Effect of cyclooxygenase and thromboxane synthetase inhibition on furosemide-stimulated plasma renin activity

1987 ◽  
Vol 65 (1) ◽  
pp. 80-83 ◽  
Author(s):  
Sunil Datar ◽  
Frances A. McCauley ◽  
Thomas W. Wilson
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Cyclooxygenase Inhibitor ◽  
Sprague Dawley ◽  
Blood Samples ◽  
Sprague Dawley Rats ◽  
Thromboxane Synthetase ◽  
Serum Thromboxane

We studied the effects of a specific thromboxane (TX) synthetase inhibitor (U-63,557A) and a cyclooxygenase inhibitor on furosemide-induced renin release. Furosemide (2.0 mg∙kg−1) was injected into Sprague–Dawley rats pretreated with indomethacin (10 mg∙kg−1, i.v.), U-63,557A (1.0–32.0 mg∙kg−1, i.v.), or vehicle (Na2CO3 0.03 M). Plasma renin activity was measured in blood samples collected 0, 10, 20, and 40 min after the injection of furosemide. Blood was also collected after the administration of vehicle, indomefhacin, or U-63,557A for serum TXB2, a measure of platelet TXA2 synthesis. The results demonstrated that plasma renin activity rose with time following furosemide in the various groups of rats; indomethacin suppressed the furosemide-induced increments in plasma renin activity, while U-63,557A at doses of 4–8 mg∙kg−1 augmented it. At doses below 4 mg∙kg−1 or above 8 mg∙kg−1, U-63,557A did not augment renin secretion. Indomethacin and U-63,557A reduced serum thromboxane by 81 and 90%, respectively. Thus, these experiments suggest that thromboxane synthetase inhibition, within a narrow dosage range, potentiates furosemide-induced renin release while cyclooxygenase inhibition suppresses it.

Beta-adrenoceptor-stimulated renin release is blunted in old rats.

1998 ◽  
Vol 9 (7) ◽  
pp. 1318-1320
Author(s):  
C Baylis ◽  
K Engels ◽  
W H Beierwaltes
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Sprague Dawley ◽  
Angiotensin I ◽  
Beta Adrenoceptors ◽  
Beta Adrenoceptor ◽  
Sprague Dawley Rats ◽  
Old Rats

Plasma renin activity (PRA) was similar in young versus old male Sprague Dawley rats under unstressed conditions (1.3 +/- 0.2 versus 1.8 +/- 0.3 ng angiotensin I/ml per min). Airjet stress increases PRA in young but not old rats (13.9 +/- 3.8 versus 2.9 +/- 0.8 ng angiotensin I/ml per min), respectively. This response is ablated in young rats by beta-adrenoceptor blockade, suggesting that the increased PRA is mediated by beta-adrenoceptors, and this response was blunted in old rats.

scholarly journals Sodium, potassium and chloride utilization by rats given various inorganic anions

1991 ◽  
Vol 66 (3) ◽  
pp. 523-532 ◽  
Author(s):  
Susan M. Kaup ◽  
Alison R. Behling ◽  
J. L. Greger
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Basal Diet ◽  
Renin Activity ◽  
Sprague Dawley ◽  
Sodium Potassium ◽  
Sprague Dawley Rats ◽  
Blood Pressures ◽  
Sodium And Potassium

The purpose of the present studies was to examine the effect of ingestion of sodium and potassium salts of various fixed anions on blood pressure, and to assess interactions among electrolytes. In the first study, Sprague-Dawley rats fed on purified diets supplemented with Na salts of chloride, sulphate, bisulphate, carbonate and bicarbonate for 7 weeks developed higher blood pressures than rats fed on the basal diet. In a second study, rats fed on Na or K salts of HSO4, HCO3 or Cl had higher blood pressures than rats fed on the basal diet. Blood pressure measurements were not correlated with plasma volume, plasma renin activity, or plasma atrial natriuretic peptide concentrations at 7 weeks. Plasma renin activity was depressed in rats fed on supplemental Na and even more in rats fed on supplemental K salts rather than the basal diet. Generally, rats fed on supplemental Na excreted Na in urine and absorbed Na in the gut more efficiently than rats fed on the basal diet or diets supplemented with K, but the anions fed also altered Na absorption and excretion. In a third study, rats fed on diets supplemented with any Cl salt, but especially KCI, absorbed K more efficiently than those fed on the basal diet. In studies 1 and 2, the efficiency of urinary excretion of K was greatest when HCO3 and CO3 salts were fed and least when HSO4 salts were fed. Despite large variations in the efficiency of absorption and excretion of Na and K, tissue levels of the electrolytes remained constant.

Failure of Loading with Sodium Bicarbonate to Protect against Acute Renal Failure Induced by Mercuric Chloride in the Rat

1977 ◽  
Vol 53 (2) ◽  
pp. 149-154 ◽  
Author(s):  
J. E. Beaumont ◽  
T. A. Kotchen ◽  
J. H. Galla ◽  
R. G. Luke
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Sodium Balance ◽  
Control Group ◽  
Sprague Dawley ◽  
Urinary Volume ◽  
Sprague Dawley Rats

1. To investigate the mechanism by which sodium loading protects against acute renal failure we compared the effects of prior chronic loading with NaCl, or with NaHCO3, on renal function after injection of HgCl2. 2. Twenty-four male Sprague-Dawley rats were divided into three groups of eight rats. One group drank isotonic NaCl solution, a second drank isotonic NaHCO3 solution and the third control group drank deionized water. Acute renal failure was induced by HgCl2 on day 9, and the rats were killed 48 h after injection. 3. Net sodium balances and plasma volumes were similar in both groups of sodium-loaded rats. After HgCl2 serum creatinine was significantly less and urinary volume was greater in NaCl-loaded than in both NaHCO3-loaded and water-drinking animals. 4. Plasma renin activity of both NaCl- and NaHCO3-loaded animals was less than that of control rats. However, renal renin content was suppressed by NaCl but not by NaHCO3 loading. 5. Loading with NaCl afforded greater protection against HgCl2-induced acute renal failure than NaHCO3. Since this difference was not related to changes in sodium balance or plasma volume before HgCl2, or plasma renin activity after HgCl2, the results support the hypothesis that intrarenal renin plays a role in the pathogenesis of HgCl2-induced acute renal failure in the rat.

Enhancement of the Antihypertensive Effect of Hydrochlorothiazide in Dogs after Suppression of Renin Release by Beta-Adrenergic Blockade

1975 ◽  
Vol 48 (2) ◽  
pp. 147-151
Author(s):  
C. S. Sweet ◽  
M. Mandradjieff
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Arterial Blood Pressure ◽  
Antihypertensive Effect ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Antihypertensive Activity ◽  
Adrenergic Blockade ◽  
Arterial Blood

1. Renal hypertensive dogs were treated with hydrochlorothiazide (8−2 μmol/kg or 33 μmol/kg daily for 7 days), or timolol (4.6 μmol/kg daily for 4 days), a potent β-adrenergic blocking agent, or combinations of these drugs). Changes in mean arterial blood pressure and plasma renin activity were measured over the treatment period. 2. Neither drug significantly lowered arterial blood pressure when administered alone. Plasma renin activity, which did not change during treatment with timolol, was substantially elevated during treatment with hydrochlorothiazide. 3. When timolol was administered concomitantly with hydrochlorothiazide, plasma renin activity was suppressed and blood pressure was significantly lowered. 4. These observations suggest that compensatory activation of the renin-angiotensin system limits the antihypertensive activity of hydrochlorothiazide in renal hypertensive dogs and suppression of diuretic-induced renin release by timolol unmasks the antihypertensive effect of the diuretic.

Effect of ovariectomy on vasopressin, ACTH, and renin activity responses to hypotension

1991 ◽  
Vol 261 (1) ◽  
pp. R223-R230 ◽  
Author(s):  
M. Keller-Wood ◽  
C. E. Wood
Keyword(s):  
Plasma Renin Activity ◽  
Arginine Vasopressin ◽  
Adrenocorticotropic Hormone ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Acth ◽  
Blood Samples

The gonadal axis is thought to modulate adrenocorticotropic hormone (ACTH), arginine vasopressin (AVP), and plasma renin activity (PRA) responses to stimuli in several species. These experiments were designed to compare the responses to hypotension in chronically ovariectomized ewes and intact ewes. The ewes were infused with nitroprusside at rates of 5, 10, or 15 micrograms.kg-1.min-1 or infused with vehicle for 10 min. The response to 15 micrograms.kg-1.min-1 was also tested with or without treatment with 10 mg of dexamethasone 2 h before nitroprusside. Blood samples were collected before and at 5, 10, 15, 20, and 30 min after the start of the infusion for measurement of plasma ACTH, AVP, and PRA. In both groups of animals there were significant responses to hypotension. There was a significant effect of ovariectomy on ACTH, AVP, and PRA responses. ACTH and PRA responses were lower in the ovariectomized ewes; AVP responses were increased in the ovariectomized ewes. Administration of dexamethasone inhibited ACTH responses and did not inhibit PRA responses in both groups of ewes. Administration of dexamethasone did not inhibit the AVP response in the intact ewes but did reduce the response in the ovariectomized ewes.

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.

Adrenergically induced renin release in conscious indomethacin-treated dogs and rats

1981 ◽  
Vol 240 (6) ◽  
pp. F515-F521
Author(s):  
A. A. Seymour ◽  
J. O. Davis ◽  
S. F. Echtenkamp ◽  
J. R. Dietz ◽  
R. H. Freeman
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Release ◽  
Adrenergic Blockade ◽  
Cyclooxygenase Inhibitor ◽  
Adrenergic Stimulation ◽  
Adrenergic Agents ◽  
Endogenous Prostaglandins ◽  
Intact Rats

To investigate the role of endogenous prostaglandins in renin release stimulated via adrenergic pathways, isoproterenol, norepinephrine (NE) and NE in the presence of phentolamine (PTA) were infused into conscious sodium-replete rats and dogs. Isoproterenol (1 microgram.kg-1.min-1) infusion into intact rats increased plasma renin activity (PRA) eightfold. AFter pretreatment with the prostaglandin (PG) cyclooxygenase inhibitor indomethacin (5 mg/kg), isoproterenol increased PRA 16-fold. In dogs, isoproterenol (0.4 microgram.kg-1.min-1) increased PRA six-fold before indomethacin and 11-fold during PG inhibition. Infusion of NE into both rats (250 ng.kg-1.min-1) and dogs (1 microgram.kg-1.min-1) failed to increase PRA before indomethacin, but during inhibition of PG synthesis NE increased PRA in both species. During partial alpha-adrenergic blockade with PTA in dogs, PTA alone increased PRA by 38% and NE given during PTA infusion increased PRA further both before indomethacin by twofold and during PG inhibition by fivefold. In rats given NE during PTA infusion, PRA increased only after indomethacin injection. Additionally, in dogs the renin responses to these adrenergic agents were even greater after indomethacin administration than before the drug. These results in both conscious rats and dogs give no indication that renal prostaglandins mediate the renin response to adrenergic stimulation.

scholarly journals Activity Assays and Immunoassays for Plasma Renin and Prorenin: Information Provided and Precautions Necessary for Accurate Measurement

2009 ◽  
Vol 55 (5) ◽  
pp. 867-877 ◽  
Author(s):  
Duncan J Campbell ◽  
Juerg Nussberger ◽  
Michael Stowasser ◽  
A H Jan Danser ◽  
Alberto Morganti ◽  
...  
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Inhibitor Therapy ◽  
Renin Activity ◽  
Renin Inhibitor ◽  
Blood Samples ◽  
Hypertensive Patients ◽  
Active Renin ◽  
Open Conformation ◽  
Background Measurement

AbstractBackground: Measurement of plasma renin is important for the clinical assessment of hypertensive patients. The most common methods for measuring plasma renin are the plasma renin activity (PRA) assay and the renin immunoassay. The clinical application of renin inhibitor therapy has thrown into focus the differences in information provided by activity assays and immunoassays for renin and prorenin measurement and has drawn attention to the need for precautions to ensure their accurate measurement.Content: Renin activity assays and immunoassays provide related but different information. Whereas activity assays measure only active renin, immunoassays measure both active and inhibited renin. Particular care must be taken in the collection and processing of blood samples and in the performance of these assays to avoid errors in renin measurement. Both activity assays and immunoassays are susceptible to renin overestimation due to prorenin activation. In addition, activity assays performed with peptidase inhibitors may overestimate the degree of inhibition of PRA by renin inhibitor therapy. Moreover, immunoassays may overestimate the reactive increase in plasma renin concentration in response to renin inhibitor therapy, owing to the inhibitor promoting conversion of prorenin to an open conformation that is recognized by renin immunoassays.Conclusions: The successful application of renin assays to patient care requires that the clinician and the clinical chemist understand the information provided by these assays and of the precautions necessary to ensure their accuracy.

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.

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