nonspecific beta-adrenergic blockade (1 mg/kg iv propranolol) in 10 mongrel dogs [19 +/- 2 (SE) kg]. A small (20%) but significant (P less than 0.05) increase in plasma atriopeptin concentration was observed from rest (43 +/- 5 pg/ml) to exercise (52 +/- 6 pg/ml) without beta-blockade. Propranolol significantly reduced heart rate at rest (89 +/- 7 vs. 104 +/- 7 beats/min) and during exercise (96 +/- 10 vs. 176 +/- 11 beats/min), and this was associated with a larger increase in plasma atriopeptin concentration during exercise (rest 46 +/- 6 pg/ml; exercise 171 +/- 22 pg/ml). Exercise under beta-blockade is associated with an increased preload of the heart. These results further support the hypothesis that atriopeptin release during exercise is under the control of atrial stretch. The higher plasma atriopeptin concentration observed during exercise under beta-blockade may contribute to the reduction of the response of plasma renin activity (1.0 +/- 0.1 vs. 3.0 +/- 0.6 ng.ml-1.h-1) and aldosterone concentration (87 +/- 36 vs. 138 +/- 25 pg/ml). Vasopressin concentration was lower at rest and during exercise under propranolol (3.5 +/- 1.3 vs. 4.9 +/- 0.9 and 6.1 +/- 2.2 vs. 9.9 +/- 1.5 pg/ml, respectively), which might reflect a dissociation between activity of the renin-angiotensin system and vasopressin release.

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.

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.

Dopaminergic Control of Aldosterone Secretion is Independent of the Renin—Angiotensin System in Rats

1980 ◽  
Vol 59 (s6) ◽  
pp. 101s-103s ◽  
Author(s):  
J. R. Sowers ◽  
M. L. Tuck ◽  
J. Barrett ◽  
M. P. Sambhi ◽  
M. S. Golub
Keyword(s):  
Plasma Renin Activity ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Dopamine Antagonist ◽  
Aldosterone Secretion ◽  
Angiotensin System ◽  
Renin Angiotensin

1. In rats, intra-arterial metoclopramide, a dopamine antagonist, resulted in an elevation of plasma aldosterone at 5 min and plasma renin activity at 10 min and peak aldosterone and renin responses at 10 and 30 min respectively. 2. Pre-administration of l-dopa blunted and delayed aldosterone and renin responses to metoclopramide, indicating that metoclopramide-induced plasma aldosterone and plasma renin activity increments are mediated by a direct effect of blockade of dopamine receptors rather than other effects of this drug. 3. Pre-administration of angiotensin converting enzyme inhibitor, captopril (SQ 14 225) and the angiotensin II antagonist, saralasin, as well as bilateral nephrectomy did not significantly affect the aldosterone response to metoclopramide, Thus dopaminergic modulation of aldosterone secretion occurs independently of alterations in the renin-angiotensin system. 4. Modulating effects of dopamine on plasma aldosterone are probably mediated by direct effects as well as by interaction with other factors influencing aldosterone secretion at the adrenal zona glomerulosa.

Urinary Prostaglandin E2 and Kallikrein Excretion in Glucocrticoid Hypertension in Rats

1983 ◽  
Vol 65 (1) ◽  
pp. 37-42 ◽  
Author(s):  
Michiko Handa ◽  
Kazuoki Kondo ◽  
Hiromichi Suzuki ◽  
Takao Saruta
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Prostaglandin E2 ◽  
Urine Volume ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Concurrent Administration ◽  
Angiotensin System

1. Oral administration of dexamethasone (about 2.5 × 10-7 mol/day) caused hypertension in rats. The blood pressure rose from 108 ± 6 (mean ± sd) to 156 ± 17 mmHg on the seventh day. The urine volume and urinary excretion of sodium were increased. The plasma renin activity and plasma aldosterone were unchanged. However, the urinary excretions of prostaglandin E2 (UPGE2V) and kallikrein (Ukall.V) were markedly decreased throughout the experiment. 2. With concurrent administration of captopril, the elevation of blood pressure was partially prevented. in this group of rats, the plasma renin activity was elevated and the reductions in UPGE2V and Ukall.V were partially prevented. 3. Based on these results, it is suggested that suppression of the kallikrein—kinin and prostaglandin systems, in addition to involvement of the renin-angiotensin system, is one of the factors contributing to the hypertensive action of dexamethasone.

Renin-angiotensin system in hypothyroid rats: effects of potassium iodide and triiodo-L-thyronine

1984 ◽  
Vol 105 (4) ◽  
pp. 505-510 ◽  
Author(s):  
E. Jiménez ◽  
M. Montiel ◽  
J. A. Narváez ◽  
M. Morell
Keyword(s):  
Plasma Renin Activity ◽  
Potassium Iodide ◽  
Renin Angiotensin System ◽  
Kinetic Studies ◽  
Plasma Renin ◽  
The Other ◽  
Renin Substrate ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Previously Treated

Abstract. Kinetic studies of the renin-angiotensin system (RAS) were carried out by measuring plasma renin activity (PRA), plasma renin concentration (PRC) and plasma renin substrate (PRS). Changes in this system were studied during hypothyroidism, after administration of propylthiouracil (PTU), and in thyroidectomized rats. A significant decrease in PRA and PRC was observed in those animals previously treated with PTU. However, a significant increase in PRC, and a decrease in PRS, were found in T animals, but no changes in PRA were observed. In these animals, after daily administration of potassium iodide for I week (T+KI), no changes in RAS were observed in comparison with T rats. Nevertheless, administration of daily doses of triiodo-ithyronine (T+T3) induced a significant increase in PRA, leaving PRC unaltered. In this case the changes in PRA were related to the increase in PRS after T3 treatment. These results suggest that two different mechanisms were involved in renin release, one activated in T rats and the other in pharmacological hypothyroidism.

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.

The Sympathetic Nervous System and the Renin-Angiotensin System in Borderline Hypertension

1981 ◽  
Vol 60 (1) ◽  
pp. 25-31 ◽  
Author(s):  
J. W. Henquet ◽  
T. Kho ◽  
M. Schols ◽  
H. Thijssen ◽  
K. H. Rahn
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Concentrations ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Catecholamine ◽  
Bicycle Ergometry ◽  
Angiotensin System ◽  
Plasma Renin Concentration ◽  
Borderline Hypertension

1. Plasma catecholamine levels as well as plasma renin activity and plasma renin concentration were compared in normotensive volunteers and in subjects with borderline hypertension. All subjects were studied at rest and during bicycle ergometry. 2. The two groups of volunteer subjects did not differ in the plasma concentrations of noradrenaline and adrenaline, both at rest and during physical activity. The same was true for plasma renin activity and plasma renin concentration. Furthermore, urinary excretion of noradrenaline, adrenaline and 4-hydroxy-3-methoxymandelic acid was similar in both groups. 3. The results do not support the assumption that there is increased sympathetic activity in subjects with borderline hypertension.

Plasma Renin Activity in Diabetes Mellitus

1979 ◽  
Vol 56 (3) ◽  
pp. 255-259 ◽  
Author(s):  
A. C. Burden ◽  
H. Thurston
Keyword(s):  
Plasma Renin Activity ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Activity ◽  
Diabetic Patients ◽  
Angiotensin System ◽  
Control Subjects ◽  
Untreated Hypertension ◽  
Age And Sex ◽  
Normotensive Control

1. The plasma renin activity (PRA) was measured in 76 diabetic patients who were attending an outpatients clinic. Of these patients 16 had untreated hypertension and 28 had diabetic complications, which ranged from microaneurysms to renal failure and blindness. 2. Compared with age- and sex-matched normotensive control subjects, both normotensive and hypertensive diabetic patients had significantly higher PRA (P < 0·001). 3. Hypertensive diabetic patients also showed a higher PRA than matched hypertensive control subjects (P < 0·005). There were no significant differences between diabetic patients with hypertension or complications compared with those without these features. 4. Although this elevation of PRA could be due to a change in another component of the renin—angiotensin system, hypersecretion of renin is the most likely explanation.

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