Acute changes in plasma volume, renin activity, and free aldosterone levels in healthy subjects following Fursemide administration

1968 ◽  
Vol 46 (1) ◽  
pp. 85-91 ◽  
Author(s):  
J. Rosenthal ◽  
R. Boucher ◽  
W. Nowaczynski ◽  
J. Genest
Keyword(s):  
Plasma Renin Activity ◽  
Intravenous Injection ◽  
Plasma Volume ◽  
Human Subjects ◽  
Plasma Renin ◽  
Renin Activity ◽  
Healthy Human ◽  
Volume Measurements ◽  
Quantitative Changes ◽  
Acute Changes

The effects of acute changes in plasma volume on renin release and plasma free aldosterone levels are not well understood. Our experiments demonstrate quantitative changes in the above-mentioned parameters following salt depletion. Plasma renin activity was assayed 10, 20, 60, and 120 min after the intravenous injection of Fursemide in healthy human subjects. Plasma free aldosterone levels and plasma volume were measured 60 and 120 min after injection. Plasma renin activity rose significantly after 10 min, as compared with control values, the highest values coinciding with peaks in urinary volume and sodium excretion as well as lowest urinary osmolality. The plasma aldosterone increase, moderate at 60 min, was significant at 120 min. Plasma volume measurements, 60 min after injection, decreased significantly, with a tendency to return to control values at 120 min. Plasma renin activity, measured by the new micromethod of Boucher at intervals of 2 to 70 min after the intravenous injection of Fursemide in rats, revealed, as in humans, a significant increase after 10 min. These data show that the increase in renin precedes that in aldosterone following the marked decrease in plasma volume due to acute diuresis and sodium loss.

Solitary Kidney and Ageing as Causes of Low Renin and Aldosterone Concentrations: Relevance to ‘Low-Renin’ Essential Hypertension

1976 ◽  
Vol 51 (s3) ◽  
pp. 177s-180s ◽  
Author(s):  
R. Gordon ◽  
Freda Doran ◽  
M. Thomas ◽  
Frances Thomas ◽  
P. Cheras
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Plasma Renin Activity ◽  
Plasma Volume ◽  
Plasma Renin ◽  
Renin Activity ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Normotensive Subjects ◽  
The Mean

1. As experimental models of reduced nephron population in man, (a) twelve men aged 15–32 years who had one kidney removed 1–13 years previously and (b) fourteen normotensive men aged 70–90 years were studied. Results were compared with those in eighteen normotensive men aged 18–28 years and eleven men aged 19–33 years with essential hypertension. 2. While the subjects followed a routine of normal diet and daily activity, measurements were made, after overnight recumbency and in the fasting state, of plasma volume and renin activity on one occasion in hospital and of blood pressure on five to fourteen occasions in the home. Blood pressure was also measured after standing for 2 min and plasma renin activity after 1 h standing, sitting or walking. Twenty-four hour urinary aldosterone excretion was also measured. 3. The measurements were repeated in the normotensive subjects and subjects in (a) and (b) above after 10 days of sodium-restricted diet (40 mmol of sodium/day). 4. The mean plasma renin activity (recumbent) in essential hypertensive subjects was higher than in normotensive subjects. In subjects of (a) and (b) above, it was lower than normotensive subjects, and was not increased by dietary sodium restriction in subjects of (a). 5. The mean aldosterone excretion level was lower in old normotensive subjects than in the other groups, and increased in each group after dietary sodium restriction. 6. Mean plasma volume/surface area was not different between the four groups and in normotensive, essential hypertensive and nephrectomized subjects but not subjects aged 70–90 years was negatively correlated with standing diastolic blood pressure.

Effect of nitric oxide synthase inhibition on cardiovascular and hormonal regulation during pregnancy in the rat

2000 ◽  
Vol 78 (5) ◽  
pp. 423-427 ◽  
Author(s):  
Yunlong Zhang ◽  
Susan Kaufman
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Plasma Renin Activity ◽  
Plasma Volume ◽  
Atrial Natriuretic Factor ◽  
Plasma Renin ◽  
Renin Activity ◽  
Pregnant Rats ◽  
Oxide Synthase ◽  
In Pregnancy

Recent studies have shown that nitric oxide (NO) biosynthesis increases in pregnancy and that inhibition of nitric oxide synthase (NOS) induces some pathological processes characteristic of preeclampsia. The current project sought to study the effect of the NOS inhibitor Nω-nitro-L-arginine methyl ester (L-NAME, 10 µg·min-1, sc for 7 days) on plasma volume, plasma atrial natriuretic factor (ANF), plasma endothelin-1 (ET), and plasma renin activity (PRA) during gestation in conscious rats. NOS inhibition caused mean arterial pressure to increase in both virgin and 21-day pregnant rats. Plasma volume fell in the pregnant rats [L-NAME, 4.5 ± 0.3 mL·100 g-1 body wt. (n = 7) vs. D-NAME, 6.8 ± 0.2 mL·100 g-1 body wt. (n = 10); P < 0.05] but not in the virgin rats [L-NAME, 4.3 ± 0.1 mL·100 g-1 body wt. (n = 6) vs. D-NAME, 4.8 ± 0.2 mL·100 g-1 body wt. (n = 8)]. There was no effect of NOS inhibition on plasma ANF levels or PRA in either the virgin or pregnant rats. However, L-NAME did decrease plasma ET levels in the pregnant rats [L-NAME, 19.6 ± 1.6 pg·mL-1 (n = 8) vs. D-NAME, 11.6 ± 2.5 pg·mL-1 (n = 9); P < 0.05]. Our results confirm that NO is involved in cardiovascular homeostasis in pregnancy; NOS inhibition selectively reduces plasma volume in pregnant rats, thus mimicking a major pathophysiological perturbation of preeclampsia. However, it does not induce the hormonal changes characteristic of preeclampsia, namely the decrease in PRA and increase in plasma ET and ANF levels. Key words: plasma volume, preeclampsia, endothelin, atrial natriuretic factor, plasma renin activity.

scholarly journals Reduction of plasma renin activity by inhibition of the fatty acid cyclooxygenase in human subjects: independence of sodium retention.

1979 ◽  
Vol 44 (6) ◽  
pp. 781-787 ◽  
Author(s):  
J C Frölich ◽  
J W Hollifield ◽  
A M Michelakis ◽  
B S Vesper ◽  
J P Wilson ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Plasma Renin Activity ◽  
Human Subjects ◽  
Plasma Renin ◽  
Renin Activity ◽  
Sodium Retention

Neurohumoral and cardiopulmonary response to sustained submaximal exercise in the dog

1987 ◽  
Vol 62 (3) ◽  
pp. 1040-1045 ◽  
Author(s):  
P. C. Kirlin ◽  
M. D. Kittleson ◽  
L. E. Johnson
Keyword(s):  
Plasma Renin Activity ◽  
Human Subjects ◽  
Plasma Renin ◽  
Respiratory Alkalosis ◽  
Left Ventricular ◽  
Submaximal Exercise ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Plasma Aldosterone Concentration ◽  
Epinephrine Concentration

Neurohumoral, cardiovascular, and respiratory parameters were evaluated during sustained submaximal exercise (3.2 km/h, 15 degrees elevation) in normal adult mongrel dogs. At the level of activity achieved (fivefold elevation of total body O2 consumption and threefold elevation of cardiac output), significant (P less than 0.05) increases in plasma norepinephrine and epinephrine concentration (from 150 +/- 23 to 341 +/- 35 and from 127 +/- 27 to 222 +/- 31 pg/ml, respectively) were present, as well as smaller but significant increases in plasma renin activity and plasma aldosterone concentration (from 2.2 +/- 0.3 to 3.1 +/- 0.6 ng X ml-1 X h-1 and from 98 +/- 8 to 130 +/- 6 pg/ml, respectively). Plasma arginine vasopressin increased variably and insignificantly. The cardiovascular response (heart rate, systemic arterial and pulmonary arterial pressures, left ventricular filling pressure, and calculated total peripheral and pulmonary arteriolar resistance) closely paralleled that of human subjects. Increased hemoglobin concentration was induced by exercise in the dogs. The ventilatory response of the animals was characterized by respiratory alkalosis. These data suggest similarities between canine and human subjects in norepinephrine, plasma renin activity, and plasma aldosterone responses to submaximal exercise. Apparent species differences during submaximal exertion include greater alterations of plasma epinephrine concentration and a respiratory alkalosis in dogs.

Glucocorticoid Inhibition of Mineralocorticoid Action in the Rat

1984 ◽  
Vol 67 (3) ◽  
pp. 329-335 ◽  
Author(s):  
C. J. Kenyon ◽  
N. A. Saccoccio ◽  
D. J. Morris
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Sodium ◽  
Long Term Effects ◽  
Physiological Dose ◽  
Acute Changes ◽  
Adrenalectomized Rats

1. The mineralocorticoid activity of corticosterone based on acute changes in urinary Na+/K+ ratios in adrenalectomized rats was 1000 times less than that of aldosterone. However, corticosterone had only kaliuretic actions whereas aldosterone had both antinatriuretic and kaliuretic properties. Corticosterone inhibited the antinatriuretic actions of aldosterone. 2. Adrenalectomized rats infused continuously with a physiological dose of corticosterone (1 mg/day) were 5 times less sensitive to the antinatriuretic and 25 times less sensitive to the kaliuretic actions of aldosterone when administered acutely than were control adrenalectomized rats. 3. The long term effects of infusions of physiological doses of aldosterone and corticosterone were assessed in adrenalectomized rats maintained in metabolic cages. Aldosterone lowered plasma renin activity and reduced fluid (0.3% NaCl) intake; these effects were diminished when aldosterone and corticosterone were infused simultaneously. Plasma renin activity and fluid intake were correlated in long term infusion experiments. Both hormones had hypokalaemic effects but these were not additive. Corticosterone, but not aldosterone, increased systolic blood pressure and plasma sodium levels. 4. We conclude that glucocorticoid effects on water and electrolyte metabolism are different from those of mineralocorticoids, that glucocorticoids may antagonize mineralocorticoid effects and that interactions between mineralocorticoids and glucocorticoids may be important in long term blood pressure regulation.

Failure of NaHCO3 and KHCO3 to inhibit renin in the rat

1976 ◽  
Vol 231 (4) ◽  
pp. 1050-1056 ◽  
Author(s):  
TA Kotchen ◽  
JH Galla ◽  
RG Luke
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Volume ◽  
Plasma Renin ◽  
Renin Activity ◽  
Sodium Balance ◽  
Renin Inhibition ◽  
Renin Content

To evaluate the contribution of chloride to NaCl- and KCl-induced renin inhibition, renin responses to NaCl or NaHCO3 and to KCl or KHCO3 loading were compared in NaCl-deprived rats. Sodium balance in animals drinking isotonic NaHCO3 and NaCl for 9 days did not differ (P greater than 0.40); K+ balance was less positive in NaHCO3-drinking animals (P less than 0.005). Plasma renin activity (PRA) in NaCl-loaded (16.5 ng/ml per h +/- 4.4 SE), but not in NaHCO3-loaded rats (57.2 +/- 9.8), was lower (P less than 0.005) than in NaCl-deprived controls (44.8 +/- 4.7). Renal renin content (RRC) of NaCl but not of NaHCO3-drinking animals was also decreased (P less than 0.02). Both PRA and RRC of KCl- but not of KHCO3-loaded rats (5 meq K+/10 g diet) were lower (P less than 0.01) than in NaCl-deprived controls. After acute intravenous expansion with isotonic NaCl or NaHCO3, increases of plasma volume and plasma K+ did not differ (P greater than 0.05). However, PRA of NaCl-expanded rats (11.8 +/- 3.8) was lower (P less than 0.05) than in NaHCO3-expanded animals (29.7 +/- 8.5). The failure of NaHCO3 and KHCO3 to inhibit renin suggests a role for chloride in mediating the renin responses to Na+ and K+.

The Early Effects of Intravenous Frusemide on Central Haemodynamics, Venous Tone and Plasma Renin Activity

1975 ◽  
Vol 49 (6) ◽  
pp. 551-555 ◽  
Author(s):  
B. Hesse ◽  
I. Nielsen ◽  
H. Lund-Jacobsen
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Volume ◽  
Plasma Renin ◽  
Right Heart Catheterization ◽  
Renin Activity ◽  
Heart Catheterization ◽  
Volume Loss ◽  
Volume Depletion ◽  
Venous Tone ◽  
Early Effects

1. Nine patients with clinically unimportant heart disease or benign essential hypertension were given frusemide intravenously during right-heart catheterization. 2. Pressures in both atria decreased rapidly and in parallel. The magnitude of the pressure decrease was clearly related to decrease in plasma volume loss. 3. Plasma renin activity increased significantly after 5 min (P < 0·01), but did not correlate with plasma volume loss. 4. Venous tone in the forearm was unchanged. 5. It is concluded that the pressure reduction was secondary to plasma volume depletion through diuresis and that increased plasma renin activity was mainly caused by intrarenal changes.

Effect of Chronic and Acute Changes in Sodium Balance on the Urinary Excretion of Prostaglandins E2 and F2α in Normal Man

1981 ◽  
Vol 60 (4) ◽  
pp. 405-410 ◽  
Author(s):  
M. Rathaus ◽  
E. Podjarny ◽  
Eli Weiss ◽  
M. Ravid ◽  
Sara Bauminger ◽  
...  
Keyword(s):  
Plasma Renin Activity ◽  
Urinary Excretion ◽  
Prostaglandin E2 ◽  
Prostaglandin F2α ◽  
Plasma Renin ◽  
Renin Activity ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Acute Changes ◽  
Prostaglandins E2 And F2α

1. The effects of changes in sodium balance on renal prostaglandins have been hitherto studied mainly in experimental animals and the results have been controversial. In this study the 24 h urinary excretion of prostaglandins E2 and F2α was measured by radioimmunoassay in seven normal subjects under basal conditions and after 5 days of a diet containing <20 mmol of sodium/day. Subsequently a sodium chloride (150 mmol/l: saline) load (300 mmol of sodium over 4 h) was infused and prostaglandins were again measured in hourly urine collections. Plasma renin activity and aldosterone were also measured under basal conditions, after the low sodium diet and at 2 and 4 h of the saline infusion. 2. Dietary sodium restriction was associated with a marked increase in prostaglandin E2 excretion (from 769.7 ± 201.6 sem to 1761.3 ± 304.9 ng/24 h, P<0.0005). Prostaglandin F2α also increased from 1187.0 ± 390.1 to 1435.6 ± 344.6 ng/24 h, but this was not statistically significant. The prostaglandin E2/prostaglandin F2α ratio increased from 0.83 ± 0.2 to 1.52 ± 0.34 (P<0.01). Plasma renin activity and aldosterone rose significantly (P<0.05 and<0.0025 respectively). 3. During the saline load prostaglandin E2 decreased after 2 h from 142.4 ± 29.9 to 86.7 ± 22.9 ng/h (P<0.05) and to 36.9 ± 5.96 ng/h after 4 h. Prostaglandin F2α decreased at a slower rate, from 98.4 ± 18.7 to 37.5 ± 8.8 ng/h at 4 h (P<0.02). At 4 h the prostaglandin E2/prostaglandin F2α ratio returned to control values (0.90 ± 0.17). Plasma renin activity and aldosterone decreased significantly after 2 h (P<0.02 and<0.0025 respectively) and reached control values after 4 h. 4. The present study demonstrates that chronic and acute changes in sodium balance induce changes in the excretion of prostaglandin E2 parallel to changes in plasma renin activity and aldosterone. The similar but quantitatively smaller changes in prostaglandin F2α and the inversion of the ratio between the two prostaglandins during sodium deprivation suggest that at least two factors are involved: increased delivery of substrate for prostaglandin synthase and decreased activity of the prostaglandin E2 9-ketoreductase. Prostaglandins probably play an important role in the adaptation of the kidney to changes in sodium balance.

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