Renin secretion and loop of Henle chloride reabsorption in the adrenalectomized rat

1985 ◽  
Vol 249 (4) ◽  
pp. F596-F602
Author(s):  
W. J. Welch ◽  
C. E. Ott ◽  
G. P. Guthrie ◽  
T. A. Kotchen
Keyword(s):  
Sodium Chloride ◽  
Chloride Transport ◽  
Plasma Renin ◽  
Saline Infusion ◽  
Renin Release ◽  
Loop Of Henle ◽  
Water Drinking ◽  
Before And After ◽  
Adrenalectomized Rats ◽  
Stimulation Of

Renin release is increased in the adrenalectomized rat and is not inhibited by sodium chloride administration. The purpose of this study was to determine whether increased renin release is related to impaired absorptive chloride transport in the loop of Henle. Chloride transport in the loop was measured before and after acute saline infusion in three groups of rats: 1) saline-drinking adrenalectomized rats (Adx); 2) saline-drinking dexamethasone-treated adrenalectomized rats (Dex); and 3) water-drinking sham-operated controls. Unrelated to differences of arterial pressure, glomerular filtration rate, or net sodium chloride balance, chloride reabsorption in the loop of Henle of Adx [836 +/- 172 peq/min (SE)] was less (P less than 0.01) than in controls (1,646 +/- 353) and Dex (1,377 +/- 318) before saline infusion. After saline infusion, chloride delivery to the loop increased (P less than 0.05) in all three groups. However, loop chloride reabsorption increased (P less than 0.01) only in controls and Dex but not in Adx. Before saline infusion, plasma renin concentration (PRC) of Adx (350 +/- 108 U/ml) was greater (P less than 0.01) than that in controls (56 +/- 6) or Dex (108 +/- 36); sodium chloride infusion failed to inhibit PRC in Adx, whereas PRC was suppressed (P less than 0.01) by saline in Dex and controls. Thus stimulation of renin release in adrenalectomized animals was associated with decreased absorptive chloride transport in the loop of Henle. Dexamethasone normalized loop function and renin responsiveness to sodium chloride.

Importance of chloride for acute inhibition of renin by sodium chloride

1978 ◽  
Vol 235 (5) ◽  
pp. F444-F450 ◽  
Author(s):  
K. A. Kirchner ◽  
T. A. Kotchen ◽  
J. H. Galla ◽  
R. G. Luke
Keyword(s):  
Sodium Chloride ◽  
Chloride Transport ◽  
Free Water ◽  
Plasma Renin ◽  
Sodium Balance ◽  
Thick Ascending Limb ◽  
Free Water Clearance ◽  
Sodium Salts ◽  
Before And After ◽  
Renin Inhibition

To evaluate the contribution of chloride to acute renin inhibition by sodium chloride, plasma renin activity (PRA) was measured before and after peripheral venous infusion of NaCl, NaHCO3, NaBr, NaNO3, lysine monohydrochloride, or lysine glutamate in NaCl-deprived rats. In contrast to controls and animals infused with other sodium salts, PRA decreased (P less than 0.01) after infusion with NaCl [from 28.3 +/- 2.8 to 13.3 +/- 1.8 ng/ml per h (SE)] and NaBr (from 40.6 +/- 6.2 to 21.8 +/- 3.9 ng/ml per h), and renal tubular halide reabsorption increased (P less than 0.05). Arterial pressure, plasma volume, inulin clearance, net sodium balance, serum Na+ and K+, and pH were not different among sodium-loaded groups. PRA was also suppressed (P less than 0.01) by infusion with lysine monohydrochloride (from 51.6 +/- 5.4 to 32.4 +/- 5.1 ng/ml per h) but not with lysine glutamate. These results suggest that inhibition of renin by sodium is dependent on an intrarenal effect of chloride. During infusion with sodium salts which suppressed renin, negative free water clearance (TcH2O) increased, whereas infusion with sodium salts that did not inhibit renin resulted in either no change or decreased TcH2O. The association of renin inhibition and increased TcH2O indirectly supports the hypothesis that renin suppression by chloride is related to the magnitude of absorptive chloride transport in the thick ascending limb of the loop of Henle.

Effect of Na and Cl infusion on loop function and plasma renin activity in rats

1990 ◽  
Vol 258 (5) ◽  
pp. F1328-F1335 ◽  
Author(s):  
J. N. Lorenz ◽  
T. A. Kotchen ◽  
C. E. Ott
Keyword(s):  
Plasma Renin Activity ◽  
Chloride Transport ◽  
Chloride Concentration ◽  
Specific Effect ◽  
Distal Tubule ◽  
Plasma Renin ◽  
Renin Activity ◽  
Thick Ascending Limb ◽  
Loop Of Henle ◽  
Before And After

Inhibition of plasma renin activity (PRA) by saline has been shown to be related to a specific effect of chloride. The purpose of this study was to test the hypothesis that inhibition of renin release by selective chloride infusion in the rat is related to increased chloride transport in the thick ascending limb of the loop of Henle (TALH). Measurements of loop of Henle function were obtained by micropuncture before and after a 5% body wt infusion of solutions containing either 0.15 mol/l NaCl, 0.15 mol/l lysine monohydrochloride (LysCl), or 0.15 mol/l Na-assorted anions (NaAA). Both NaCl and LysCl infusion lowered PRA (60.8 +/- 11.9 to 22.6 +/- 3.7 ng angiotensin I (ANG I).ml-1.h-1 and 53.3 +/- 6.8 to 34.5 +/- 4.6 ng ANG I.ml-1.h-1; P less than 0.05), whereas NaAA infusion had no effect on PRA (66.7 +/- 15.1 to 59.1 +/- 12.4 ng ANG I.ml-1.h-1). Analysis of late proximal and early distal fluid showed that chloride transport in the TALH was significantly elevated by infusion in all three groups, and there were no differences among the groups after infusion. Distal chloride concentration increased in the NaCl and LysCl groups (26 +/- 2 to 37 +/- 1 meq/l and 26 +/- 2 to 36 +/- 2 meq/l; P less than 0.05), but distal chloride concentration decreased in the NaAA group (28 +/- 2 to 22 +/- 1 meq/l; P less than 0.05). There was no correlation between PRA and fluid flow rate or chloride delivery to the distal tubule.(ABSTRACT TRUNCATED AT 250 WORDS)

Suppression of renin release by antagonism of endogenous opiates in the dog

1986 ◽  
Vol 250 (4) ◽  
pp. R633-R637
Author(s):  
J. E. Szilagyi ◽  
J. Chelly ◽  
M. F. Doursout
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Endogenous Opioids ◽  
Renin Activity ◽  
Renin Release ◽  
Endogenous Opioid ◽  
Endogenous Opiates ◽  
Arterial Blood ◽  
Before And After ◽  
Arterial Constriction

The influence of blockade of endogenous opioids on the release of renin due to partial renal arterial constriction was determined acutely and chronically in unilaterally nephrectomized dogs. In acute preparations changes in plasma renin activity, arterial blood pressure, and heart rate were determined after 15 min of 60% renal arterial constriction before and after administration of either a saline vehicle, the opiate antagonist naloxone (0.05 mg/kg), or morphine (2 mg/kg). Acute antagonism of endogenous opiates abolished the increase in plasma renin activity and mean arterial pressure associated with renal arterial constriction. Repeated renal arterial constrictions in saline- or morphine-treated animals did not alter the humoral or hemodynamic responses. In chronic preparations long-term naloxone infusion attenuated the development of renovascular hypertension and diminished the increase in plasma renin activity. These data suggest that endogenous opioid peptides are modulators in the control of renin release and may be important participants in the pathogenesis of hypertension.

Effect of deoxycorticosterone on sodium appetite of intact and adrenalectomized rats

1965 ◽  
Vol 208 (6) ◽  
pp. 1281-1285 ◽  
Author(s):  
George Wolf
Keyword(s):  
Sodium Chloride ◽  
Low Doses ◽  
Sodium Appetite ◽  
Self Selection ◽  
Saline Preference ◽  
High Doses ◽  
Adrenalectomized Rats ◽  
Stimulation Of ◽  
Intact Rats

The effect of DOC on sodium chloride (saline) intake was studied in intact and adrenalectomized rats under "two-bottle" self-selection conditions. It was found that in adrenalectomized rats low doses of DOC produced a decrease in saline intake (restoration of sodium-retaining ability), whereas high doses produced an increase in saline intake (stimulation of sodium appetite). At high doses, however, intact rats consumed more saline and manifested a greater preference for it than did similarly treated adrenalectomized rats. Treatment with corticosterone increased both absolute saline intake and saline preference of DOC-treated adrenalectomized rats.

α1-Adrenoceptor Blockade: Dissociation of Its Effects on Renin Release and Arterial Blood Pressure in Man

1981 ◽  
Vol 61 (s7) ◽  
pp. 307s-309s ◽  
Author(s):  
A. Morganti ◽  
Carla Sala ◽  
Anna Palermo ◽  
Lucia Turolo ◽  
A. Zanchetti
Keyword(s):  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Pressor Response ◽  
Plasma Renin ◽  
Test Dose ◽  
Blocking Agent ◽  
Renin Activity ◽  
Renin Release ◽  
Arterial Blood ◽  
Before And After

1. The possibility that the juxtaglomerular α1-adrenoceptors mediate an inhibitory action on renin release in man was examined in seven patients with essential hypertension, by measuring (i) the acute effects of prazosin (0.25 mg intravenously), a selective α1-adrenoceptor-blocking agent, on arterial pressure and plasma renin activity, the degree of α-blockade induced by the drug being assessed by comparing the pressor response with that to a test dose of phenylephrine before and after prazosin administration, and (ii) the increases in plasma renin activity in response to isoprenaline before and during the prazosin-induced α-blockade. 2. Twenty minutes after the infusion of prazosin, when the pressor response to phenylephrine was reduced by 80% with respect to control, (i) mean arterial pressure was practically unchanged, (ii) plasma renin activity was almost doubled and (iii) the increases in plasma renin activity in response to isoprenaline were significantly greater, both in absolute and percentage values, than those observed before prazosin. 3. The increments in baseline plasma renin activity induced by prazosin in the absence of decrease in arterial pressure and the enhancement in renin responsiveness to the β-adrenoceptor stimulus suggest that, in man, the juxtaglomerular α1-adrenoceptors exert a direct, suppressive action on renin release.

Exaggerated responsiveness of immunoreactive atrial natriuretic peptide to saline infusion in chronic renal failure

1987 ◽  
Vol 72 (1) ◽  
pp. 19-24 ◽  
Author(s):  
Robert G. Walker ◽  
Charles P. Swainson ◽  
Tim G. Yandle ◽  
M. Gary Nicholls ◽  
Eric A. Espiner
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Renin ◽  
Saline Infusion ◽  
Physiological Importance ◽  
Before And After ◽  
Intravenous Sodium ◽  
Atrial Natriuretic

1. Plasma levels of immunoreactive alpha human atrial natriuretic peptide (IR-ANP) were measured in nine patients with chronic renal failure before and after removal of 1.3–3.7 litres of fluid by ultrafiltration and again during volume repletion with intravenous sodium chloride solution (150 mmol/l: saline). 2. Baseline levels of IR-ANP were elevated but fell by 22% during ultrafiltration. 3. Saline infusion induced a rapid and steep rise in IR-ANP levels which were 150% of baseline while body weight was still 2% below baseline. 4. Changes in plasma renin, angiotensin II, aldosterone and vasopressin during the study were slight compared with the change in IR-ANP, but noradrenaline levels rose threefold during ultrafiltration. 5. There was a significant positive relationship between arterial pressure and IR-ANP levels before and after ultrafiltration. 6. These results lend support to the suggestion that atrial peptides are of physiological importance, especially in states of chronic fluid overload such as chronic renal failure.

Modulation of renin by thromboxane: studies with thromboxane synthase inhibitor, receptor antagonists, and mimetic

1989 ◽  
Vol 257 (4) ◽  
pp. F554-F560 ◽  
Author(s):  
W. J. Welch ◽  
C. S. Wilcox ◽  
K. R. Dunbar
Keyword(s):  
Blood Pressure ◽  
Salt Intake ◽  
Plasma Renin ◽  
Renal Hemodynamics ◽  
Thromboxane Synthase ◽  
Anesthetized Rats ◽  
Before And After ◽  
Synthase Inhibitor ◽  
By Products ◽  
Stimulation Of

The regulation of plasma renin activity (PRA) by thromboxane (Tx) A2 was studied in anesthetized rats by measuring PRA before and after administration of drugs that block cyclooxygenase (CO) (indomethacin [INDO], 5 mg/kg), thromboxane synthase (TS) (UK 38485 [UK], 100 mg/kg), or Tx receptors (SQ 29548 [SQ], 8 mg/kg or L 641953 [L], 50 mg/kg) or that activate Tx receptors (U 46619 [U], 10 ng.kg-1.min-1). PRA (ng ANG I.ml-1.h-1) was unaffected by vehicle; it was reduced by INDO (25 +/- 2 to 13 +/- 3, n = 13, P less than 0.001) but was increased by UK (24 +/- 3 to 50 +/- 6, n = 18, P less than 0.005), SQ (27 +/- 4 to 44 +/- 7, n = 6, P less than 0.05), and L (32 +/- 4 to 51 +/- 7, n = 10, P less than 0.05). U reduced PRA in each rat (17 +/- 3 to 10 +/- 3, n = 6, P less than 0.005). UK caused dose-dependent stimulation of PRA (mean effective dose 50 mg/kg) and inhibition of TxB2 excretion (mean inhibitory dose 15 mg/kg). After INDO, SQ no longer changed PRA (-1 +/- 10, n = 7). Prolonged administration of SQ for 4-6 days (20 mg.kg-1.day-1 ip) did not change Na+ or K+ balances, blood pressure, renal hemodynamics, or urine flow. However, SQ stimulated PRA (P less than 0.007) independent of prior salt intake. In conclusion in anesthetized rats 1) PRA is stimulated by products of CO but inhibited by products of TS and by a Tx mimetic; 2) stimulation of PRA by SQ depends on ongoing PG and Tx synthesis; 3) rise in PRA with Tx antagonists is not closely related to changes in salt balance, blood pressure, or renal hemodynamics.

Effects of altered NaCl intake on renal hemodynamic and renin release responses to RNS

1987 ◽  
Vol 253 (5) ◽  
pp. F976-F981 ◽  
Author(s):  
J. L. Osborn ◽  
D. D. Kinstetter
Keyword(s):  
Sodium Chloride ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Renin Release ◽  
Renal Vasculature ◽  
Renal Nerve ◽  
High Sodium ◽  
Low Sodium ◽  
Anesthetized Dogs ◽  
Neurogenic Vasoconstriction

Relationships between frequency of renal nerve stimulation (RNS) and renal blood flow (RBF), glomerular filtration rate (GFR), and plasma renin activities (PRA) were evaluated in anesthetized dogs placed on low (5 meq/day)-, normal (40 meq/day)-, and high (200 meq/day)-sodium chloride diets. Arterial pressure, RBF, GFR, and renal venous and arterial PRA were determined before and during direct electrical RNS at 0.5, 1.0, and 2.0 Hz (15 V, 1.0 ms). Dogs on low sodium intakes increased renal venous PRA at 0.5, 1.0-, and 2.0-Hz RNS, whereas dogs on normal sodium intakes did not increase renal venous PRA until RNS reached 2.0 Hz. High sodium dogs did not increase PRA at any frequency of RNS tested. RNS at 0.5 Hz was not associated with any changes in GFR or RBF in any of the groups. Dogs on normal sodium and high sodium intakes decreased both GFR and RBF during 1.0- and 2.0-Hz RNS. Low-sodium dogs, however, only decreased GFR and RBF during 2.0-Hz RNS, and these hemodynamic responses were significantly less than 2.0-Hz GFR and RBF responses of high sodium dogs. These data indicate that renal vasoconstrictor responses to RNS are potentiated, and renin release responses to RNS are reduced by elevation of sodium chloride intake. We suggest that during low sodium intake, activation of sympathetic nerve activity elicits an enhanced renin release response, whereas the renal vasculature may be protected against neurogenic vasoconstriction.

Body temperature modification of osmotically induced vasopressin secretion and thirst in humans

1995 ◽  
Vol 269 (4) ◽  
pp. R874-R880 ◽  
Author(s):  
A. Takamata ◽  
G. W. Mack ◽  
N. S. Stachenfeld ◽  
E. R. Nadel
Keyword(s):  
Hypertonic Saline ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
Saline Infusion ◽  
Body Core Temperature ◽  
Healthy Humans ◽  
Before And After ◽  
Vasopressin Secretion ◽  
Plasma Arginine ◽  
Hypertonic Saline Infusion

We examined the effect of increased body core temperature (Tes) on the plasma arginine vasopressin concentration ([AVP]p) and thirst responses to increased plasma osmolality (Posm) induced by 3% NaCl infusion for 120 min in seven healthy humans. Tes was increased by immersion of the lower legs in 41 degrees C water in a 28 degrees C room (passive heating; HT). Immersion of the lower legs in 34.5 degrees C water on a separate day served as the control (thermoneutral; NT). The 120-min hypertonic saline infusion was initiated 30 min after the onset of leg immersion and was followed by a 30-min rehydration period. Tes in HT increased by 0.21 +/- 0.04 degree C before infusion and by 0.86 +/- 0.08 degree C at the end of infusion. The change in Tes in NT before and after the infusion was negligible. Posm was increased by 15.0 +/- 1.0 mosmol/kgH2O by infusion in both NT and HT. [AVP]p increased by 3.48 +/- 0.72 pg/ml in NT and by 7.59 +/- 1.02 pg/ml in HT. Thus the increase in [AVP]p at a given increase in Posm was markedly higher in HT than in NT. The plasma renin activity response to hypertonic saline infusion in both conditions was similar. Subjective thirst rating and cumulative water intake during rehydration were higher in HT than in NT.(ABSTRACT TRUNCATED AT 250 WORDS)

Decreased Plasma Renin Activity and Renin Release in Rats with Phaeochromocytoma

1977 ◽  
Vol 53 (5) ◽  
pp. 447-452
Author(s):  
J. C. S. Fray ◽  
P. V. H. Mayer
Keyword(s):  
Sodium Chloride ◽  
Plasma Renin Activity ◽  
Perfusion Pressure ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
High Sodium ◽  
Sodium Chloride Loading ◽  
And Control ◽  
Renin Content

1. We have examined the response of renin to chronic low and high sodium chloride intake in rats with transplanted phaeochromocytoma. 2. Phaeochromocytoma suppressed the usual elevated plasma renin activity observed during sodium deprivation. 3. Studies in isolated perfused kidneys indicated that sodium-deprived phaeochromocytoma rats released substantially less renin than sodium-deprived control rats despite an almost identical renal renin content in both sets of animals. In addition, low perfusion pressure (50 mmHg) failed to stimulate renin release in kidneys from these phaeochromocytoma rats. 4. Additional experiments demonstrated that chronic sodium chloride loading suppressed plasma renin activity, renin content and renin release in both phaeochromocytoma and control rats. Both sodium-loaded phaeochromocytoma and sodium-loaded control rats were unresponsive to low perfusion pressure. 5. We conclude that noradrenaline-secreting phaeochromocytoma impairs the response of plasma renin activity in the rat by inhibiting renin release. We also conclude that chronic sodium chloride loading has a similar effect, but the mechanisms remain to be determined.

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