Renin release in rats during blockade of nitric oxide synthesis

1994 ◽  
Vol 266 (6) ◽  
pp. R1723-R1729 ◽  
Author(s):  
R. A. Johnson ◽  
R. H. Freeman
Keyword(s):  
Nitric Oxide ◽  
Plasma Renin Activity ◽  
Perfusion Pressure ◽  
Plasma Renin ◽  
Treated Group ◽  
Renal Perfusion ◽  
Renin Activity ◽  
Renin Release ◽  
Nitric Oxide Synthesis ◽  
Renal Perfusion Pressure

The influence of renal perfusion pressure on renin release was examined in rats administered the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME). Compared with the control plasma renin of 6.0 +/- 0.7 ng angiotensin I (ANG I).ml-1.h-1, plasma renin activity was suppressed (1.8 +/- 0.2 ng ANG I.ml-1.h-1, P < 0.05) in L-NAME-treated animals in which the renal perfusion pressure was permitted to increase and reached 141 +/- 8 mmHg. Plasma renin activity also was suppressed (2.5 +/- 0.4 ng ANG I.ml-1.h-1, P < 0.05) in a second L-NAME-treated group in which the renal perfusion pressure was controlled to a level of 105 +/- 5 mmHg via tightening of a suprarenal aortic snare. Plasma renin activity was increased (12.0 +/- 1.4 ng ANG I.ml-1.h-1, P < 0.05) in a third L-NAME-treated group in which renal perfusion pressure was reduced to 59 +/- 1 mmHg. Overall, these findings suggest that the intrarenal pressure-sensing mechanism for renin release does not stringently require nitric oxide synthesis. In a second experimental series, bilaterally renal-denervated rats were administered L-NAME, and again plasma renin activity was suppressed significantly whether renal perfusion pressure was permitted to increase or was controlled. Thus L-NAME also suppressed plasma renin activity independently of reflex reductions in renal neuroadrenergic activity even when renal perfusion pressure was controlled. Infusions of sodium nitroprusside completely inhibited L-NAME-induced suppression of plasma renin activity in these renal-denervated rats. Nitric oxide may function as a paracrine stimulatory mechanism for the local regulation of renin release.

Renal perfusion pressure and renin secretion in the rainbow trout, Salmo gairdneri

1981 ◽  
Vol 59 (7) ◽  
pp. 1220-1226 ◽  
Author(s):  
J. R. Bailey ◽  
D. J. Randall
Keyword(s):  
Plasma Renin Activity ◽  
Perfusion Pressure ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Renin Secretion ◽  
Renin Activity ◽  
Renin Release ◽  
Salmo Gairdneri ◽  
Renal Perfusion Pressure

In the trout, Salmo gairdneri, a significant correlation between the amount of blood loss and plasma renin activity was established. This increase in plasma renin activity could be due to stimulation of an intrarenal receptor, thus an isolated nonfiltering perfused kidney preparation was developed to test this hypothesis. It was found that a decrease in renal perfusion pressure resulted in an increase in renin release (as measured by perfusate renin activity) but an increase in renal perfusion pressure had no effect on renin release. The increase in renin secretion in response to a decreased renal perfusion pressure was not affected by sympathetic nervous system blocking agents, whereas angiotensin II will apparently inhibit renin secretion in vitro. It was concluded that a baroreceptor response, similar to that found in mammals, is found in fishes and a model mechanism for renin secretion in fishes is proposed.

Plasma renin activity responses to graded decreases in renal perfusion pressure in fetal and newborn lambs

1992 ◽  
Vol 262 (3) ◽  
pp. R524-R529 ◽  
Author(s):  
N. D. Binder ◽  
D. F. Anderson
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Perfusion Pressure ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Renin Activity ◽  
Renal Perfusion Pressure ◽  
Arterial Blood ◽  
The Right ◽  
The Relationship

We examined the relationship between acute reductions in renal perfusion pressure, as approximated by femoral arterial blood pressure, and plasma renin activity in the uninephrectomized fetal lamb. Renal perfusion pressure was reduced and maintained at a constant value by controlled partial occlusion of the aorta above the renal artery. After 15 min of reduced blood pressure, blood samples were taken for determination of plasma renin activity. This protocol was performed 22 times in 11 fetal lambs. Additionally, three of the fetuses were delivered by cesarean section and studied as newborns for the first week of life. In the fetus, there was a linear relationship between log plasma renin activity and femoral arterial blood pressure (P less than 0.01). After birth, the relationship still existed, although it was shifted to the right (P less than 0.0001). We conclude that there is a significant relationship between plasma renin activity and renal perfusion pressure in the fetal lamb, and as early as 1 day after birth, this relationship shifts to the right in the newborn lamb.

Plasma epinephrine and control of plasma renin activity: possible extrarenal mechanisms

1979 ◽  
Vol 236 (6) ◽  
pp. H854-H859 ◽  
Author(s):  
M. D. Johnson ◽  
E. R. Fahri ◽  
B. R. Troen ◽  
A. C. Barger
Keyword(s):  
Plasma Renin Activity ◽  
Perfusion Pressure ◽  
Potassium Concentration ◽  
Plasma Renin ◽  
Plasma Potassium ◽  
Renal Perfusion ◽  
Renin Activity ◽  
Renal Nerves ◽  
Epinephrine Infusion ◽  
Renal Perfusion Pressure

Previous work from our laboratory has shown that physiological increments of circulating epinephrine concentration increase plasma renin activity (PRA) by an extrarenal beta-receptor mechanism. In the present experiments, epinephrine was infused intravenously at 125 ng.kg-1.min-1 for 45 min in trained, conscious dogs. PRA rose 3 to 5-fold, as previously described, and was accompanied by a transient decline of mean arterial pressure, decreased plasma potassium concentration, and increased hematocrit. Prior splenectomy to maintain hematocrit constant did not attenuate the PRA response to epinephrine. The kidneys of 4 dogs were denervated and constrictor cuff was placed around the renal artery. Renal denervation did not alter the PRA response to intravenous epinephrine infusion. A transient decline in renal perfusion pressure produced by cuff constriction only transiently increase PRA. Neither maintenance of a constant plasma potassium concentration nor oral administration of indomethacin altered the PRA response to epinephrine. We conclude that intravenous epinephrine increases PRA by a mechanism independent of the renal nerves, changes in renal perfusion pressure, hematocrit, plasma potassium concentration, and plasma prostaglandins.

Effects of Carotid Occlusion and Clonidine on Renin Secretion in Anaesthetized Dogs

1976 ◽  
Vol 51 (s3) ◽  
pp. 109s-111s ◽  
Author(s):  
I. A. Reid ◽  
A. Jones
Keyword(s):  
Plasma Renin Activity ◽  
Perfusion Pressure ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Renin Secretion ◽  
Renin Activity ◽  
Carotid Occlusion ◽  
Renal Perfusion Pressure ◽  
Sympathetic Reflexes ◽  
Blood Pressure Responses

1. Sympathetic reflexes were activated by carotid occlusion in anaesthetized dogs in which changes in renal perfusion pressure were prevented. This produced a prompt and reversible increase in plasma renin activity. 2. Administration of clonidine decreased plasma renin activity, arterial pressure and heart rate and blocked the renin secretory and blood pressure responses to carotid occlusion. 3. These results support the hypothesis that the suppression of renin secretion by clonidine is a consequence of the decrease in sympathetic activity produced by this drug.

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.

scholarly journals Role of the endothelium-dependent relaxing factor nitric oxide on renal function.

1992 ◽  
Vol 2 (9) ◽  
pp. 1371-1387 ◽  
Author(s):  
J C Romero ◽  
V Lahera ◽  
M G Salom ◽  
M L Biondi
Keyword(s):  
Nitric Oxide ◽  
Renal Function ◽  
Perfusion Pressure ◽  
Sodium Intake ◽  
Systemic Circulation ◽  
Renal Perfusion ◽  
Renin Release ◽  
High Sodium ◽  
Renal Perfusion Pressure

The role of nitric oxide in renal function has been assessed with pharmacologic and physiologic interventions. Pharmacologically, the renal vasodilation and, to some extent, the natriuresis produced by endothelium-dependent vasodilators such as acetylcholine and bradykinin are mediated by nitric oxide and also by prostaglandins. However, prostaglandins and nitric oxide do not participate in the renal effects produced by endothelium-independent vasodilators such as atrial natriuretic peptide, prostaglandin I2, and nitroprusside. Physiologically, nitric oxide and prostaglandins exert a strong regulation on the effects produced by changes in renal perfusion pressure. Increments in renal perfusion pressure within the range of RBF autoregulation appear to inhibit prostaglandin synthesis while simultaneously enhancing the formation of nitric oxide. Nitric oxide modulates autoregulatory vasoconstriction and at the same time inhibits renin release. Conversely, a decrease of renal perfusion pressure to the limit of or below RBF autoregulation may inhibit the synthesis of nitric oxide but may trigger the release of prostaglandins, whose vasodilator action ameliorates the fall in RBF and stimulates renin release. Nitric oxide and prostaglandins are also largely responsible for mediating pressure-induced natriuresis. However, unlike prostaglandins, mild impairment of the synthesis of nitric oxide in systemic circulation produces a sustained decrease in sodium excretion, which renders blood pressure susceptible to be increased during high-sodium intake. This effect suggests that a deficiency in the synthesis of nitric oxide could constitute the most effective single disturbance to foster the development of a syndrome similar to that seen in salt-sensitive hypertension.

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.

Intravertebral ANG II effects on plasma renin and Na excretion in dogs at constant renal artery pressure

1995 ◽  
Vol 268 (2) ◽  
pp. F296-F301
Author(s):  
E. W. Quillen ◽  
I. A. Reid
Keyword(s):  
Renal Function ◽  
Perfusion Pressure ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Urine Flow ◽  
Renin Release ◽  
Central Action ◽  
Ang Ii ◽  
Renal Perfusion Pressure ◽  
Vascular Catheters

Studies were performed to determine whether intravertebral angiotensin II infusion (iva ANG II) decreases renin release by increasing renal perfusion pressure (RPP) and to investigate possible effects of iva ANG II on renal function. RPP was electronically servocontrolled in 12 conscious dogs equipped with chronic vascular catheters and a suprarenal aortic balloon constrictor while iva ANG II was infused bilaterally for 60 min at 0.33 ng.kg-1.min-1. Without servocontrol, iva ANG II increased mean arterial pressure (MAP) from 101 +/- 4 to 106 +/- 5 mmHg, urine flow (V) from 0.36 +/- 0.03 to 0.45 +/- 0.04 ml/min, and sodium excretion (UNaV) from 36.2 +/- 7.0 to 62.7 +/- 6.6 mumol/min. Plasma renin activity (PRA) decreased from 6.9 +/- 0.7 to 5.0 +/- 0.6 ng ANG I.ml-1.3 h-1. With servocontrol, iva ANG II increased MAP from 102 +/- 4 to 109 +/- 5 mmHg while RPP remained constant with a variation of less than +/- 1 mmHg. PRA did not change significantly (5.9 +/- 0.3 to 7.0 +/- 0.7 ng ANG I.ml-1.3 h-1). V decreased from 0.33 +/- 0.02 to 0.26 +/- 0.01 ml/min, and UNaV decreased from 49.0 +/- 5.7 to 29.7 +/- 4.4 mumol/min. The data provide evidence that iva ANG II decreases renin release by increasing RPP and stimulating the renal baroreceptor and/or the macula densa mechanisms. In addition, at constant RPP, ANG II exerts a central action to decrease UNaV.

Renal baroreceptor-stimulated renin in the eNOS knockout mouse

2002 ◽  
Vol 282 (1) ◽  
pp. F59-F64 ◽  
Author(s):  
William H. Beierwaltes ◽  
D'Anna L. Potter ◽  
Edward G. Shesely
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Knockout Mice ◽  
Perfusion Pressure ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Renal Perfusion Pressure ◽  
Oxide Synthase ◽  
Renal Vascular ◽  
Endothelial Nitric Oxide

The role of endothelium-derived nitric oxide (NO) in renal baroreceptor stimulation of renin was tested comparing endothelial nitric oxide synthase (eNOS)-deficient mice with C57BL/6J (C57) controls. We measured blood pressure, renal blood flow (RBF), and plasma renin concentration (PRC) in Inactin-anesthetized mice. Blood pressure in eNOS knockout mice was higher than in controls (100 ± 3 vs. 86 ± 1 mmHg, respectively; P < 0.001), but RBF was similar (1.71 ± 0.06 vs. 1.66 ± 0.09 ml · min−1 · 100 mg kidney wt−1, respectively), so that renal vascular resistance was also higher in the knockouts (59.81 ± 2.07 vs. 51.81 ± 2.66 resistance units, respectively; P < 0.025). PRC was similar (8.24 ± 1.57 in eNOS knockouts vs. 7.10 ± 1.19 ng ANG I · ml−1 · h−1 in C57). NOS inhibition with nitro-l-arginine methyl ester (l-NAME) in C57 controls increased blood pressure (from 85 ± 2 to 106 ± 1 mmHg, P < 0.001) and decreased RBF (from 1.66 ± 0.09 to 1.08 ± 0.02; P< 0.005), but l-NAME had no effect in eNOS knockout mice. When renal perfusion pressure was reduced in C57 controls to 55 mmHg, PRC increased from 6.6 ± 0.9 to 14.5 ± 1.9 μg · ml−1 · h−1 ( P< 0.025), but this response was blocked by l-NAME. However, in eNOS knockouts, reduced renal perfusion pressure increased PRC from 7.6 ± 1.4 to 15.0 ± 2.8 μg · ml−1 · h−1 ( P< 0.001). Thus in the chronic absence of eNOS, blood pressure was elevated, but RBF was normal. Additionally, the absence of eNOS did not modify baroreceptor-stimulated renin, suggesting that eNOS-derived NO does not directly mediate this renin-regulating pathway.

Determinants of renal vasoconstriction after systemic inhibition of nitric oxide synthesis in rats

1996 ◽  
Vol 270 (6) ◽  
pp. R1203-R1207
Author(s):  
E. Brand-Schieber ◽  
M. Pucci ◽  
A. Nasjletti
Keyword(s):  
Nitric Oxide ◽  
Vascular Resistance ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Vascular Resistance ◽  
Tubuloglomerular Feedback ◽  
Nitric Oxide Synthesis ◽  
Renal Vasoconstriction ◽  
Renal Perfusion Pressure ◽  
Renal Vascular

The effects of NG-nitro-L-arginine (L-NNA, 10 mg/kg i.v.) on renal hemodynamics were examined in control rats, rats in which renal perfusion pressure was prevented from rising after L-NNA by constricting the abdominal aorta, and rats in which tubuloglomerular feedback was inhibited by furosemide pretreatment, ureteral ligation, or both interventions combined. In control rats, L-NNA increased (P < 0.05) renal vascular resistance (274 +/- 27%) along with systemic arterial (54 +/- 4%) and renal perfusion (54 +/- 5%) pressures and decreased (P < 0.05) renal blood flow (57 +/- 4%). In rats in which renal perfusion pressure was prevented from increasing along with systemic arterial pressure (54 +/- 4%), the L-NNA-induced elevation of renal vascular resistance (173 +/- 27%) was less intense (P < 0.05). In another study, where renal perfusion pressure was fixed at pre-L-NNA levels, L-NNA-induced increases in renal vascular resistance (130 +/- 20%) were attenuated (P < 0.05) further with furosemide pretreatment (52 +/- 12%), with ureteral ligation (75 +/- 10%), and with furosemide pretreatment and ureteral ligation combined (32 +/- 8%). These data suggest that vasoconstrictor mechanisms linked to tubuloglomerular feedback and perfusion pressure elevation contribute to renal vasoconstriction after systemic inhibition of nitric oxide synthesis with L-NNA.

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