Corticosteroid-induced stimulation of atrial natriuretic peptide in man

1988 ◽  
Vol 118 (2) ◽  
pp. 179-186 ◽  
Author(s):  
Hermann Saxenhofer ◽  
Martin Angst ◽  
Peter Weidmann ◽  
Sidney G. Shaw ◽  
Claudia Ferrier
Keyword(s):  
Oral Administration ◽  
Potential Role ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Elevated Plasma ◽  
Glucocorticoid Treatment ◽  
Volume State ◽  
Normal Humans ◽  
Fludrocortisone Acetate ◽  
Stimulation Of

Abstract. Previously, we reported elevated plasma immunoreactive ANP (irANP) levels from the 2nd to the 9th day of administering either prednisone, 50 mg/day, or 9α-fludrocortisone acetate (9αF), 0.6 mg/day, to normal humans. To investigate the course of plasma irANP levels during the first 48 h of corticosteroid adminstration, 9 healthy men (mean age ± sem, 24 ± 1 years) received in randomised sequence A) a 4-h iv infusion of prednisolone sodium tetrahydrophthalate followed by oral administration of prednisone for 2 days; or B) a 4-h infusion of aldosterone followed by oral administration of 9αF for 2 days. Basal supine plasma irANP levels averaged 32 ± 5 ng/l in study A and 30 ± 6 ng/l in study B; they were unchanged or even deceased up to 24 h of glucocorticoid or mineralocorticoid administration, but rose (P < 0.01) to 56 ± 9 and 62 ± 12 ng/l at 48 h, respectively, of the two interventions. During glucocorticoid treatment, blood pressure (BP) and indices of the sodium-fluid volume state were unchanged after 48 h. During 9αF administration, body weight increased (1.1 ± 0.3%, P < 0.001), whereas urinary sodium excretion (63 ±7%, P < 0.001), hematocrit (4.1 ± 1.1%, P < 0.001), and plasma renin activity (38 ± 4%, P < 0.001) decreased. Conclusions: The increase in circulating irANP at 48 h of administration of either a glucocorticoid or a mineralocorticoid demonstrates a distinct but slow response of the ANP system to these corticosteroids in normal humans. ANP may play a potential role in mediating and/or modulating physiological and pathophysiological effects of corticosteroids.

Dissociation between plasma renin and plasma aldosterone induced by dietary glycine hydrochloride

1988 ◽  
Vol 254 (2) ◽  
pp. E187-E192
Author(s):  
T. A. Kotchen ◽  
G. P. Guthrie ◽  
L. D. Boucher ◽  
J. N. Lorenz ◽  
C. E. Ott
Keyword(s):  
Plasma Renin Activity ◽  
Indirect Effect ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Elevated Plasma ◽  
Sprague Dawley ◽  
Low Sodium ◽  
High Chloride ◽  
Stimulation Of

We evaluated the effects of selective dietary chloride loading (without sodium) on plasma renin activity (PRA) and plasma aldosterone in the sodium-deprived Sprague-Dawley rat. Three groups of animals were fed one of the following diets for 13 days: 1) low NaCl; 2) high NaCl; or 3) low sodium, high chloride, provided as glycine hydrochloride. Compared with NaCl-deprived animals, PRA and plasma aldosterone were lower (P less than 0.01) in animals fed low sodium high chloride, whereas aldosterone in animals fed glycine hydrochloride was higher (P less than 0.01) than that of NaCl-deprived animals. In contrast, plasma concentrations of corticosterone and 18-hydroxycorticosterone were not increased by selective chloride loading. Glycine chloride-fed animals were acidotic and had elevated plasma concentrations of potassium and ionized calcium. Thus stimulation of aldosterone by selective chloride loading is not related to PRA or ACTH but may be due to a direct effect of acidosis or an indirect effect of acidosis on potassium and/or calcium. Additionally, selective chloride loading appears to stimulate the conversion of 18-hydroxycorticosterone to aldosterone.

Role of intrarenal ANG II in reflex neural stimulation of plasma renin activity and renal sodium reabsorption

1993 ◽  
Vol 265 (2) ◽  
pp. R392-R398
Author(s):  
L. D. Nelson ◽  
J. L. Osborn
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Renin Activity ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Volume Depletion ◽  
Converting Enzyme Inhibition ◽  
Renal Sympathetic ◽  
Stimulation Of

Renal sympathetic stimulation of plasma renin activity (PRA) and sodium reabsorption was examined in conscious dogs before and during intrarenal angiotensin II (ANG II)-type 1 receptor blockade with losartan (Dup-753) and converting enzyme inhibition. In uninephrectomized dogs, renal function and PRA responses to 14% blood volume depletion (BVD) were measured. BVD was utilized to activate renal sympathetic outflow in the absence of hypotension. In eight vehicle-treated dogs, 14% BVD increased PRA from 1.38 +/- 0.32 to 2.79 +/- 0.66 ng ANG I.ml-1 x h-1 and decreased urinary sodium excretion (UNaV) from 85.1 +/- 11.3 to 45.4 +/- 7.5 mueq/min. During losartan (n = 6) and captopril (n = 5) infusion, plasma renin responses were enhanced in response to 14% BVD (1.93 +/- 0.48 to 5.74 +/- 2.25 and 3.03 +/- 0.73 to 9.19 +/- 1.94 ng ANG I.ml-1 x h-1, respectively), whereas antinatriuretic responses were similar to vehicle-infused dogs. Thus, neurogenic antinatriuresis is not mediated by secondary generation of ANG II, since UNaV decreased similarly to control in all conditions of ANG II blockade. Tonic intrarenal and/or circulating ANG II synthesis of dogs on a normal sodium diet inhibit neurogenic stimulation of renin release, since PRA responses were enhanced after blockade of ANG II.

Hemodynamic and humoral effects of prostaglandin inhibition in exercising humans

1984 ◽  
Vol 56 (1) ◽  
pp. 39-45 ◽  
Author(s):  
J. Staessen ◽  
A. Cattaert ◽  
R. Fagard ◽  
P. Lijnen ◽  
E. Moerman ◽  
...  
Keyword(s):  
Statistical Significance ◽  
Plasma Catecholamines ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Systemic Circulation ◽  
Controlled Study ◽  
Double Blind ◽  
Humoral Factors ◽  
Exercise Induced ◽  
Stimulation Of

This double-blind placebo-controlled study investigated whether indomethacin-induced (500 mg/3 days) prostaglandin synthesis inhibition (PG inhibition) affected systemic hemodynamics and several humoral factors in nine sodium-replete normal humans, during exercise. Independent of the level of physical activity, PG inhibition was accompanied by small but significant (P less than 0.001) increases in systolic (+4.3 mmHg) and diastolic (+1.8 mmHg) intra-arterial pressure: the changes in cardiac output (determined noninvasively), systemic vascular resistance, and exercise capacity did not reach a level of statistical significance. After PG inhibition, plasma 13,14-dihydro-15-keto/prostaglandin F2 alpha, plasma renin, and aldosterone were reduced (P less than 0.001) at rest sitting and exercise, but PG inhibition did not prevent the exercise-induced stimulation of the plasma renin-aldosterone system. The urinary sodium excretion, averaging 156 meq/24 h during placebo, decreased (P less than 0.001) by 28 meq/24 h during PG inhibition: urinary aldosterone and kallikrein and the plasma catecholamines remained unchanged. In resting and exercising sodium-replete subjects, prostaglandins seem to exert a depressor effect on the systemic circulation and to increase plasma renin activity, but they are probably not involved in the exercise-related stimulation of the plasma renin-aldosterone system.

Overexpression of kidney neutral endopeptidase (EC 3.4.24.11) and renal function in experimental cirrhosis

2006 ◽  
Vol 290 (6) ◽  
pp. F1337-F1343 ◽  
Author(s):  
G. Sansoè ◽  
M. Aragno ◽  
R. Mastrocola ◽  
J. C. Cutrin ◽  
S. Silvano ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Specific Inhibitor ◽  
Free Water ◽  
Plasma Renin ◽  
Neutral Endopeptidase ◽  
Experimental Cirrhosis ◽  
Proximal Tubule Cells ◽  
Advanced Cirrhosis ◽  
Normal Humans ◽  
Renal Proximal Tubule Cells

Neutral endopeptidase degrades atrial natriuretic peptide (ANP) and bradykinin and may generate endothelin-1 from big-endothelin. In advanced cirrhosis, sodium retention is accompanied by elevated plasma ANP levels, and infusion of ANP causes hypotension, but in normal humans increasing the concentration of ANP through the inhibition of neutral endopeptidase, localized in renal proximal tubule cells, causes natriuresis without any arterial pressure drop. The purpose of this study was the assessment of kidney neutral endopeptidase expression and responses to candoxatrilat (a specific inhibitor of this enzyme) in rats with CCl4-induced cirrhosis. Two groups of control rats ( n = 5) were injected with vehicle or 3 mg/kg candoxatrilat. Three groups of cirrhotic rats with ascites ( n = 10) received vehicle alone or 3 or 10 mg/kg candoxatrilat. In cirrhotic rats, Western blot analysis revealed a 170% increase in renal neutral endopeptidase protein content ( P < 0.03), mainly in the proximal nephron and macula densa, and both candoxatrilat dosages increased plasma ANP levels, urinary volume, and urinary excretion of sodium, ANP, and cGMP compared with vehicle alone (all P < 0.03). Candoxatrilat (10 mg/kg) also reduced tubular solute-free water reabsorption ( P < 0.03) in cirrhotic rats, but renal blood flow, arterial pressure, and plasma renin activity were unaffected. Neutral endopeptidase inhibition has natriuretic and aquaretic actions in cirrhosis without any effect on blood pressure and kidney perfusion due to a significant overexpression of this enzyme in renal cortex.

Comparison of the Renin Response to Dopamine and Noradrenaline in Normal Subjects and Patients with Autonomic Insufficiency

1974 ◽  
Vol 46 (4) ◽  
pp. 481-488 ◽  
Author(s):  
C. S. Wilcox ◽  
M. J. Aminoff ◽  
A. B. Kurtz ◽  
J. D. H. Slater
Keyword(s):  
Autonomic Failure ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Control Groups ◽  
Autonomic Reflexes ◽  
Fractional Increase ◽  
The Mean ◽  
Autonomic Insufficiency ◽  
Stimulation Of

1. The effect on plasma renin activity (PRA) of dopamine and noradrenaline infusions was studied in three patients with Shy—Drager syndrome, three patients with Parkinson's disease and normal autonomic reflexes, and three healthy volunteers. The patients with the Shy—Drager syndrome had functional evidence of a peripheral lesion of the sympathetic nervous system and subnormal PRA on a controlled sodium intake. 2. In all subjects catecholamines were infused step-wise for 4 min until a 30% rise in systolic blood pressure occurred. 3. In each subject, PRA fell after noradrenaline but rose after dopamine. The mean fractional increase in PRA after dopamine was no less in the Shy—Drager patients than in the control groups. 4. The results suggest, first, that stimulation of dopamine receptors can release renin, and secondly, that inadequate renin stores cannot explain the low PRA found in our patients with autonomic failure.

Elevated Plasma Renin Activity Associated with Renal Dysfunction

Nephron ◽  
1986 ◽  
Vol 44 (1) ◽  
pp. 51-57 ◽  
Author(s):  
Bernard Kehoe ◽  
Godfrey R. Keeton ◽  
Christine Hill
Keyword(s):  
Plasma Renin Activity ◽  
Renal Dysfunction ◽  
Plasma Renin ◽  
Renin Activity ◽  
Elevated Plasma

Renal denervation alters cardiovascular and endocrine responses to hemorrhage in conscious newborn lambs

1998 ◽  
Vol 275 (1) ◽  
pp. H285-H291 ◽  
Author(s):  
Francine G. Smith ◽  
Isam Abu-Amarah
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Renal Denervation ◽  
Plasma Renin ◽  
Sympathetic Nerves ◽  
Renal Nerves ◽  
Elevated Plasma ◽  
Baseline Levels ◽  
Renal Sympathetic

To investigate the role of renal sympathetic nerves in modulating cardiovascular and endocrine responses to hemorrhage early in life, we carried out three experiments in conscious, chronically instrumented lambs with intact renal nerves (intact; n = 8) and with bilateral renal denervation (denervated; n = 5). Measurements were made 1 h before and 1 h after 0, 10, and 20% hemorrhage. Blood pressure decreased transiently after 20% hemorrhage in intact lambs and returned to control levels. In denervated lambs, however, blood pressure remained decreased after 60 min. After 20% hemorrhage, heart rate increased from 170 ± 16 to 207 ± 18 beats/min in intact lambs but not in denervated lambs, in which basal heart rates were already elevated to 202 ± 21 beats/min. Despite an elevated plasma renin activity (PRA) measured in denervated (12.0 ± 6.4 ng ANG I ⋅ ml−1 ⋅ h−1) compared with intact lambs (4.0 ± 1.1 ng ANG I ⋅ ml−1 ⋅ h−1), the increase in PRA in response to 20% hemorrhage was similar in both groups. Plasma levels of arginine vasopressin increased from 11 ± 8 to 197 ± 246 pg/ml after 20% hemorrhage in intact lambs but remained unaltered in denervated lambs from baseline levels of 15 ± 10 pg/ml. These observations provide evidence that in the newborn, renal sympathetic nerves modulate cardiovascular and endocrine responses to hemorrhage.

The renin-aldosterone system in pre-eclampsia, essential and transient hypertension during pregnancy, and normotensive pregnant and non-pregnant control subjects

1982 ◽  
Vol 101 (2) ◽  
pp. 273-280 ◽  
Author(s):  
E. B. Pedersen ◽  
A. B. Rasmussen ◽  
P. Johannesen ◽  
H. J. Kornerup ◽  
S. Kristensen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Third Trimester ◽  
Plasma Aldosterone Concentration ◽  
The Third ◽  
Control Subjects ◽  
Hypertension In Pregnancy ◽  
Normotensive Pregnancy ◽  
In Pregnancy

Abstract. Plasma renin concentration (PRC), plasma aldosterone concentration (PAC), and blood pressure were determined in the third trimester in pregnancy, 5 days and 6 months after delivery in pre-eclampsia, essential and transient hypertension in pregnancy and in normotensive pregnant and non-pregnant control subjects. PRC and PAC were elevated several fold above non-pregnant level in all groups during pregnancy. In pre-eclampsia PRC and PAC were 220 and 160%, respectively, above the levels 6 months after delivery, and thus lower than the corresponding values, 360 and 402%, in normotensive pregnancy. In essential and transient hypertension PRC and PAC increased to the same degree as during normotensive pregnancy. Urinary sodium excretion, serum sodium and creatinine clearance were reduced in pre-eclampsia, but not in essential and transient hypertension when compared to normotensive pregnant controls. All the parameters determined were the same as in non-pregnant controls 6 months after delivery in all groups. There were no correlations between blood pressure and PRC or PAC in any of the groups neither in pregnancy nor after delivery. It is concluded that the renin-aldosterone system is stimulated in lesser degree in pre-eclampsia than in both essential hypertension, transient hypertension and normotensive pregnancy, and there was no evidence for a causal relationship between the renin-aldosterone system and blood pressure neither in normotensive nor hypertensive pregnancy.

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