Plasma renin system during exercise in normal men

1987 ◽  
Vol 63 (1) ◽  
pp. 188-194 ◽  
Author(s):  
J. Staessen ◽  
R. Fagard ◽  
P. Hespel ◽  
P. Lijnen ◽  
L. Vanhees ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Peak Exercise ◽  
Ang Ii ◽  
Similar Extent ◽  
Bicycle Ergometry ◽  
Arterial Blood ◽  
Intensity Of Exercise ◽  
Normal Men

The exercise-related increase in plasma renin activity (PRA) and in the plasma concentration of angiotensin II (ANG II) and aldosterone (Aldo) was studied in 43 healthy volunteers whose 24-h urinary sodium excretion (UVNa) ranged from 10 to 250 mmol. Arterial blood samples were obtained at rest and during bicycle ergometry. Compared with rest, PRA, ANG II, and Aldo rose to a similar extent during light and moderate exercise. However, at peak exercise ANG II increased significantly more (P less than 0.001) than PRA and Aldo. Thus, with increasing intensity of exercise, the slope of the linear regression of ANG II on PRA became significantly (P less than 0.001) steeper, whereas at maximal exercise the Aldo response did not follow the acute rise in ANG II. At rest as well as during exercise, Aldo rose with increasing ANG II, but the stimulatory effect of ANG II on Aldo was attenuated with higher sodium intake, as estimated from UVNa. Finally, independent of the level of physical activity, UVNa was negatively correlated with PRA, ANG II, and Aldo.

Chronic activation of plasma renin is log-linearly related to dietary sodium and eliminates natriuresis in response to a pulse change in total body sodium

2008 ◽  
Vol 294 (1) ◽  
pp. R17-R25 ◽  
Author(s):  
Mads Kjolby ◽  
Peter Bie
Keyword(s):  
Sodium Excretion ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Dietary Sodium ◽  
Ang Ii ◽  
Low Sodium ◽  
Arterial Blood ◽  
Body Sodium ◽  
Custom Made ◽  
Total Body

Responses to acute sodium loading depend on the load and on the level of chronic sodium intake. To test the hypothesis that an acute step increase in total body sodium (TBS) elicits a natriuretic response, which is dependent on the chronic level of TBS, we measured the effects of a bolus of NaCl during different low-sodium diets spanning a 25-fold change in sodium intake on elements of the renin-angiotensin-aldosterone system (RAAS) and on natriuresis. To custom-made, low-sodium chow (0.003%), NaCl was added to provide four levels of intake, 0.03–0.75 mmol·kg−1·day−1for 7 days. Acute NaCl administration increased PV (+6.3–8.9%) and plasma sodium concentration (∼2%) and decreased plasma protein concentration (−6.4–8.1%). Plasma ANG II and aldosterone concentrations decreased transiently. Potassium excretion increased substantially. Sodium excretion, arterial blood pressure, glomerular filtration rate, urine flow, plasma potassium, and plasma renin activity did not change. The results indicate that sodium excretion is controlled by neurohumoral mechanisms that are quite resistant to acute changes in plasma volume and colloid osmotic pressure and are not down-regulated within 2 h. With previous data, we demonstrate that RAAS variables are log-linearly related to sodium intake over a >250-fold range in sodium intake, defining dietary sodium function lines that are simple measures of the sodium sensitivity of the RAAS. The dietary function line for plasma ANG II concentration increases from theoretical zero at a daily sodium intake of 17 mmol Na/kg (intercept) with a slope of 16 pM increase per decade of decrease in dietary sodium intake.

Salt-sensitive hypertension in ANP knockout mice is prevented by AT1 receptor antagonist losartan

1999 ◽  
Vol 277 (3) ◽  
pp. R624-R630 ◽  
Author(s):  
Luis G. Melo ◽  
Anthony T. Veress ◽  
Chee K. Chong ◽  
Uwe Ackermann ◽  
Harald Sonnenberg
Keyword(s):  
Receptor Antagonist ◽  
Knockout Mice ◽  
Plasma Renin ◽  
Plasma Catecholamine ◽  
Ang Ii ◽  
Dietary Salt ◽  
Water Control ◽  
Dietary Regimen ◽  
Arterial Blood ◽  
Salt Sensitive Hypertension

Mice harboring a functional deletion of the pro-atrial natriuretic peptide (ANP) gene (−/−) develop salt-sensitive hypertension relative to their wild-type (+/+) counterparts after prolonged (>1 wk) maintenance on high-salt (HS, 8% NaCl) diet. We reported recently that the sensitization of arterial blood pressure (ABP) to dietary salt in the −/− mice is associated with failure to downregulate plasma renin activity. To further characterize the role and mechanism of ANG II in the sensitization of ABP to salt in the ANP “knockout” mice, we measured ABP, heart rate (HR), and plasma catecholamine and aldosterone concentrations in −/− and +/+ mice maintained on HS for 4 wk and treated with daily injections of AT1 receptor antagonist DuP-753 (losartan) or distilled water (control). Daily food and water intake and fluid and electrolyte excretion were also measured during the first and last weeks of the dietary regimen. Cumulative urinary excretion of fluid and electrolytes did not differ significantly between genotypes and was not altered by chronic treatment with losartan. Basal ABP and HR were significantly elevated in control −/− mice compared with control +/+ mice. Losartan did not affect ABP or HR in +/+ mice, but reduced ABP and HR in the −/− mice to the levels in the +/+ mice. Total plasma catecholamine was elevated by approximately ten-fold in control −/− mice compared with control +/+ mice. Losartan reduced plasma catecholamine concentration significantly in −/− mice and abrogated the difference in plasma catecholamine between −/− and +/+ mice on HS diet. Plasma aldosterone did not differ significantly between genotypes and was not altered by losartan. We conclude that salt sensitivity of ABP in ANP knockout mice is mediated, at least in part, by a synergistic interaction between ANG II and sympathetic nerve activity.

Angiotensin II overflow from canine skeletal muscle in vivo: importance of plasma angiotensin I

1994 ◽  
Vol 266 (5) ◽  
pp. R1664-R1669 ◽  
Author(s):  
J. H. Schwieler ◽  
J. Nussberger ◽  
T. Kahan ◽  
P. Hjemdahl
Keyword(s):  
De Novo ◽  
Ex Vivo ◽  
Plasma Renin ◽  
Gracilis Muscle ◽  
Ang Ii ◽  
Concentration Difference ◽  
Beta Adrenoceptor ◽  
Arterial Blood ◽  
Catheter System

The overflows (i.e., veno-arterial concentration differences multiplied by plasma flow) of angiotensin-(1-10) decapeptide (ANG I) and angiotensin-(1-8) octapeptide (ANG II) from blood-perfused canine gracilis muscle in situ were studied. Special precautions were taken to minimized ex vivo generation and/or degradation of angiotensins in the sampled blood. ANG I was found to be generated in the catheter system supplying the gracilis muscle with arterial blood, but plasma renin activity and ANG II levels were uninfluenced by the catheter system. A positive venoarterial concentration difference over the muscle itself was found for ANG II but not for ANG I under basal conditions. Isoprenaline elicited vasodilatation, reduced ANG I overflow, and tended to increase ANG II overflow, whereas beta-adrenoceptor blockade by propranolol had no effect on these variables. In conclusion, we found no evidence for a local de novo synthesis of ANG II from the gracilis muscle vasculature in vivo. The net overflow of ANG II was most likely caused by local conversion in the tissue of ANG I artifactually generated in the arterial catheter system. beta-Adrenoceptor stimulation enhanced the local conversion of ANG I to ANG II, probably by exposing a greater endothelial surface containing angiotensin-converting enzyme activity.

The Renal Extraction and the Natriuretic Action of GLP-1 in Humans Depend on Interaction With the GLP-1 Receptor

2020 ◽  
Vol 106 (1) ◽  
pp. e11-e19
Author(s):  
Ali Asmar ◽  
Per K Cramon ◽  
Meena Asmar ◽  
Lene Simonsen ◽  
Charlotte M Sorensen ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Fold Increase ◽  
Receptor Activation ◽  
Ang Ii ◽  
Healthy Humans ◽  
Natriuretic Effect ◽  
Glucagon Like Peptide 1 ◽  
Arterial Plasma

Abstract Purpose The natriuretic effect of glucagon-like peptide-1 (GLP-1) in humans is independent of changes in renal plasma flow (RPF) and glomerular filtration rate (GFR) but may involve suppression of angiotensin II (ANG II) and a significant (~45%) renal extraction of GLP-1. The current study was designed to investigate the consequences for the renal extraction and the natriuretic effect of blocking GLP-1 receptors with the specific GLP-1 receptor antagonist, Exendin 9–39 (Ex 9–39). Methods Under fixed sodium intake for 4 days before each study day, 6 healthy male participants were recruited from our recent study where GLP-1 or vehicle was infused (1). In the present new experiments, participants were examined during a 3-hour infusion of GLP-1 (1.5 pmol/kg/min) together with a 3.5-hour infusion of Ex 9–39 (900 pmol/kg/min). Timed urine collections were conducted throughout the experiments. Renal extraction of GLP-1 as well as RPF and GFR were measured via Fick’s principle after catheterization of a renal vein. Arterial plasma renin, ANG II, and aldosterone concentrations were measured. Results Co-infusion of Ex 9–39 significantly reduced renal extraction of GLP-1 to ~25% compared with GLP-1 infusion alone (~45%). Urinary sodium excretions remained at baseline levels during co-infusion of Ex 9–39 as well as vehicle. By contrast, GLP-1 infusion alone resulted in a 2-fold increase in natriuresis. Ex 9–39 abolished the GLP-1-induced decrease in arterial ANG II concentrations. RPF and GFR remained unchanged during all experiments. Conclusions Renal extraction of GLP-1 and its effect on natriuresis are both dependent on GLP-1 receptor activation in healthy humans.

Obesity augments vasoconstrictor reactivity to angiotensin II in the renal circulation of the Zucker rat

2007 ◽  
Vol 293 (4) ◽  
pp. H2537-H2542 ◽  
Author(s):  
David W. Stepp ◽  
Erika I. Boesen ◽  
Jennifer C. Sullivan ◽  
James D. Mintz ◽  
Clark D. Hair ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Angiotensin Ii ◽  
Vascular Reactivity ◽  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Zucker Rats ◽  
Ang Ii ◽  
Renal Vasoconstriction ◽  
Insulin Resistant

Obesity is an emerging risk factor for renal dysfunction, but the mechanisms are poorly understood. Obese patients show heightened renal vasodilation to blockade of the renin-angiotensin system, suggesting deficits in vascular responses to angiotensin II (ANG II). This study tested the hypothesis that obesity augments renal vasoconstriction to ANG II. Lean (LZR), prediabetic obese (OZR), and nonobese fructose-fed Zucker rats (FF-LZR) were studied to determine the effects of obesity and insulin resistance on reactivity of blood pressure and renal blood flow to vasoconstrictors. OZR showed enlargement of the kidneys, elevated urine output, increased sodium intake, and decreased plasma renin activity (PRA) vs. LZR, and renal vasoconstriction to ANG II was augmented in OZR. Renal reactivity to norepinephrine and mesenteric vascular reactivity to ANG II were similar between LZR and OZR. Insulin-resistant FF-LZR had normal reactivity to ANG II, indicating the insulin resistance was an unlikely explanation for the changes observed in OZR. Four weeks on a low-sodium diet (0.08%) to raise PRA reduced reactivity to ANG II in OZR back to normal levels without effect on LZR. From these data, we conclude that in the prediabetic stages of obesity, a decrease in PRA is observed in Zucker rats that may lead to increased renal vascular reactivity to ANG II. This increased reactivity to ANG II may explain the elevated renal vasodilator effects observed in obese humans and provide insight into early changes in renal function that predispose to nephropathy in later stages of the disease.

CHANGES IN PLASMA ALDOSTERONE, CORTISOL, CORTICOSTERONE, AND RENIN CONCENTRATION IN A PATIENT WITH SODIUM-LOSING RENAL DISEASE

1966 ◽  
Vol 35 (3) ◽  
pp. 311-320 ◽  
Author(s):  
ROBERT FRASER ◽  
V. H. T. JAMES ◽  
J. J. BROWN ◽  
D. L. DAVIES ◽  
A. F. LEVER ◽  
...  
Keyword(s):  
Plasma Proteins ◽  
Urinary Infection ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Renal Calculi ◽  
Urinary Sodium Excretion ◽  
Plasma Corticosterone ◽  
Sodium Depletion ◽  
Severe Hyponatraemia ◽  
Abnormal Pattern

SUMMARY A woman with recurrent urinary infection, bilateral renal calculi, and an abnormal pattern of plasma proteins was unable to reduce urinary sodium excretion when sodium intake was restricted. When the intake of sodium was reduced depletion developed rapidly, and severe hyponatraemia was associated with increased plasma renin and aldosterone concentrations, and a less marked although definite, increase in plasma corticosterone. Plasma cortisol was unchanged during sodium depletion, although it increased normally after the administration of corticotrophin.

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.

Hemodynamic, hormonal, and drinking responses to reduced venous return in the dog

1982 ◽  
Vol 243 (3) ◽  
pp. R354-R362 ◽  
Author(s):  
T. N. Thrasher ◽  
L. C. Keil ◽  
D. J. Ramsay
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Water Intake ◽  
Venous Return ◽  
Control Level ◽  
Vena Cava ◽  
Plasma Renin ◽  
Ang Ii ◽  
Arterial Blood ◽  
Dog Plasma

The effect of an acute reduction in venous return, caused by reversible constriction of the thoracic vena cava, on drinking and secretion or arginine vasopressin (AVP) was examined in the dog. Plasma AVP levels rose immediately from a control level of 1.4 +/- 0.1 pg/ml (mean +/- SE) to a plateau ranging between 36 and 42 pg/ml during the first 30 min after constriction but declined to 12.6 +/- 4.2 pg/ml 2 h after constriction even though systemic arterial hypotension was maintained. Drinking occurred with a latency of 22 +/- 6 min and 13.2 +/- 1.8 ml H2O/kg was consumed during 2 h of vena caval constriction. Water intake was significantly correlated with the average reduction in blood pressure (r = 0.86; n = 8; P less than 0.01) but not with plasma renin activity. The role of angiotensin II (ANG II) in the drinking and secretion of AVP in response to decreased venous return was evaluated using the ANG II receptor blocker, saralasin, infused intravenously (iv) or intracerebroventricularly (icv). Intravenous, but not icv, infusion of saralasin during vena caval constriction reduced the ability of the dogs to maintain arterial blood pressure (P less than 0.05). However, neither iv nor icv saralasin significantly affected water intake or the rise in plasma AVP in response to vena caval constriction when compared to their respective controls. Taken together, these data show that angiotensin is important in the maintenance of systemic arterial blood pressure but is not essential for the rise in plasma AVP or drinking in response to an acute reduction in venous return. It is suggested that either arterial baroreceptors or "low-pressure" volume receptors or both mediate the drinking and AVP responses in the presence of central blockade of the effects of circulating angiotensin.

Angiotensin causes vasoconstriction during hemorrhage in baroreceptor-denervated dogs

1983 ◽  
Vol 245 (4) ◽  
pp. H667-H673
Author(s):  
D. B. Averill ◽  
A. M. Scher ◽  
E. O. Feigl
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Aortic Pressure ◽  
Ang Ii ◽  
Arterial Blood ◽  
Aortic Blood ◽  
Aortic Blood Pressure ◽  
Mean Aortic Pressure

The participation of angiotensin II (ANG II) in the maintenance of arterial blood pressure during hypotensive hemorrhage was examined in unanesthetized, baroreceptor-denervated dogs. When mean aortic blood pressure was reduced to 69.0 +/- 2.2 mmHg, plasma renin activity increased from 0.6 +/- 0.3 ng ANG I X ml-1 X h-1 during the prehemorrhage control period to 4.5 +/- 1.6. Twenty minutes after the hemorrhage, mean aortic blood pressure rose to 78.9 +/- 3.1 mmHg. Subsequent infusion of the angiotensin II antagonist saralasin (5.2-14.0 micrograms X kg-1 X min-1) decreased mean aortic pressure to 59.6 +/- 3.3 mmHg. When 5% dextrose was infused in place of saralasin, mean aortic pressure was 79.3 +/- 4.3 mmHg. The lower aortic blood pressure caused by saralasin infusion was the result of a significant decrease in total peripheral resistance. Resistance was 10.3 +/- 3.2 mmHg X l-1 X min lower during saralasin infusion than during dextrose infusion. We conclude that baroreceptor reflexes are not essential for the elevation of plasma renin activity during hemorrhage. In baroreceptor-denervated dogs subjected to hypotensive hemorrhage, the increased formation of ANG II has a vasoconstrictor action that contributes to the maintenance of arterial blood pressure.

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