Insulin-Induced Renin Release: Blockade by Indomethacin in the Rat

1980 ◽  
Vol 58 (5) ◽  
pp. 415-418 ◽  
Author(s):  
W. B. Campbell ◽  
Judith A. Zimmer
Keyword(s):  
Urinary Excretion ◽  
Prostaglandin E2 ◽  
Plasma Catecholamines ◽  
Plasma Renin ◽  
Plasma Potassium ◽  
The Other ◽  
Renin Release ◽  
Plasma Adrenaline ◽  
A Site ◽  
Induced Changes

1. Since prostaglandins appear to mediate adrenergically stimulated renin release, the effect of indomethacin was examined on insulin-induced renin and catecholamine release in conscious rats. Insulin (10 units/kg subcutaneously) increased plasma renin activity from 2.8 ± 0.5 to 9.0 ± 1.1 pmol h−1 ml−1 (P<0.001) while also increasing plasma adrenaline, noradrenaline and the urinary excretion of prostaglandin E2 and F2α. Plasma potassium and glucose were reduced by 16 and 54%respectively. 2. Indomethacin (14 μmol/kg subcutaneously) reduced the urinary excretion of prostaglandin E2 and F2α by 67 and 54%respectively, without altering the other parameters. 3. Indomethacin inhibited insulin-induced renin release by 67%(P<0.01) and blocked the insulin-induced increases in urinary postaglandin E2 and F2α. The insulin-induced changes in plasma catecholamines, potassium and glucose were unaltered by indomethacin. 4. These findings suggest that renal prostaglandins mediate this form of adrenergically stimulated renin release by acting at a site distal to the β-adrenoreceptor.

Plasma Catecholamines and Plasma Renin Activity at Birth and during the First Days of Life

1980 ◽  
Vol 59 (s6) ◽  
pp. 319s-321s ◽  
Author(s):  
G. Leonetti ◽  
C. Bianchini ◽  
G. B. Picotti ◽  
A. Cesura ◽  
Letizia Caccamo ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Umbilical Cord Blood ◽  
Plasma Catecholamines ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Noradrenaline ◽  
Plasma Adrenaline ◽  
Noradrenaline And Adrenaline ◽  
Noradrenaline Levels

1. Plasma noradrenaline and adrenaline concentrations and plasma renin activity were measured in 21 mothers at delivery and in their babies at birth (umbilical cord blood) and on days 1 and 5 of extrauterine life. 2. At birth plasma renin activity was significantly higher in the newborn than in mothers. Plasma renin activity increased further, but not significantly, on day 1 of life and significantly decreased on day 5. On day 5, 10 min head-up tilting caused no change in plasma renin activity. 3. Plasma noradrenaline in the newborn was higher than in mothers at birth and significantly decreased thereafter. Plasma adrenaline levels at birth were similar in the newborn and their mothers and significantly lower in the newborn in subsequent days. Tilting caused no increase in either plasma adrenaline or noradrenaline levels. 4. No correlation was found between plasma noradrenaline and adrenaline levels and plasma renin activity, or between noradrenaline, adrenaline or plasma renin activity and blood pressure.

Effect of propranolol on renin release in the dog

1977 ◽  
Vol 55 (4) ◽  
pp. 747-754 ◽  
Author(s):  
John C. H. Yun ◽  
Gerald D. Kelly ◽  
Frederic C. Bartter
Keyword(s):  
Plasma Renin ◽  
Plasma Potassium ◽  
Sodium Concentration ◽  
Plasma Aldosterone ◽  
Renin Release ◽  
Plasma Sodium ◽  
Renin Substrate ◽  
Arterial Blood ◽  
Consistent Change ◽  
Change In Mean

Infusion of d,l-propranolol in both anesthetized and conscious dogs caused decreases in heart rate (HR), plasma renin activity (PRA), and plasma aldosterone. There was no consistent change in mean arterial blood pressure, plasma renin substrate concentration, packed cell volume, plasma potassium, or plasma sodium concentration following the infusion of propranolol. In five conscious animals, infusion of propranolol (1 mg/kg followed by 0.47–0.65 mg kg−1 h−1) reduced HR from 117.6 ± 4.0 beats per minute (mean ± SE) during control periods to 73.2 ± 2.0 beats per minute (P < 0.005) 90 min after the start of infusion. PRA decreased from 9.97 ± 1.79 ng ml−1 h−1 during control periods to reach 1.50 ± 0.42 ng ml−1 h−1 (P < 0.005) at the end of the 90-min infusions. Plasma aldosterone also decreased during this time from 17.60 ± 1.93 ng% during control periods to reach 6.64 ± 0.98 ng% (P < 0.005). The data suggest that propranolol at the dose administered suppresses renin and aldosterone secretion in unstimulated dogs. They suggest also that β-receptor activity contributes to basal renin release.

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.

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.

Role of Haemodynamics, Catecholamines and Renin in Acute Hypercalcaemic Hypertension in Man

1980 ◽  
Vol 59 (s6) ◽  
pp. 369s-371s ◽  
Author(s):  
C. Marone ◽  
C. Beretta-Piccoli ◽  
P. Weidmann
Keyword(s):  
Blood Pressure ◽  
Plasma Volume ◽  
Plasma Catecholamines ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Peripheral Vascular ◽  
Plasma Adrenaline ◽  
Adrenaline Release ◽  
Calcium Infusion

1. The effect of acute hypercalcaemia on blood pressure, blood volume, haemodynamic indices, plasma catecholamines, renin and aldosterone levels was investigated in 10 patients. 2. Calcium infusion (15 mg/kg over 3 h) increased (P&lt;0.05) plasma calcium and adrenaline levels, blood pressure, total peripheral resistance and packed cell volume. Plasma volume was decreased, and heart rate, cardiac output and plasma renin, aldosterone or dopamine levels were not significantly changed. Plasma noradrenaline was increased only minimally after 3 h of calcium infusion. 3. Mean blood pressure before and during calcium infusion correlated with concomitant serum calcium (r = 0.39; P&lt;0.02) or adrenaline levels (r = 0.57; P&lt;0.01); changes in blood pressure correlated with variations in plasma adrenaline (r = 0.68; P&lt;0.001). 4. Acute hypercalcaemic hypertension is mediated by an increase in peripheral vascular resistance and may be induced by a direct effect of calcium on blood vessels. The calcium-mediated increase in adrenaline release may play a contributory, and plasma volume contraction an inhibitory, role.

scholarly journals The renin-aldosterone axis in two models of reduced renal mass in the rat.

1998 ◽  
Vol 9 (1) ◽  
pp. 72-76 ◽  
Author(s):  
H N Ibrahim ◽  
T H Hostetter
Keyword(s):  
Renal Mass ◽  
Statistical Significance ◽  
Systolic Arterial Pressure ◽  
Plasma Renin ◽  
Surgical Excision ◽  
Plasma Potassium ◽  
Plasma Aldosterone ◽  
The Other ◽  
Scar Region ◽  
Progressive Renal Disease

The renin-angiotensin-aldosterone system participates in chronic progressive renal disease. The studies presented here assessed the importance of aldosterone in two different methods of reduced kidney mass in the rat, i.e., the infarction model (INF; uninephrectomy plus infarction of approximately two-thirds of the other kidney) and surgical excision or polectomy (POL; uninephrectomy plus surgical excision of both poles of the other kidney). Equivalent degrees of reduction in renal mass were confirmed by the similarity of serum creatinines 3 d after the ablative procedure. Measurements were made thereafter at 2 and 4 wk postablation. Systolic arterial pressure was greater with INF at both 2 and 4 wk. Proteinuria was also greater in the INF group at both time periods. The percentage of glomeruli with sclerosis measured at 4 wk tended to be greater in the INF group; however, this difference was not of statistical significance. At 2 wk, plasma renin activity and plasma aldosterone levels were lower in the POL group. The renin concentration in the scar region of the kidneys in the INF group was higher than in the kidney of the POL group. In conjunction with the lower plasma aldosterone, rats in the POL group had higher plasma potassium concentrations at 2 wk. In summary, higher aldosterone and plasma renin levels distinguish the INF model from the POL and likely contribute to the greater proteinuria and hypertension in the INF model.

High potassium intake selectively increases urinary PGF2 alpha excretion in the rat

1985 ◽  
Vol 248 (3) ◽  
pp. F382-F388 ◽  
Author(s):  
A. Nasjletti ◽  
A. Erman ◽  
L. M. Cagen ◽  
D. P. Brooks ◽  
J. T. Crofton ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Reductase Activity ◽  
Control Period ◽  
Plasma Renin ◽  
Experimental Period ◽  
Plasma Potassium ◽  
High Potassium ◽  
Potassium Intake ◽  
Dietary Potassium ◽  
Low Potassium

This study was designed to investigate relationships between dietary potassium and the renal prostaglandin system in rats. The potassium content of the diet was 0.162 mmol/g during the control period and 0.004, 0.162, 1.351, or 2.702 mmol/g during the experimental period. Relative to control data in rats fed a 0.162 mmol/g potassium diet, the urinary excretion of 6-keto-PGF1 alpha was not affected by high potassium intake but increased (P less than 0.05) by 25% in rats fed a low potassium diet for 13 days and was associated with reduction of plasma potassium and with elevation of both plasma renin and net release of 6-keto-PGF1 alpha from renal inner medulla slices incubated in Krebs solution. The excretion of PGF2 alpha was not affected by low potassium intake but increased (P less than 0.05) by about twofold in rats fed a potassium-rich diet (1.351 and 2.702 mmol/g) for 13 days and was associated with elevation of plasma potassium concentration, renal prostaglandin 9-keto-reductase activity, and urinary excretion of kallikrein and vasopressin. The urinary excretion of PGE2 was not altered in rats fed either low or high potassium diets. Altogether, these results indicate selective influence of dietary potassium on the urinary excretion of prostaglandins in the rat.

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