Acute Reduction in Inactive Renin after Stimulation of Active Renin by Converting Enzyme Inhibition (CEI) in Man

1982 ◽  
Vol 63 (s8) ◽  
pp. 175s-177s ◽  
Author(s):  
W. A. Hsueh ◽  
R. Goldstone ◽  
E. J. Carlson ◽  
R. Horton
Keyword(s):  
Single Dose ◽  
Salt Intake ◽  
Repeated Administration ◽  
Active Renin ◽  
Low Salt ◽  
Inactive Renin ◽  
Converting Enzyme Inhibition ◽  
Normal Man ◽  
Circulating Levels ◽  
Stimulation Of

1. Administration of a single dose of captopril, 50 mg, to normal man (n = 7) on a low salt intake induced a 12.5 ± 0.9-fold rise in active renin. The rise in active renin was associated with a reciprocal decrease in circulating inactive renin to 10% or less of control levels. 2. Repeated administration of captopril (50 mg p.o. q 6 h × 3 days) to normal man resulted in increases in both active and inactive renin concentration in plasma. 3. When a single dose of captopril was administered to three patients with hyporeninaemic hypoaldosteronism, no changes in their circulating levels of active or inactive renin occurred. 4. These observations suggest that renal conversion of inactive to active renin may be important in active renin production.

Acid-Activated Renin Responses to Hydrochlorothiazide, Propranolol and Indomethacin

1978 ◽  
Vol 55 (s4) ◽  
pp. 151s-153s ◽  
Author(s):  
J. K. McKenzie ◽  
E. Reisin
Keyword(s):  
Blood Pressure ◽  
Serum Potassium ◽  
Potassium Concentration ◽  
Hypertensive Patients ◽  
Serum Potassium Concentration ◽  
Active Renin ◽  
Serum Aldosterone ◽  
Low Salt ◽  
Inactive Renin ◽  
Marked Suppression

1. Six essential hypertensive patients (five with low renin) were treated in successive weeks with placebo; hydrochlorothiazide 100 mg (382 μmol)/day; hydrochlorothiazide and 50 mmol of sodium/day diet; hydrochlorothiazide, 50 mmol of sodium diet and propranolol 160 mg (544 μmol)/day; and hydrochlorothiazide, 50 mmol of sodium and indomethacin 100 mg (287 μmol)/day. 2. Although blood pressure remained unchanged and serum potassium fell on diuretic with or without low salt, there was a marked increase of active renin and a lesser increase of inactive renin, resulting in an increased proportion of active to total renin. 3. Propranolol decreased both active and inactive renin, but not significantly. 4. Indomethacin produced a marked suppression of active renin, a smaller reduction in inactive renin, and a reduction of the ratio of active to total renin almost to placebo values. 5. Blood pressure rose to control values on indomethacin despite the fall in renin whereas it fell with propranolol with little change in renin. 6. Serum aldosterone rose with stimulation but remained elevated despite effective renin suppression with indomethacin and continuing reduced serum potassium concentration.

Active and Inactive Renin in Individual Juxtaglomerular Apparatuses

1980 ◽  
Vol 59 (s6) ◽  
pp. 35s-36s
Author(s):  
A. Gillies ◽  
T. Morgan ◽  
W. Fitzgibbon
Keyword(s):  
Salt Intake ◽  
Active Form ◽  
Juxtaglomerular Apparatus ◽  
Macula Densa ◽  
Active Renin ◽  
High Salt Intake ◽  
Before And After ◽  
Inactive Renin ◽  
Inhibitor Of Protein Synthesis

1. Renin was measured in individual juxtaglomerular apparatuses before and after acidification in vitro.. 2. Active renin increased with delivery of extra sodium by microperfusion to the macula densa and this increase was similar to that achieved with acidification. 3. In rats pretreated with an inhibitor of protein synthesis active renin increased when extra sodium was delivered to the macula densa. 4. Salt intake changed the amount of renin present in the juxtaglomerular apparatus. In rats on a high salt intake the total renin was low and was all in an active form.

Active and inactive renin in primary and secondary adrenal insufficiency and during ACTH infusion

1983 ◽  
Vol 102 (2) ◽  
pp. 265-270
Author(s):  
Lutz Belkien ◽  
Petra Exner ◽  
Wolfgang Oelkers
Keyword(s):  
Plasma Renin ◽  
Renal Secretion ◽  
Young Males ◽  
Active Renin ◽  
Group I ◽  
Inactive Renin ◽  
Group Ii ◽  
Peripheral Activation ◽  
The Relationship ◽  
Stimulation Of

Abstract. Prolonged low-dose ACTH infusion leads to a transient stimulation of plasma renin activity (PRA) and angiotensin II. In part 1 of the present study (infusion of 10 IU of ACTH per day for 38 h into 6 normal young males), it was shown that the concentration of active renin (aPRC) increases in parallel to PRA. Thus, the rise in PRA is either due to net active renin secretion by the kidney or to increased conversion of inactive into active renin. Since the plasma concentration of inactive renin (iPRC) tended to rise rather than to fall during ACTH infusion, peripheral activation of inactive renin is probably not the cause of the rise in aPRC. Part 2 of the study consisted in the measurement of plasma ACTH, cortisol, PRA, aPRC and iPRC in 10 patients (group I) with primary adrenocortical insufficiency (8 Addisonians, 2 adrenalectomized Cushing's) and in 9 patients with hypopituitarism (group II) after short-term withdrawal of hydrocortisone substition therapy. ACTH was 1770 ± 390 pg/ml in the former and 20 ± 4 pg/ml in the latter group. PRA and aPRC were higher and the ratio iPRC:aPRC lower in group I than in group II. This might indicate stimulation of active renin formation by ACTH. However, it is unlikely that the higher aPRC levels in group I are due to increased peripheral activation of inactive renin, since the relationship between aPRC and the ratio iPRC:aPRC fell on the same curve in both groups. ACTH or an ACTH-dependent mechanism raises aPRC, probably by stimulating its renal secretion rather than by peripheral activation of inactive renin.

Evidence for Activation of Circulating Inactive Renin by the Human Kidney

1979 ◽  
Vol 56 (2) ◽  
pp. 115-120 ◽  
Author(s):  
F. H. M. Derkx ◽  
G. J. Wenting ◽  
A. J. Man In't Veld ◽  
R. P. Verhoeven ◽  
M. A. D. H. Schalekamp
Keyword(s):  
Renal Vein ◽  
Human Kidney ◽  
Activation Process ◽  
Peripheral Vein ◽  
Active Renin ◽  
A Value ◽  
Before And After ◽  
Inactive Renin ◽  
Propranolol Treatment ◽  
Stimulation Of

1. In eight patients with essential hypertension (EHT) and six patients with renovascular hypertension (RVHT) peripheral venous enzymatically active and inactive renin values were followed after acute stimulation of renin release by the vasodilating agent diazoxide (300 mg intravenously). Active renin rose during the first hour after diazoxide and remained high during the following 15 h, but inactive renin fell during the first hour and rose thereafter. Peripheral venous active and inactive renin were not different from arterial values both before and after diazoxide. 2. Sixteen patients with EHT received propranolol, 80 mg, four times a day. Six of them had a first injection of diazoxide the day before propranolol was started and a second one after 10–14 days of propranolol treatment. Peripheral vein active renin was lowered by propranolol, but inactive renin was raised. Both the diazoxide-induced rapid rise of active renin and the fall of inactive renin observed in untreated patients were absent during treatment with propranolol. 3. In four patients with EHT and seven patients with RVHT renal vein sampling was performed before and 30 min after diazoxide. Increased release of active renin from kidneys that were not markedly contracted was associated with a fall of the renal vein to peripheral vein ratio of inactive renin to a value less than one. 4. It is concluded that under certain circumstances stimulated release of active renin is associated with removal of inactive renin from the circulation by the kidney. This may in fact be due to intrarenal transformation of circulating inactive renin into its active counterpart. The findings suggest that a β-adrenoreceptor might be involved in this activation process.

Stimulation of plasma inactive renin by dexamethasone in the cat

1989 ◽  
Vol 257 (6) ◽  
pp. E879-E884
Author(s):  
N. Glorioso ◽  
C. Troffa ◽  
G. Tonolo ◽  
M. G. Melis ◽  
P. Manunta ◽  
...  
Keyword(s):  
Time Course ◽  
Consensus Sequence ◽  
Recovery Period ◽  
Base Line ◽  
Active Renin ◽  
Human Renin ◽  
Inactive Form ◽  
Inactive Renin ◽  
Selective Increase ◽  
Stimulation Of

An inactive form of renin in human plasma is the biosynthetic precursor, prorenin. The cat is a good animal model for studies of inactive renin. The gene for human renin contains sequences homologous to the glucocorticoid consensus sequence. The response of cat plasma (active and inactive renin) and of angiotensinogen to administration of dexamethasone (0.5 mg/kg im, daily) was studied in ketamine-sedated cats (20 mg/kg im). Inactive renin increased by twofold after 7 days of dexamethasone (P less than 0.01). After a 7-day recovery period, it returned to base line. Active renin did not change. Angiotensinogen fell by 35% (P less than 0.01). The time course of the selective increase of plasma inactive renin showed that inactive renin began to rise after 2 days, peaking after 5 days. Ketamine alone induced inactive renin to rise slightly but significantly (P less than 0.05), although the magnitude of the increment was much less than that observed in ketamine-sedated cats receiving dexamethasone (P less than 0.01). Active renin did not change, whereas angiotensinogen was reduced by 25% (P less than 0.01). Our findings support the hypothesis that glucocorticoids might have a selective role in the synthesis and/or secretion of the precursor of renin, at least in the cat.

Effects of isoprostane on tubuloglomerular feedback: roles of TP receptors, NOS, and salt intake

2005 ◽  
Vol 288 (4) ◽  
pp. F757-F762 ◽  
Author(s):  
William J. Welch
Keyword(s):  
Salt Intake ◽  
Tubuloglomerular Feedback ◽  
Loop Of Henle ◽  
Dietary Salt ◽  
Low Salt ◽  
Luminal Perfusion ◽  
Tp Receptors ◽  
Flow Pressure ◽  
Stop Flow ◽  
Stimulation Of

A thromboxane prostanoid receptor (TP-R) agonist U-46,619 enhances tubuloglomerular feedback (TGF). Glomerular expression of TP-R and enhancement of TGF by U-46,619 increase with salt intake. We investigated the hypothesis that 8-isoprostaglandin F2α (8-Iso) activates TGF via TP-R. The maximal TGF response in rats was assessed from the fall in proximal stop flow pressure (PSF; an index of glomerular capillary pressure) during loop of Henle (LH) microperfusion of artificial tubular fluid (ATF) at 40 nl/min. Microperfusion of 8-Iso (10−4 M) into the efferent arteriole (EA) enhanced TGF responses by 20 ± 3% ( P < 0.01). TGF response to 8-Iso was independent of dietary salt [ΔTGF%, low salt (LS): 21 ± 5%; normal salt (NS): 17 ± 4%; high salt (HS): 29 ± 8%, not significant (ns)], unlike the salt-dependent effect of U-46,619 (ΔTGF%, LS: 41 ± 5%; NS: 52 ± 4%; HS: 112 ± 21%). Ifetroban, the TP-R antagonist, abolished TGF responses to 8-Iso and U-46,619 at all levels of salt intake. During luminal perfusion of N-monomethyl-l-arginine (l-NMA), the effect of 8-Iso on TGF was enhanced in NS and HS but not in LS (LS: 22 ± 6 vs. LS + l-NMA: 28 ± 6%, ns; NS: 18 ± 4 vs. NS + l-NMA: 40 ± 4, P < 0.01; HS: 27 ± 3 vs. HS + l-NMA: 65 ± 6, P < 0.01). However, U-46,619 did not further increase TGF after l-NMA in all salt groups (LS: 43 ± 7 vs. LS + l-NMA: 51 ± 6, ns; NS: 52 ± 7 vs. NS + l-NMA: 48 ± 8, ns; HS: 114 ± 21 vs. HS + l-NMA: 74 ± 22, ns). In conclusion, activation of TP receptors by U-46,619 and 8-Iso-PGF2α enhances TGF. In addition, the effect of U-46,619 was salt dependent, whereas the effect of 8-Iso-PGF2α was salt independent. However, stimulation of NO by 8-isoprostanes masks its salt-sensitive effect on TGF.

Release of active and inactive renin from hog renal cortical slices in vitro

1984 ◽  
Vol 246 (6) ◽  
pp. F765-F771 ◽  
Author(s):  
T. Okamura ◽  
T. Inagami
Keyword(s):  
Renin Release ◽  
Dibutyryl Camp ◽  
Active Renin ◽  
Renal Kallikrein ◽  
Inactive Renin ◽  
Cortical Slices ◽  
Selective Mechanism ◽  
Hog Kidney ◽  
Stimulation Of

Both inactive and active renin were released from renal cortical slices of the hog. Isoproterenol, prostaglandin E1, and dibutyryl cAMP stimulated the release of both inactive and active renin. Renal kallikrein caused selective stimulation of the release of active renin and suppressed the release of inactive renin. Bradykinin and kallidin did not stimulate renin release. The effect of kallikrein was abolished by aprotinin but not by indomethacin. These observations indicate that the effect of kallikrein is not mediated via kinin formation or prostaglandin generation. The data suggest that there may be at least two types of mechanism for renin release from hog kidney. One is of the nonselective type by which both active and inactive renin are released, as in the case of beta-adrenergic or prostaglandin stimulation. The other is a selective mechanism by which only active renin is preferentially released, as in the case of urinary or renal kallikrein stimulation.

Ontogeny of neuronally released norepinephrine on renin secretion in sheep

1989 ◽  
Vol 257 (4) ◽  
pp. R765-R770 ◽  
Author(s):  
K. T. Nakamura ◽  
J. M. Klinkefus ◽  
F. G. Smith ◽  
T. Sato ◽  
J. E. Robillard
Keyword(s):  
Renin Secretion ◽  
Renal Nerves ◽  
Nerve Terminals ◽  
Norepinephrine Release ◽  
Fetal Sheep ◽  
Postnatal Maturation ◽  
Active Renin ◽  
Inactive Renin ◽  
Cortical Slices

The role of renal nerves and norepinephrine release on renin secretion during fetal and postnatal maturation has not been studied. Experiments were performed to determine the effect of veratridine, a substance known to promote norepinephrine release from nerve terminals, on active and inactive renin secretion from renal cortical slices of fetal (134-138 days gestation; term is 145 days), newborn (4-9 days of age), and adult nonpregnant sheep. Veratridine (10-300 microM) significantly increased active renin secretion and produced a small but nonsignificant rise in inactive renin secretion in all three groups of animals (P less than 0.05). The percent rise in active renin secretion during veratridine stimulation was similar among all groups. Veratridine-stimulated (300 microM) active renin secretion was antagonized by tetrodotoxin (0.5 and 5.0 microM) and DL-propranolol (1 microM) in fetal renal cortical slices. However, neither tetrodotoxin nor propranolol completely inhibited the stimulatory effect of veratridine on active renin secretion. These results suggest that 1) norepinephrine released from nerve terminals may regulate active renin secretion early during development; 2) the effect of veratridine on active renin secretion was similar in fetal, newborn, and adult sheep; 3) veratridine had no significant effect on inactive renin secretion; and 4) active renin secretion due to depolarization of nerve terminals in fetal sheep is dependent on activation of beta-adrenoceptors as it is in adults.

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