Effects of variations in renal hemodynamics on the time course of renin secretion rate

1983 ◽  
Vol 245 (6) ◽  
pp. F784-F791
Author(s):  
S. Simchon ◽  
S. Chien
Keyword(s):  
Time Constant ◽  
Time Course ◽  
Renal Perfusion ◽  
Renal Hemodynamics ◽  
Secretion Rate ◽  
Renin Secretion ◽  
Renin Release ◽  
Pump System ◽  
Renal Vasoconstriction ◽  
Nitroprusside Infusion

The effects of variations in renal hemodynamics on the time course of renin secretion were studied in dogs anesthetized with pentobarbital-chloralose. Hemodynamic changes were induced either locally in kidneys perfused in situ via an extracorporeal circuit (with or without a pump system) or systemically by hemorrhage or nitroprusside infusion. In the autoperfused kidney the reduction of renal perfusion pressure to approximately one-half of the arterial pressure by inflow occlusion caused an increase in renal conductance (renal vasodilation) and an increase in renin secretion rate (RSR). In the pump-perfused kidney, a step increase in renal blood flow (RBF) caused renal vasoconstriction and a decrease in RSR; a step decrease in RBF caused renal vasodilation and an increase in RSR. Following step changes in RBF, the time constant of the alterations of renal conductance was 56.5 s, and the time constant of the RSR responses was 80.1 s. The total time required to reach a steady state for RSR lagged behind that for renal conductance by approximately 5 min. These differences reflect the time needed for the kidney to release renin in response to changes in renal vascular caliber. The results suggest that renin release occurs in response to the autoregulatory dilation of the renal arterioles. When systemic hypotension was induced by nitroprusside infusion, RSR also increased together with the renal conductance. Following hemorrhage, however, RSR increased despite a decrease in renal conductance, reflecting the role of neurohumoral factors in causing renin release in this case. The comparison of renin secretion following different types of hemodynamic alterations serves to elucidate the mechanisms of renin secretion.

α-Adrenergic Suppression of Renin Secretion in the Rat Independent of Renal Vasoconstriction

1979 ◽  
Vol 57 (s5) ◽  
pp. 161s-163s
Author(s):  
R. Vandongen ◽  
K. D. Strang ◽  
Marianne H. Poesse ◽  
W. H. Birkenhager
Keyword(s):  
Perfusion Pressure ◽  
Rat Kidney ◽  
Renal Perfusion ◽  
Inhibitory Effect ◽  
Renin Secretion ◽  
Renin Release ◽  
Adrenergic Stimulation ◽  
Renal Vasoconstriction ◽  
Adrenergic Mechanism ◽  
Perfused Rat Kidney

1. The effect of α-adrenergic stimulation, with phenylephrine, on isoprenaline-provoked renin secretion was studied in the isolated perfused rat kidney. 2. Infusion of phenylephrine increased renal perfusion pressure and prevented renin secretion in response to isoprenaline. 3. Renal vasoconstriction was abolished and the response in renin secretion to isoprenaline was restored by α-adrenoreceptor blockade with phenoxybenzamine. 4. In contrast, when renal vasoconstriction was prevented by dihydrallazine, suppression of renin release by phenylephrine still occurred. 5. These observations support an inhibitory effect of a non-vascular α-adrenergic mechanism on renin release. It is suggested that the α-receptor mediating this effect is directly related to the renin-producing juxtaglomerular cell.

Impaired control of renal hemodynamics and renin release during hyperkalemia in rabbits

1988 ◽  
Vol 254 (5) ◽  
pp. F704-F710 ◽  
Author(s):  
H. B. Lin ◽  
D. B. Young
Keyword(s):  
Perfusion Pressure ◽  
Plasma Potassium ◽  
Renal Perfusion ◽  
Renal Hemodynamics ◽  
Renin Release ◽  
Control Group ◽  
Rabbit Plasma ◽  
Suprarenal Aorta ◽  
Impaired Control ◽  
Significant Impairment

We analyzed the changes in control of renal hemodynamics and renin release resulting from hyperkalemia in the rabbit. Plasma potassium activity was maintained at a controlled elevated level by intravenous infusion of KCl. The potassium activity of the control group (n = 23) averaged 3.20 +/- 0.06 meq/l and that of the hyperkalemic group (n = 13) averaged 5.80 +/- 0.13 meq/l. Renal blood flow (RBF), glomerular filtration rate (GFR), and renin release were measured over a range of renal perfusion pressures achieved by constriction of the suprarenal aorta. The control group's RBF and GFR exhibited excellent autoregulatory capability from 100 to 80 mmHg. However, significant impairment of autoregulation was apparent in the hyperkalemic group. At 100 mmHg, RBF and GFR in the hyperkalemic group averaged 33 and 34% greater, respectively, than those of the control group (P less than 0.005); both variables in the hyperkalemic group were greater than the values of the control group over the autoregulatory range (100-80 mmHg). The renin release values for the two groups were not different at the 100-mmHg pressure level, although renin release of the hyperkalemic group increased to higher levels than those of the control group as perfusion pressure was reduced. At the 70- and 60-mmHg levels renin release from the hyperkalemic group averaged approximately 300% greater than that of the control group (P less than 0.05). However, when expressed as percentage change, the stimulatory effect of hyperkalemia was not apparent.(ABSTRACT TRUNCATED AT 250 WORDS)

Interaction of renal beta 1-adrenoceptors and prostaglandins in reflex renin release

1983 ◽  
Vol 244 (4) ◽  
pp. F418-F424 ◽  
Author(s):  
U. Kopp ◽  
G. F. DiBona
Keyword(s):  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Carotid Sinus ◽  
Urinary Sodium Excretion ◽  
Renal Perfusion ◽  
Prostaglandin Synthesis ◽  
Urinary Sodium ◽  
Secretion Rate ◽  
Renin Secretion ◽  
Renal Perfusion Pressure

Anesthetized dogs with isolated carotid sinus preparation were used to examine the mechanisms involved in the increase in renin secretion rate produced by carotid baroreceptor reflex renal nerve stimulation (RNS) at constant renal perfusion pressure. Lowering carotid sinus pressure by 41 +/- 5 mmHg for 10 min increased mean arterial pressure and heart rate, caused no or minimal renal hemodynamic changes, decreased urinary sodium excretion, and increased renin secretion rate. Metoprolol, a beta 1-adrenoceptor antagonist, given in the renal artery, did not affect the decrease in urinary sodium excretion but attenuated the increase in renin secretion rate, from 1,764 +/- 525 to 412 +/- 126 ng/min (70 +/- 8%). Indomethacin or meclofenamate, prostaglandin synthesis inhibitors, did not affect the decrease in urinary sodium excretion but attenuated the increase in renin secretion rate, from 1,523 +/- 416 to 866 +/- 413 ng/min (51 +/- 18%). Addition of metoprolol to indomethacin-pretreated dogs attenuated the increase in renin secretion rate from 833 +/- 327 to 94 +/- 60 ng/min (86 +/- 10%). These results indicate that reflex RNS at constant renal perfusion pressure results in an increase in renin secretion rate that is largely mediated by renal beta 1-adrenoceptors and is partly dependent on intact renal prostaglandin synthesis. The beta 1-adrenoceptor-mediated increase in renin secretion rate is independent of and not in series with renal prostaglandins.

Role of the Renal Nerves in Renin Release during Suprarenal Aortic Stenosis in Cats

1976 ◽  
Vol 51 (s3) ◽  
pp. 85s-87s
Author(s):  
A. Stella ◽  
F. Calaresu ◽  
A. Zanchetti
Keyword(s):  
Aortic Stenosis ◽  
Time Course ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renin Release ◽  
Renal Nerves ◽  
Renal Perfusion Pressure ◽  
The Difference

1. Renin release from an intact, innervated kidney and from the contralateral denervated kidney was measured before and during a period of suprarenal aortic stenosis. 2. Aortic stenosis of 10 min duration reduced renal perfusion pressure to 50 mmHg and increased renin release from both kidneys, but the response from the innervated kidney was greater. 3. A study of the time-course of the response during 30 min of aortic stenosis showed that the difference in rate of renin release between the innervated and the denervated kidney is greatest during the first few minutes of aortic stenosis.

Measurement of renin secretion in single perfused rabbit glomeruli

1990 ◽  
Vol 258 (5) ◽  
pp. F1460-F1465 ◽  
Author(s):  
H. A. Bock ◽  
M. Hermle ◽  
A. Fiallo ◽  
R. W. Osgood ◽  
T. A. Fried
Keyword(s):  
Perfusion Pressure ◽  
Secretion Rate ◽  
Renin Secretion ◽  
Renin Release ◽  
Afferent Arteriole ◽  
Adrenergic Nervous System ◽  
A New Technique ◽  
New Perspective ◽  
Bowman's Capsule

A new technique is presented that allows the measurement of the renin secretion rate of single rabbit glomeruli during in vitro perfusion at controlled afferent arteriolar perfusion pressure. Rabbit glomeruli with intact afferent arteriole and Bowman's capsule are obtained by microdissection and cannulated with a pipette system that allows continuous afferent arteriolar pressure measurement. The renin secretion rate of 10 glomeruli, perfused at 40 mmHg, was measured in 15-min intervals with an antibody-trapping microassay. Renin secretion rate was low relative to total renin content (1.2-2.0% of content/perfusion h) and increased three- to fivefold in response to isoproterenol (10(-5) M). The afferent arteriole contracted to norepinephrine (10(-5) M) in each instance. This novel, although difficult, technique allows the study of renin release in vitro at controlled perfusion pressure, without the interfering effects of the macula densa, arterial angiotensin II, and the adrenergic nervous system. It should allow a new perspective on issues such as the pressure-flow dependence of renin release and the interaction of the afferent arteriolar endothelium with the renin-secreting juxtaglomerular cells.

Mechanism of effect of diphenylhydantoin on renal renin release

1984 ◽  
Vol 247 (3) ◽  
pp. F418-F422
Author(s):  
P. Cadnapaphornchai ◽  
C. Pontes ◽  
F. D. McDonald
Keyword(s):  
Renal Artery ◽  
Renal Denervation ◽  
Secretion Rate ◽  
Renin Secretion ◽  
Separate Group ◽  
Renin Release ◽  
Renal Nerves ◽  
Percent Increase ◽  
Anesthetized Dogs

This study was undertaken to delineate the mechanism of the effect of diphenylhydantoin (DPH) on renal renin release. DPH at a dose of 0.18 mg X kg-1 X min-1 was infused for 30 min into the renal artery of anesthetized dogs with acute unilateral renal denervation. In the innervated kidney, DPH infusion increased renin secretion rate (RSR) from 189 +/- 54 to 939 +/- 279 ng ANG I X h-1 X min-1. In the contralateral denervated kidneys, RSR did not change. An identical study was done in a second group of dogs in which unilateral renal denervation was done 24 h prior to DPH infusion. In this group, DPH infusion increased RSR from 63 +/- 57 to 643 +/- 180 ng ANG I X h-1 X min-1 in the innervated kidneys. In the contralateral denervated kidneys, RSR did not change. In a separate group of indomethacin-treated nondenervated dogs, intrarenal infusion of DPH increased RSR from 131 +/- 32 to 452 +/- 88 ng ANG I X h-1 X min-1. The percent increase in RSR in the indomethacin-treated dogs was not significantly different from the non-indomethacin-treated dogs. These data suggest that the stimulatory effect of DPH on renin release is mediated by or requires the presence of renal nerves. The step(s) after the renal nerves is (are) not mediated by prostaglandins.

cGMP-Mediated Inhibition of cAMP Degradation Stimulates Renin Secretion Without Affecting Renal Hemodynamics.

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 711-711
Author(s):  
Cecilia M Sayago ◽  
William H Beierwaltes
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Direct Effect ◽  
Venous Blood ◽  
Second Messenger ◽  
Renal Hemodynamics ◽  
Secretion Rate ◽  
Renin Secretion ◽  
Before And After

P100 The stimulatory second messenger for renin is cAMP, which is degraded by phosphodiesterase (PDE)-3. PDE-3 is inhibited by cGMP, while PDE-5 degrades cGMP. We hypothesized that if endogenous cGMP was increased, it could inhibit PDE-3, increasing cAMP, and stimulating renin. We used the selective PDE-5 inhibitor Zaprinast at a dose we determined would not change either blood pressure or renal blood flow (RBF). In inactin-anesthetized rats, renin secretion rate (RSR) was determined by collecting arterial and renal venous blood while measuring RBF before and 75 min after administering 20 mg/kg bw Zaprinast (n=9) ip, or vehicle (n=7). Blood pressure before and after Zaprinast was unchanged at 102 ±2 and 98 ±2 mmHg, respectively, similar to vehicle controls (107 ±3 to 105 ±4 mmHg). RBF was unchanged by either Zaprinast (5.57 ±0.38 to 5.77 ±0.41 ml/min/gkw) or vehicle (6.21 ±0.47 to 6.25 ±0.42 ml/min/gkw). Zaprinast increased RSR 6-fold (from 2.95 ±1.74 to 17.62 ±5.46 ng Ang1/hr/min, p <0.024), while vehicle had no effect (4.08 ±2.02 to 3.87 ±1.53 ng Ang1/hr/min). Zaprinast also increased renal cGMP excretion from 12.75 ±1.57 to 18.67 ±1.87 p mol/min (p<0.003), while cGMP excretion was unchanged by vehicle (13.07 ±1.76 to 12.42 ±2.16 p mol/min). Thus, inhibition of cGMP degradation by the PDE-5 inhibitor Zaprinast increased endogenous cGMP (as reflected in excretion) and also stimulated renin secretion, despite not significantly changing renal hemodynamics. These data suggest that endogenous cGMP may indirectly regulate renin through its direct effect on cAMP degradation.

Inhibition of intrarenal NO stimulates renin secretion through a macula densa-mediated mechanism

1997 ◽  
Vol 272 (3) ◽  
pp. R879-R886 ◽  
Author(s):  
C. G. Schnackenberg ◽  
B. L. Tabor ◽  
M. H. Strong ◽  
J. P. Granger
Keyword(s):  
Kidney Function ◽  
Fractional Excretion ◽  
Macula Densa ◽  
Secretion Rate ◽  
Renin Secretion ◽  
Renin Release ◽  
Normal Kidney ◽  
Synthesis Inhibition ◽  
Normal Kidney Function ◽  
Fractional Excretion Of Sodium

Because endothelium-derived factors are known to have multiple actions throughout the body, the role of nitric oxide (NO) produced within the kidney in the regulation of renin release is still unclear. Therefore, the objectives of this study were to determine the effect of local NO synthesis inhibition within the kidney on renin secretion rate (RSR) and to determine whether the macula densa mechanism mediates the effect of NO on renin secretion rate in dogs. The NO synthesis inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) was administered via the renal artery at 5 microg x kg(-1) x min(-1) to dogs with normal kidney function and to dogs with the macula densa mechanism blocked, established by using the nonfiltering kidney model. In dogs with normal kidney function, renal arterial pressure (RAP) and glomerular filtration rate (GFR) remained constant throughout the experiment (131 +/- 5 mmHg and 22.6 +/- 3.0 ml/min, respectively). However, intrarenal NO synthesis inhibition decreased renal blood flow (RBF) by 16% (240 +/- 22 to 201 +/- 23 ml/min) and increased renal vascular resistance (RVR) by 24% (0.59 +/- 0.08 to 0.73 +/- 0.09 mmHg x ml(-1) x min). In addition, L-NAME decreased the fractional excretion of lithium by 27% (30.0 +/- 3.7 to 21.6 +/- 4.3%) and decreased the fractional excretion of sodium by 35% (0.86 +/- 0.29 to 0.56 +/- 0.21%). Associated with these changes in renal function, renin secretion rate increased by 194 and 235%. In marked contrast, renin secretion rate remained constant in dogs with the macula densa mechanism blocked. Intrarenal NO synthase blockade decreased RSR by 4 and 10% in dogs with the macula densa mechanism blocked. The RAP, RBF, and RVR responses to intrarenal NO synthesis inhibition in dogs with the macula densa mechanism blocked were similar to the renal hemodynamic response in dogs with normal kidney function. In summary, we have demonstrated that intrarenal NO synthesis blockade enhances renin secretion in dogs. The macula densa mechanism appears to play an important role in mediating the effect of intrarenal NO synthesis inhibition on renin release.

Effects of alpha-agonist on renin and prostaglandin E2 release in anesthetized dogs

1984 ◽  
Vol 247 (5) ◽  
pp. E604-E608
Author(s):  
K. Takahashi ◽  
H. Hisa ◽  
S. Satoh
Keyword(s):  
Secretion Rate ◽  
Renin Secretion ◽  
Renin Release ◽  
Slight Degree ◽  
Pge2 Release ◽  
Anesthetized Dogs ◽  
Dose Dependent Decrease ◽  
The Relationship ◽  
Dose Dependent ◽  
Alpha Agonist

The relationship between renin release and renal prostaglandin (PG) production induced by the alpha-agonists methoxamine and alpha-methylnorepinephrine was examined in anesthetized dogs. Both intrarenal infusions of methoxamine (1, 3, and 5 micrograms/min) and alpha-methylnorepinephrine (0.37, 1, and 2 micrograms/min) resulted in a dose-dependent decrease in renal blood flow to a slight degree. Methoxamine dose-dependently increased the renin secretion rate but failed to increase the PGE2 secretion rate. In contrast, alpha-methylnorepinephrine failed to affect the renin secretion rate but dose-dependently increased the PGE2 secretion rate. The effect of methoxamine (5 micrograms/min) on renin release was abolished by the intrarenal alpha 1-adrenoceptor blockade with prazosin (3 micrograms/min) but was not affected by the intrarenal alpha 2-adrenoceptor blockade with yohimbine (30 micrograms/min). The effect of alpha-methylnorepinephrine (2 micrograms/min) on PGE2 release was abolished by yohimbine but not by prazosin. These results suggest that there is a dissociation between renin release and renal PG production induced by alpha-agonists and that renal alpha 1- and alpha 2-adrenoceptors may participate in renin and PGE2 release, respectively.

Renin secretion as a function of renal renin content in dogs

1978 ◽  
Vol 234 (6) ◽  
pp. F506-F509 ◽  
Author(s):  
C. S. Park ◽  
R. L. Malvin ◽  
R. D. Murray ◽  
K. W. Cho
Keyword(s):  
Total Content ◽  
Renal Perfusion ◽  
Secretion Rate ◽  
Renin Secretion ◽  
Fractional Rate ◽  
Rate Dependent ◽  
Secretion Rates ◽  
Renin Content

The in vivo and in vitro rates of renin secretion were measured in kidneys from five groups of dogs in which renal perfusion pressure, salt diet, and neural input were varied to cause large changes in renin secretion rates and renal renin content. It was found that both the in vivo and in vitro secretory rates were proportional to the renal renin content. However, in vitro secretion rates were dependent on content up to 100 ng angiotensin I/mg tissue per h. At higher renin contents no increment in in vitro secretion rate was seen. In vivo secretion rate did not appear to reach a maximum until renal renin content was above 250 ng AI/mg tissue per h. The data are interpreted to support the hypothesis that there exist at least two pools of renin. One releases renin at a fractional rate of about 1.5% of the total content per hour. The other releases renin at a rate dependent on the magnitude of the stimuli acting on the kidneys. It is also suggested that the rate of renin synthesis may be a determinant of the basla rate of renin secretion.

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