Renal perfusion pressure and renin secretion in bilaterally renal denervated sheep

1994 ◽  
Vol 72 (7) ◽  
pp. 782-787 ◽  
Author(s):  
L. Fan ◽  
S. Mukaddam-Daher ◽  
J. Gutkowska ◽  
B. S. Nuwayhid ◽  
E. W. Quillen Jr.
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Factor ◽  
Perfusion Pressure ◽  
Excretion Rate ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Renin Secretion ◽  
Renal Nerves ◽  
Renal Perfusion Pressure ◽  
Plasma Angiotensin

To further investigate the influence of renal nerves on renin secretion, the renin secretion responses to step reductions of renal perfusion pressure (RPP) were studied in conscious sheep with innervated kidneys (n = 5) and with bilaterally denervated kidneys (n = 5). The average basal level of RPP in sheep with denervated kidneys (82 ± 4 mmHg; 1 mmHg = 133.3 Pa) was similar to that in sheep with innervated kidneys (83 ± 3 mmHg). RPP was reduced in four sequential 15-min steps, to a final level of 54 ± 2 mmHg in sheep with innervated kidneys and to 57 ± 1 mmHg in denervated sheep. The renin secretion rate was increased as RPP was reduced in sheep with innervated kidneys. Baseline peripheral plasma renin activity was reduced and there was almost no response of renin secretion rate to reduction of RPP in sheep with denervated kidneys. Also, baseline renal blood flow, urine flow rate, sodium excretion rate, and potassium excretion rate were higher in sheep with denervated kidneys than those with innervated kidneys. Baseline plasma angiotensin II was similar in both groups of sheep. As RPP was decreased, plasma angiotensin II was increased in sheep with innervated kidneys, but was not significantly altered in sheep with denervated kidneys. Plasma atrial natriuretic factor was unaltered by either reduction of RPP or renal denervation. In conclusion, hormonal factors, such as angiotensin II and atrial natriuretic factor, do not account for the dramatic suppression of renin secretion in response to the reduction of RPP in sheep with bilateral renal denervation. Renal nerves are a necessary component in the control of renin secretion during reduction of RPP and may contribute to the regulation of baseline plasma renin activity and sodium excretion rate in conscious ewes.Key words: renin secretion, renal perfusion pressure, renal nerves, denervation, sheep.

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.

Influences of renal nerves and pregnancy on renin secretion in sheep

1994 ◽  
Vol 266 (3) ◽  
pp. R668-R673 ◽  
Author(s):  
L. Fan ◽  
D. Archambault ◽  
S. Chavez ◽  
A. W. Aljabari ◽  
E. W. Quillen
Keyword(s):  
Plasma Renin ◽  
Conscious State ◽  
Renal Perfusion ◽  
Renin Secretion ◽  
Slow Phase ◽  
Renal Nerves ◽  
Pregnant Sheep ◽  
Plasma Angiotensin ◽  
The Relationship

To investigate the role of the renal nerves in the control of renin secretion during pregnancy, we prepared sheep with one denervated kidney, bilateral renal vein catheters, and an inflatable aortic occluder. The renin secretory responses to step reductions of renal perfusion pressure (RPP) of the innervated and denervated kidneys were compared in eight nonpregnant and nine pregnant (115-130 days gestation) sheep in a normal conscious state. Nonpregnant sheep had average basal levels of mean arterial pressure (MAP) of 91 +/- 3 mmHg, plasma renin activities (PRA) of 2.3 +/- 0.4 ng ANG I.ml-1.3 h-1, and plasma angiotensin (ANG) concentrations of 8.4 +/- 1.1 pg/ml. Pregnant sheep had reduced levels (P < 0.01) of MAP (76 +/- 3 mmHg) but elevated levels of PRA (3.8 +/- 0.4 ng ANG I.ml-1.h 3-1; P < 0.5) and ANG II (12.0 +/- 1.6 pg/ml; P = 0.08). Four successively reduced levels of RPP were observed for 15 min each in both groups of sheep. In both groups, RPP was reduced to a final level of 51 +/- 2 mmHg. The renal venous-arterial difference of PRA (v-aPRA) from the innervated kidneys was increased as RPP was reduced. However, there was little response of v-aPRA to RPP in denervated kidneys. In nonpregnant sheep, the relationship between RPP and renin secretion rate was characterized by an initially slow phase, over which small reductions of RPP resulted in small increases in renin secretion. As RPP fell, this relationship became progressively steeper in nonpregnant ewes.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

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.

Role of the Renal Nerves in Modulating Renin Release During Pressure Reduction at the Feline Kidney

1985 ◽  
Vol 69 (2) ◽  
pp. 185-195 ◽  
Author(s):  
Edward J. Johns
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renin Secretion ◽  
Renal Nerves ◽  
Pressure Reduction ◽  
Renal Perfusion Pressure

1. Experiments were undertaken in pentobarbitone-anaesthetized cats to determine how reflex activation of the renal nerves altered the responsiveness of the kidney to release renin during reductions in renal perfusion pressure. Reflex activation of the renal nerves was achieved by reducing carotid sinus perfusion pressure by 30 mmHg, which increased systemic blood pressure. During this period renal perfusion pressure was regulated at control levels and neither renal blood flow nor glomerular filtration rate changed, but there was a significant decrease in sodium excretion and increase in renin secretion. Renal denervation abolished both these latter responses. 2. Renal perfusion pressure reduction, by 25-30 mmHg, had no effect on renal blood flow or glomerular filtration rate but significantly decreased sodium excretion and increased renin secretion. Simultaneous reduction of carotid sinus and renal perfusion pressures had no effect on renal blood flow or glomerular filtration rate, decreased sodium excretion, and the magnitude of the increase in renin secretion was significantly greater than that obtained with reduction in renal perfusion pressure alone. Renal denervation abolished the increase in renin secretion during these manoeuvres. 3. During atenolol administration, renal haemodynamics and sodium excretion responses to renal pressure reduction were similar to those obtained in the absence of the drug. Renin secretion was increased, but significantly less than in the absence of atenolol. Simultaneous carotid sinus and renal pressure reductions during atenolol administration had no effect on renal haemodynamics, reduced sodium excretion and increased renin secretion, the magnitude of which was significantly greater than that recorded with only renal pressure reduction in the presence of atenolol. 4. Direct electrical stimulation of the renal nerves, at frequencies which caused a 5-10% reduction in renal blood flow, did not change glomerular filtration rate, decreased sodium excretion by 30% and increased the rate of renin secretion twofold. In the presence of atenolol, such renal nerve stimulation reduced renal blood flow to the same degree, did not change filtration rate, decreased sodium excretion by 37% but did not change renin secretion. 5. These results show that the magnitude of the release of renin in response to renal pressure reduction is dependent on activity within the renal nerves, being blunted after denervation, and enhanced during reflex activation of the renal nerves.

Selective neuronal nitric oxide synthase inhibition blocks furosemide-stimulated renin secretion in vivo

1995 ◽  
Vol 269 (1) ◽  
pp. F134-F139 ◽  
Author(s):  
W. H. Beierwaltes
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Nitric Oxide Synthase ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Macula Densa ◽  
Renin Secretion ◽  
Renal Perfusion Pressure ◽  
Neuronal Nos ◽  
Oxide Synthase

The macula densa is a regulatory site for renin. It contains exclusively the neuronal isoform of nitric oxide synthase (NOS), suggesting NO could stimulate renin secretion through the macula densa pathway. To test whether neuronal NOS mediates renin secretion, renin was stimulated by either the renal baroreceptor or the diuretic furosemide (acting through the macula densa pathway). Renin secretion rate (RSR) was measured in 12 Inactin-anesthetized rats at normal (104 +/- 3 mmHg) and reduced renal perfusion pressure (65 +/- 1 mmHg), before and after selective blockade of the neuronal NOS with 7-nitroindazole (7-NI, 50 mg/kg ip). 7-NI had no effect on basal blood pressure (102 +/- 2 mmHg) or renal blood flow (RBF). Decreasing renal perfusion pressure doubled RSR from 11.8 +/- 3.3 to 22.9 +/- 5.7 ng ANG I.h-1.min-1 (P < 0.01) (ANG I is angiotensin I). Similarly, in 7-NI-treated rats, reduced perfusion doubled RSR from 8.5 +/- 1.8 to 20.5 +/- 6.2 ng ANG I.h-1.min-1 (P < 0.01). Renal hemodynamics and RSR were measured in response to 5 mg/kg iv furosemide in 12 control rats and 11 rats treated with 7-NI. Blocking neuronal NOS did not alter blood pressure (102 +/- 2 mmHg), RBF (5.8 +/- 0.4 ml.min-1.g kidney wt-1), or renal vascular resistance (18.7 +/- 1.4 mmHg.ml-1.min.g kidney wt).(ABSTRACT TRUNCATED AT 250 WORDS)

Membrane potential measurements in renal afferent and efferent arterioles: actions of angiotensin II

1997 ◽  
Vol 273 (2) ◽  
pp. F307-F314 ◽  
Author(s):  
R. Loutzenhiser ◽  
L. Chilton ◽  
G. Trottier
Keyword(s):  
Angiotensin Ii ◽  
Perfusion Pressure ◽  
Rat Kidney ◽  
Renal Perfusion ◽  
Membrane Potentials ◽  
Ang Ii ◽  
Ca Channels ◽  
Renal Perfusion Pressure

An adaptation of the in vitro perfused hydronephrotic rat kidney model allowing in situ measurement of arteriolar membrane potentials is described. At a renal perfusion pressure of 80 mmHg, resting membrane potentials of interlobular arteries (22 +/- 2 microns) and afferent (14 +/- 1 microns) and efferent arterioles (12 +/- 1 microns) were -40 +/- 2 (n = 8), -40 +/- 1 (n = 45), and -38 +/- 2 mV (n = 22), respectively (P = 0.75). Using a dual-pipette system to stabilize the impalement site, we measured afferent and efferent arteriolar membrane potentials during angiotensin II (ANG II)-induced vasoconstriction. ANG II (0.1 nM) reduced afferent arteriolar diameters from 13 +/- 1 to 8 +/- 1 microns (n = 8, P = 0.005) and membrane potentials from -40 +/- 2 to -29 +/- mV (P = 0.012). ANG II elicited a similar vasoconstriction in efferent arterioles, decreasing diameters from 13 +/- 1 to 8 +/- 1 microns (n = 8, P = 0.004), but failed to elicit a significant depolarization (-39 +/- 2 for control; -36 +/- 3 mV for ANG II; P = 0.27). Our findings thus indicate that resting membrane potentials of pre- and postglomerular arterioles are similar and lie near the threshold activation potential for L-type Ca channels. ANG II-induced vasoconstriction appears to be closely coupled to membrane depolarization in the afferent arteriole, whereas mechanical and electrical responses appear to be dissociated in the efferent arteriole.

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.

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.

ACE inhibition prevents Na and water retention and MABP increase during reduction of renal perfusion pressure

1995 ◽  
Vol 269 (3) ◽  
pp. R481-R489 ◽  
Author(s):  
W. Boemke ◽  
E. Seeliger ◽  
L. Rothermund ◽  
M. Corea ◽  
R. Pettker ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Water Retention ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Plasma Aldosterone ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Converting Enzyme ◽  
Renal Perfusion Pressure ◽  
Arterial Blood

Two groups of six dogs were studied during 4 control days and 4 days of reduced renal perfusion pressure (rRPP) servo controlled at 20% below the individual dog's 24-h mean arterial blood pressure (MABP) during control days, i.e., below the threshold for renin release. On rRPP days, endogenous activation of plasma aldosterone and angiotensin II was inhibited by the angiotensin-converting enzyme inhibitor captopril. The dogs were kept on a high-Na and high-water intake. Unlike studies during rRPP alone, there was no Na and water retention during rRPP+captopril. Glomerular filtration rate dropped by approximately 9%, and MABP remained in the range of control days. Plasma renin activity rose to values 14 times greater than control, whereas plasma aldosterone decreased by approximately 60%. Atrial natriuretic peptide remained in the range of controls. In conclusion, angiotensin-converting enzyme inhibition can prevent the otherwise obligatory Na and water retention and systemic MABP increase during a 20% reduction in renal perfusion pressure. This is achieved most likely via the captopril-induced fall in angiotensin II and plasma aldosterone levels.

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