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.

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.

Mechanism of renin release in exercising dog

1984 ◽  
Vol 246 (1) ◽  
pp. E71-E76 ◽  
Author(s):  
E. J. Zambraski ◽  
M. S. Tucker ◽  
C. S. Lakas ◽  
S. M. Grassl ◽  
C. G. Scanes
Keyword(s):  
Plasma Renin Activity ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Heavy Exercise ◽  
Nerve Activity ◽  
Control Exercise

Exercise is associated with an increase in plasma renin activity (PRA). The purpose of this study was to determine the role of the prostaglandin (PG) and adrenergic pathways in the renin release with exercise in the dog. One group of animals (n = 4) was exercised under control untreated and indomethacin- and meclofenamate- (2 mg/kg) treated conditions. A 155% increase in PRA was not influenced by PG inhibition. In a second group (n = 7) PRA was 1.22 +/- 0.32, 3.29 +/- 1.59, 6.28 +/- 2.85, and 5.30 +/- 2.00 ng ANG I X ml-1 X h-1 at rest and during light, moderate, and heavy exercise, respectively. Guanethidine treatment (15 mg/kg) decreased mean PRA by 41, 50, 70, and 73% at rest and during the three levels of exercise, respectively. In a third group (n = 5) control exercise runs were repeated after metoprolol treatment. Selective beta 1-blockade completely abolished the increment in PRA observed with exercise. These data demonstrate that the elevation of PRA during exercise in the dog is mediated by increased sympathetic nerve activity involving beta 1-receptors and that it is not dependent on alterations in PG synthesis.

Effects of indomethacin on plasma renin activity in the conscious rat

1981 ◽  
Vol 240 (3) ◽  
pp. E286-E289 ◽  
Author(s):  
S. Suzuki ◽  
R. Franco-Saenz ◽  
S. Y. Tan ◽  
P. J. Mulrow
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Sodium Retention ◽  
Conscious Rat ◽  
Basal Plasma ◽  
Inhibition Of Prostaglandin Synthesis

The role of prostaglandins in the control of renin release in vivo was evaluated in the conscious rat. Indomethacin suppressed urinary prostaglandin E2 (PGE2) excretion from 5.3 +/- 0.5 to 2.6 +/- 0.5 ng/3 h (P less than 0.001). Basal plasma renin activity (PRA) fell from 6.20 +/- 1.07 to 2.98 +/- 0.45 ng . ml-1 . h-1 (P less than 0.02). Indomethacin suppressed PRA stimulated by furosemide, insulin-induced hypoglycemia, hydralazine, isoproterenol, arachidonic acid, and sodium-free diet, whereas PRA stimulated by PGE2 was not suppressed by indomethacin. The suppression of PRA by indomethacin in the sodium-deplete state rules out sodium retention as the mechanism of action of indomethacin. These results indicate that inhibition of prostaglandin synthesis by indomethacin partially blocks the renin response to several of the known stimulators, suggesting that prostaglandins may play a pivotal role in the control of renin release.

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.

Water deprivation-induced drinking in rats: role of angiotensin II

1983 ◽  
Vol 244 (2) ◽  
pp. R244-R248 ◽  
Author(s):  
C. C. Barney ◽  
R. M. Threatte ◽  
M. J. Fregly
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Water Intake ◽  
Water Deprivation ◽  
Plasma Renin ◽  
Sodium Concentration ◽  
Renin Activity ◽  
Deprivation Period ◽  
Dependent Component

The role of angiotensin II in the control of water intake following deprivation of water for varying lengths of time was studied. Male rats were deprived of water for 0, 12, 24, 36, or 48 h. Water intakes were measured with and without pretreatment with the angiotensin I-converting enzyme inhibitor, captopril (50 mg/kg, ip). Captopril had no significant effect on water intake following either 0 or 12 h of water deprivation. However, captopril significantly attenuated water intake following 24-48 h of water deprivation with the magnitude of the attenuation increasing as the length of the period of water deprivation increased. Plasma renin activity was significantly increased over control levels after 24-48 h of water deprivation but not after 12 h of water deprivation. Plasma renin activity tended to increase as the length of the water-deprivation period increased. Serum osmolality and sodium concentration were significantly increased over control levels following 12-48 h of water deprivation. Serum osmolality and sodium concentration failed to show any further increases with increasing length of water deprivation beyond the increases following 12 h of water deprivation. The data indicate that the water intake of water-deprived rats can be divided into an angiotensin II-dependent component and angiotensin II-independent component. The angiotensin II-independent component appears to be more important in the early stages of water deprivation whereas the angiotensin II-dependent component becomes more important as the length of the water-deprivation period increases.

Effects of meclofenamate on the renin response to aortic constriction in the rat

1984 ◽  
Vol 247 (3) ◽  
pp. R546-R551 ◽  
Author(s):  
D. Villarreal ◽  
J. O. Davis ◽  
R. H. Freeman ◽  
W. D. Sweet ◽  
J. R. Dietz
Keyword(s):  
Perfusion Pressure ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Renin Release ◽  
Aortic Constriction ◽  
Renal Perfusion Pressure ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Intact Kidney ◽  
Stimulus Secretion Coupling

This study examines the role of the renal prostaglandin system in stimulus-secretion coupling for renal baroreceptor-dependent renin release in the anesthetized rat. Changes in plasma renin activity (PRA) secondary to suprarenal aortic constriction were evaluated in groups of rats with a single denervated nonfiltering kidney (DNFK) with and without pretreatment with meclofenamate. Suprarenal aortic constriction was adjusted to reduce renal perfusion pressure to either 100 or 50 mmHg. In addition, similar experiments were performed in rats with a single intact filtering kidney. Inhibition of prostaglandin synthesis with meclofenamate failed to block or attenuate the increase in PRA in response to the decrement in renal perfusion pressure after both severe and mild aortic constriction for both the DNFK and the intact-kidney groups. The adequacy of prostaglandin inhibition was demonstrated by complete blockade with meclofenamate of the marked hypotensive and hyperreninemic responses to sodium arachidonate. The results in the DNFK indicate that in the rat, renal prostaglandins do not function as obligatory mediators of the isolated renal baroreceptor mechanism for the control of renin release. Also the findings in the intact filtering kidney suggest that prostaglandins are not essential in the renin response of other intrarenal receptor mechanisms that also are stimulated by a reduction in renal perfusion pressure.

Pharmacological and genetic evidence that cathepsin B is not the physiological activator of rodent prorenin

2010 ◽  
Vol 391 (12) ◽  
Author(s):  
M. David Percival ◽  
Sylvie Toulmond ◽  
Nathalie Coulombe ◽  
Wanda Cromlish ◽  
Sylvie Desmarais ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Cathepsin B ◽  
Plasma Renin ◽  
Renin Activity ◽  
Spontaneously Hypertensive ◽  
Protein Levels ◽  
Arterial Blood ◽  
Gene Compensation

Abstract Renin is the first enzyme in the renin-angiotensin-aldosterone system which is the principal regulator of blood pressure and hydroelectrolyte balance. Previous studies suggest that cathepsin B is the activator of the prorenin zymogen. Here, we show no difference in plasma renin activity, or mean arterial blood pressure between wild-type and cathepsin B knockout mice. To account for potential gene compensation, a potent, selective, reversible cathepsin B inhibitor was developed to determine the role of cathepsin B on prorenin processing in rats. Pharmacological inhibition of cathepsin B in spontaneously hypertensive and double transgenic rats did not result in a reduction in renal mature renin protein levels or plasma renin activity. We conclude that cathepsin B does not play a significant role in this process in rodents.

Vasopressin Effects on Plasma Renin Activity in Male and Female Rats

1978 ◽  
Vol 55 (3) ◽  
pp. 301-307 ◽  
Author(s):  
I. W. Henderson ◽  
R. J. Balment ◽  
J. Ann Oliver
Keyword(s):  
Plasma Renin Activity ◽  
Diabetes Insipidus ◽  
Antidiuretic Hormone ◽  
Plasma Renin ◽  
Renin Activity ◽  
Female Rats ◽  
Male Rats ◽  
Adrenergic Blockade ◽  
Male And Female ◽  
Male And Female Rats

1. The influence of gonadal and pituitary factors on the plasma renin response to exogenous vasopressin was examined in anaesthetized rats. 2. Plasma renin activity (PRA) was measured in Brattleboro rats (with and without hypothalamic diabetes insipidus) and Long-Evans male and female rats, before and after single intravenous injection of antidiuretic hormone (ADH) or saline. 3. Control saline injections did not change PRA. ADH reduced PRA in male, but increased PRA in female rats. Rats with diabetes insipidus displayed the greatest changes and were used in subsequent experiments. Extrarenal renin activity (nephrectomized rats) gave qualitatively similar responses to ADH. Plasma renin concentration, which was also measured with PRA in intact and nephrectomized male and female rats with diabetes insipidus, increased in the females and decreased in the males after ADH. 4. Castration, 24 h before study, abolished the ADH-induced fall in PRA, and testosterone implanted before castration did not restore the response. Cyproterone acetate reversed the ADH effect in males, so that PRA then rose after ADH. Hypophysectomized male rats, with depressed basal plasma renin activities, also showed a reduced PRA after ADH. 5. Ovariectomy had little effect on the ADH-induced renin release and the response was similar at oestrus, metoestrus and dioestrus. In hypophysectomized female rats ADH reduced PRA; a male pattern of response was seen in hypophysectomized female rats. 6. In both sexes PRA responses to ADH were blunted but not abolished by β-adrenergic blockade (propranolol). α-Adrenergic blockade (phenoxybenzamine) had little influence on the male response but in females the typical increase disappeared so that ADH reduced PRA. 7. It is concluded that pituitary hormones, including gonadotrophins and gonadal factors as well as adrenal sex steroids, appear to affect significantly the interplay between antidiuretic hormone and the renin—angiotensin system.

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.

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