Suppression Of Exercise-Induced Plasminogen Activator And Plasma Renin Activity Following Aspirin Ingestion

1981 ◽  
Author(s):  
D H Osmond ◽  
A M Hedlin ◽  
A Y Loh ◽  
D Sakac ◽  
R R Topp
Keyword(s):  
Plasma Renin Activity ◽  
Plasminogen Activator ◽  
Plasma Renin ◽  
Bicycle Ergometer ◽  
Renin Activity ◽  
Post Exercise ◽  
Before And After ◽  
Exercise Induced ◽  
Aspirin Ingestion

The influence of aspirin on the fibrinolytic and renin systems was studied in 10 healthy young men, who served as their own controls. Basal blood samples were obtained after a 15-minute rest, immediately after exercise, and following a 15-min post-exercise rest. Later, (7-14 days) 1250 mg aspirin was ingested 1 hr. before test samples were obtained, as before. Exercise on a bicycle ergometer induced doubling of the resting heart rate within 2 min., and was continued for 3 min. longer. Aspirin induced a significant reduction in the level of plasminogen activator, before and after exercise, and also some decrease in hemoglobin and hematocrit levels. Exercise almost doubled the baspl plasma renin activity (PRA, angiotensin I, ng/ml plasma/hr., by radioimmunoassay) in the control and aspirin experiments. Aspirin did not significantly blunt this exercise-induced rise in PRA. However, after 15-minute rest, the control PRA remained elevated, while the postaspirin PRA was 37% below it (p < 0.025). After cold activation of the plasmas (-4°C, 72 hr.), the PRA increment over corresponding non-activated samples was used to estimate “prorenin”. Prorenin as % of active renin before aspirin was 347.2, 210.5, and 210.8, for the basal and 2 post-exercise periods respectively; after aspirin the values were 460.5, 354.9, and 353.4. Clearly, exercise depresses the proportion of prorenin, suggesting an exercise-induced enhancement of prorenin conversion, possibly related to the exercise-induced stimulation of the fibrinolytic system. After aspirin, all 3 prorenin percentages are higher, implying that it interferes with prorenin conversion. Thus, exercise increases both fibrinolysis and PRA. The increase in PRA could be due in part to fibrinolytic enzyme conversion of prorenin (plasmin activates prorenin in vitro). Aspirin suppresses plasminogen activator, and thus prorenin activation.

Suppression of renin release by antagonism of endogenous opiates in the dog

1986 ◽  
Vol 250 (4) ◽  
pp. R633-R637
Author(s):  
J. E. Szilagyi ◽  
J. Chelly ◽  
M. F. Doursout
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Endogenous Opioids ◽  
Renin Activity ◽  
Renin Release ◽  
Endogenous Opioid ◽  
Endogenous Opiates ◽  
Arterial Blood ◽  
Before And After ◽  
Arterial Constriction

The influence of blockade of endogenous opioids on the release of renin due to partial renal arterial constriction was determined acutely and chronically in unilaterally nephrectomized dogs. In acute preparations changes in plasma renin activity, arterial blood pressure, and heart rate were determined after 15 min of 60% renal arterial constriction before and after administration of either a saline vehicle, the opiate antagonist naloxone (0.05 mg/kg), or morphine (2 mg/kg). Acute antagonism of endogenous opiates abolished the increase in plasma renin activity and mean arterial pressure associated with renal arterial constriction. Repeated renal arterial constrictions in saline- or morphine-treated animals did not alter the humoral or hemodynamic responses. In chronic preparations long-term naloxone infusion attenuated the development of renovascular hypertension and diminished the increase in plasma renin activity. These data suggest that endogenous opioid peptides are modulators in the control of renin release and may be important participants in the pathogenesis of hypertension.

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

1978 ◽  
Vol 15 (1-6) ◽  
pp. 250-252 ◽  
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.

The Effect of Mental Stress on Catecholamines, their Metabolites and Plasma Renin Activity in Patients with Essential Hypertension and in Healthy Subjects

1979 ◽  
Vol 57 (s5) ◽  
pp. 229s-231s ◽  
Author(s):  
W. Januszewicz ◽  
M. Sznajderman ◽  
B. Wocial ◽  
T. Feltynowski ◽  
T. Klonowicz
Keyword(s):  
Essential Hypertension ◽  
Plasma Renin Activity ◽  
Urinary Excretion ◽  
Mental Stress ◽  
Healthy Subjects ◽  
Plasma Renin ◽  
Renin Activity ◽  
Vanillylmandelic Acid ◽  
Before And After ◽  
Noradrenaline And Adrenaline

1. Ten patients with essential hypertension and ten healthy men were submitted to mental stress consisting of Kraepelin's arithmetic test combined with noise. Concentrations of plasma and urine catecholamines and of their metabolites as well as plasma renin activity before and after the test were studied. 2. In both groups a significant increase of noradrenaline and adrenaline in blood and noradrenaline in urine was observed. The urinary excretion of dopamine fell significantly in both groups after stress. 3. After mental stress a significant increase in urinary excretion of 3-methoxy-4-hydroxyphenylglycol was observed in both groups. The excretion of vanillylmandelic acid decreased significantly only in healthy subjects. 4. The plasma renin activity rose significantly in both groups but the increase was more pronounced in healthy subjects.

α1-Adrenoceptor Blockade: Dissociation of Its Effects on Renin Release and Arterial Blood Pressure in Man

1981 ◽  
Vol 61 (s7) ◽  
pp. 307s-309s ◽  
Author(s):  
A. Morganti ◽  
Carla Sala ◽  
Anna Palermo ◽  
Lucia Turolo ◽  
A. Zanchetti
Keyword(s):  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Pressor Response ◽  
Plasma Renin ◽  
Test Dose ◽  
Blocking Agent ◽  
Renin Activity ◽  
Renin Release ◽  
Arterial Blood ◽  
Before And After

1. The possibility that the juxtaglomerular α1-adrenoceptors mediate an inhibitory action on renin release in man was examined in seven patients with essential hypertension, by measuring (i) the acute effects of prazosin (0.25 mg intravenously), a selective α1-adrenoceptor-blocking agent, on arterial pressure and plasma renin activity, the degree of α-blockade induced by the drug being assessed by comparing the pressor response with that to a test dose of phenylephrine before and after prazosin administration, and (ii) the increases in plasma renin activity in response to isoprenaline before and during the prazosin-induced α-blockade. 2. Twenty minutes after the infusion of prazosin, when the pressor response to phenylephrine was reduced by 80% with respect to control, (i) mean arterial pressure was practically unchanged, (ii) plasma renin activity was almost doubled and (iii) the increases in plasma renin activity in response to isoprenaline were significantly greater, both in absolute and percentage values, than those observed before prazosin. 3. The increments in baseline plasma renin activity induced by prazosin in the absence of decrease in arterial pressure and the enhancement in renin responsiveness to the β-adrenoceptor stimulus suggest that, in man, the juxtaglomerular α1-adrenoceptors exert a direct, suppressive action on renin release.

Plasma Renin in Long-Term Diuretic Treatment of Hypertension: Effect of Discontinuation and Restarting Therapy

1982 ◽  
Vol 63 (2) ◽  
pp. 121-125 ◽  
Author(s):  
S. Swart ◽  
R. F. Bing ◽  
J. D. Swales ◽  
H. Thurston
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Juxtaglomerular Apparatus ◽  
Significant Rise ◽  
Renin Activity ◽  
Hypertensive Patients ◽  
Diuretic Treatment ◽  
Low Renin Hypertension ◽  
Before And After

1. Plasma renin activity, body weight and blood pressure were measured before and after 7 days' treatment with bendrofluazide in ten hypertensive subjects. They were then treated with bendrofluazide alone (5 mg daily) for a minimum of 3 years. The diuretic was then discontinued and the measurements were repeated before and again after 7 days with bendrofluazide. The results were compared with those obtained before chronic treatment with the diuretic. 2. Chronic diuretic treatment was associated with a persistent and progressive rise in plasma renin activity, that fell promptly to pretreatment levels when diuretics were discontinued. This was associated with significant weight gain but no immediate significant rise in blood pressure. 3. When acutely challenged with bendrofluazide the patients showed a greater increase in plasma renin activity on the second occasion than on the first. Three out of five patients with an initially subnormal response had normal responses after chronic diuretic treatment. 4. Chronic diuretic treatment increased the responsiveness of the juxtaglomerular apparatus in some hypertensive patients. 5. Classification of hypertensive patients into renin subgroups may be influenced by previous therapy, even when that therapy has been discontinued for 4 weeks. In particular ‘low renin hypertension’ may be masked by recent use of diuretics, as shown by three of the five patients in this subgroup in the present study.

Angiotensin II Blockade before and after Marked Sodium Depletion in Patients with Hypertension

1978 ◽  
Vol 54 (1) ◽  
pp. 75-83 ◽  
Author(s):  
P. Van Hoogdalem ◽  
A. J. M. Donker ◽  
F. H. H. Leenen
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Hypotensive Effect ◽  
Renin Activity ◽  
Mean Blood Pressure ◽  
Sodium Depletion ◽  
Before And After

1. Angiotensin II blockade before and after marked sodium depletion in patients with hypertension [unilateral renovascular (eight), bilateral renovascular (four) and essential (four)] was performed by intravenous administration of the angiotensin II antagonist Sar1-Ala8-angiotensin II (saralasin). 2. On normal sodium intake, saralasin decreased mean blood pressure by 8 mmHg in the unilateral renovascular group, by 6 mmHg in the bilateral renovascular group and increased it by 3 mmHg in the essential hypertensive group. After sodium depletion saralasin decreased mean blood pressure by 33 mmHg, 35 mmHg and 18 mmHg respectively. The saralasin-induced decrease in blood pressure significantly correlated with the log of the initial plasma renin activity. 3. Saralasin infusion decreased effective renal plasma flow (ERPF) in all three hypertension subgroups, both on normal sodium intake and after sodium depletion. Glomerular filtration rate decreased in direct relation to the hypotensive effect of saralasin but ERPF showed this relationship only after sodium depletion. On normal sodium intake saralasin increased filtration fraction by 17%, but decreased it by 7% after sodium depletion. 4. It is concluded that the hypotensive action of saralasin closely correlates with the value of circulating plasma renin activity, apparently independent of the aetiology of the hypertension. The decrease in ERPF during saralasin infusion in the patients on normal sodium intake seems mainly related to the agonistic activity of saralasin, but that after sodium depletion to the hypotensive effect of saralasin.

scholarly journals High plasma renin activity associates with obesity-related diabetes and arterial hypertension, and predicts persistent hypertension after bariatric surgery

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Lucia La Sala ◽  
Elena Tagliabue ◽  
Elaine Vieira ◽  
Antonio E Pontiroli ◽  
Franco Folli
Keyword(s):  
Bariatric Surgery ◽  
Glucose Tolerance ◽  
Plasma Renin Activity ◽  
Laparoscopic Gastric Banding ◽  
Plasma Renin ◽  
High Plasma ◽  
Renin Activity ◽  
Glucose Levels ◽  
Before And After ◽  
Severely Obese

Abstract Background Information about the renin–angiotensin–aldosterone system (RAAS) in obese individuals before and after bariatric surgery is scarce. Aim of this study was to analyze the RAAS in severely obese subjects, in relation to anthropometric and metabolic variables, with special reference to glucose tolerance. Methods 239 subjects were evaluated at baseline, and 181 one year after bariatric surgery [laparoscopic gastric banding (LAGB)]. Results At baseline, renin (plasma renin activity, PRA) was increased from normal to glucose tolerance and more in diabetes, also correlating with ferritin. After LAGB, the decrease of PRA and aldosterone was significant in hypertensive, but not in normotensive subjects, and correlatied with decrease of ferritin. PRA and glucose levels were predictive of persistent hypertension 1 year after LAGB. Conclusions These data support the role of RAAS in the pathophysiology of glucose homeostasis, and in the regulation of blood pressure in obesity. Ferritin, as a proxy of subclinical inflammation, could be another factor contributing to the cross-talk between RAAS and glucose metabolism.

Decrease in α-Adrenoceptor-Mediated Vasoconstriction Parallels the Antihypertensive Response to Propranolol in Patients with Normal Renin Essential Hypertension

1981 ◽  
Vol 61 (s7) ◽  
pp. 445s-448s ◽  
Author(s):  
F. W. Amann ◽  
P. Bolli ◽  
L. Hulthén ◽  
W. Kiowski ◽  
F. R. Bühler
Keyword(s):  
Essential Hypertension ◽  
Plasma Renin Activity ◽  
Forearm Blood Flow ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Adrenaline ◽  
Before And After ◽  
Β Receptor ◽  
Antihypertensive Response ◽  
Propranolol Therapy

1. α1-Adrenoceptor-mediated vasoconstriction was studied before and during propranolol therapy in eight normal renin essential hypertensive patients; four were known ‘responders’ and four, age-matched ‘non-responders’ to previous β-receptor blocker monotherapy. Plasma renin activity, plasma adrenaline and noradrenaline concentrations as well as forearm blood flow were measured before and during regional postjunctional α1-adrenoceptor blockade with prazosin. All measurements were done on placebo and again after 6 weeks’ propranolol monotherapy (320 mg/day). 2. Propranolol reduced heart rate and plasma renin activity to the same extent in ‘responders’ and ‘non-responders’. Resting plasma adrenaline concentrations tended to be higher in ‘responders’ before propranolol; they remained unchanged in both groups on propranolol. Plasma noradrenaline concentrations were similar in both groups before and on propranolol. 3. Before propranolol forearm flow was not different in ‘responders’ and ‘non-responders’. Non-specific vasodilatation with sodium nitroprusside produced a similar increase in forearm flow before and after propranolol in both groups. 4. Prazosin-induced increments in forearm flow tended to be higher in ‘responders’ before propranolol. After propranolol the vasodilator effect of prazosin was attenuated in ‘responders’ but it remained unchanged in ‘non-responders’ (P &lt; 0.01). 5. In patients with normal renin essential hypertension the antihypertensive response to propranolol monotherapy is paralleled by a decrease in postjunctional α1-adrenoceptor-mediated vasoconstriction.

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