Release by Vasopressin of E-Type Prostaglandins from the Rat Kidney

1977 ◽  
Vol 52 (1) ◽  
pp. 103-106
Author(s):  
C. Bell ◽  
M. K. K. Mya
Keyword(s):  
Smooth Muscle ◽  
Perfusion Pressure ◽  
Rat Kidney ◽  
Renal Perfusion ◽  
Prostaglandin Synthesis ◽  
Prostaglandin E ◽  
Receptor Stimulation ◽  
Renal Vasoconstriction ◽  
Renal Perfusion Pressure ◽  
Stimulation Of

1. In order to test whether the release of E-type prostaglandins from the kidney by various vasoconstrictor stimuli is related specifically to adrenoreceptor activation, we have compared release of prostaglandin E-like material from perfused rat kidneys during infusion of noradrenaline or vasopressin. 2. Concentrations of noradrenaline or vasopressin that produced comparable rises in renal perfusion pressure also released comparable amounts of prostaglandin E-like material. This effect was abolished by infusion of an inhibitor of prostaglandin synthesis into the kidney. 3. We conclude that liberation of E-type prostaglandins during renal vasoconstriction is probably related to the activation of intra-renal smooth muscle and does not involve any specific hormonal receptor. Stimulation of release of prostaglandin E may explain certain reported renal actions of vasopressin.

The Stimulation of Renin Secretion by Non-Vasocontrictor Infusions of Adrenaline and Noradrenaline in the Isolated Rat Kidney

1975 ◽  
Vol 49 (6) ◽  
pp. 609-612
Author(s):  
R. Vandongen ◽  
Dianne M. Greenwood
Keyword(s):  
Perfusion Pressure ◽  
Rat Kidney ◽  
Renal Perfusion ◽  
Renin Secretion ◽  
Renal Vasoconstriction ◽  
Renal Perfusion Pressure ◽  
Perfused Rat Kidney ◽  
Secretion Rates ◽  
Control Study ◽  
Stimulation Of

1. The effect of adrenaline and noradrenaline on renin secretion in the isolated perfused rat kidney was examined. The doses of catecholamines used were such that renal vasoconstriction and therefore increases in renal perfusion pressure were avoided. Under these conditions adrenaline and noradrenaline significantly increased renin secretion rates, compared with control experiments in which no catecholamine was infused. 2. Mean renal perfusion pressure during both adrenaline and noradrenaline infusion paralleled the control study by showing a progressive fall. 3. Administration of phenoxybenzamine did not impair the stimulation of renin secretion by adrenaline whereas this was prevented by racemic propranolol. 4. These observations suggest that catecholamines stimulate renin secretion by an intrarenal effect which is largely independent of changes in renal perfusion pressure. It is postulated that the beta-adrenoceptors mediating renin secretion are an integral component of the renin-producing cell.

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.

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.

Low concentrations of ANP cause pressure-dependent natriuresis in the isolated kidney

1988 ◽  
Vol 255 (3) ◽  
pp. F391-F396 ◽  
Author(s):  
J. D. Firth ◽  
A. E. Raine ◽  
J. G. Ledingham
Keyword(s):  
Filtration Rate ◽  
Perfusion Pressure ◽  
Rat Kidney ◽  
Fractional Excretion ◽  
Renal Perfusion ◽  
Isolated Kidney ◽  
Renal Perfusion Pressure ◽  
Low Concentrations ◽  
Fractional Excretion Of Sodium ◽  
Perfused Rat Kidney

The effect of alteration in renal perfusion pressure on the response of the isolated perfused rat kidney to concentrations of alpha-human atrial natriuretic peptide (ANP) within the pathophysiological range has been examined. At a perfusion pressure of 90 mmHg ANP concentrations of 50, 200, and 1,000 pmol/l were without effect on any parameter tested. At a perfusion pressure of 130 mmHg 50 pmol/l ANP produced an increase of 3.13 +/- 0.68 mumol/min in sodium excretion (UNa V), compared with a fall of 0.33 +/- 1.04 mumol/min in controls (P less than 0.02); fractional excretion of sodium (FENa) rose by 1.45 +/- 0.36% vs. -0.12 +/- 0.47% (P less than 0.05); glomerular filtration rate (GFR) was unchanged. At 200 and 1,000 pmol/l larger changes in UNa V and FENa were seen; only at 1,000 pmol/l was a significant effect on GFR observed. In contrast, frusemide (furosemide) at concentrations of 10 and 100 mumol/l was natriuretic at both 90 and 130 mmHg, with lesser absolute but greater proportional changes being seen at the lower pressure. It was concluded 1) the response of the isolated kidney to ANP is critically dependent on perfusion pressure, 2) at elevated levels of perfusion pressure the isolated kidney can respond to levels of ANP within the upper physiological and pathophysiological range.

Stimulation of renin release by hyperkalemia in the nonfiltering kidney

1991 ◽  
Vol 260 (2) ◽  
pp. F170-F176 ◽  
Author(s):  
H. B. Lin ◽  
D. B. Young ◽  
M. J. Smith
Keyword(s):  
Pressure Range ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Pressure Level ◽  
Renin Release ◽  
Control Group ◽  
Acute Effects ◽  
Renal Perfusion Pressure ◽  
The Difference ◽  
Stimulation Of

This study was designed to analyze the acute effects of hyperkalemia on renin release in the normal filtering kidney and the nonfiltering kidney. Plasma K was increased by acute intravenous KCl infusion. In the normal filtering kidney experiment plasma K was 5.7 vs. 3.5 meq/l. Hyperkalemia resulted in a 45% increase in renal blood flow (RBF) and a 35% increase in glomerular filtration rate (GFR) at the 120-mmHg pressure level. Renin release was significantly greater in the hyperkalemic group than in the control group (P less than 0.01) with the greatest effect over the lower pressure range. In the nonfiltering kidney experiment plasma K was 6.09 vs. 3.5 meq/l. RBF was 33% greater in the hyperkalemic than in the normokalemic group at the 130-mmHg pressure level. Renin release was also greater in the hyperkalemic group than in the normokalemic group (P less than 0.01). However, unlike the normal filtering kidney experiments, in the nonfiltering kidneys the difference in renin release was most prominent at the highest level of renal perfusion pressure. These experiments demonstrate that acute hyperkalemia can cause renal vasodilation and stimulate renin release in both filtering and nonfiltering kidney preparations and that potassium may affect renin release both through a direct effect on the juxtaglomerular cells and indirectly by affecting delivery of fluid and/or NaCl to the macula densa.

Stimulation of Renin Secretion by Frusemide and Diazoxide in the Isolated Rat Kidney

1976 ◽  
Vol 51 (s3) ◽  
pp. 101s-104s
Author(s):  
R. Vandongen ◽  
Dianne M. Greenwood
Keyword(s):  
Perfusion Pressure ◽  
Rat Kidney ◽  
Renal Perfusion ◽  
Urine Flow ◽  
Renin Secretion ◽  
Stimulatory Action ◽  
Vasodilatory Effect ◽  
Perfused Rat Kidney ◽  
Site Of Action ◽  
Stimulation Of

1. The effect of diazoxide (17·3 μmol min—1 g—1) and frusemide (0·12 μmol min—1 g—1) on renin secretion was examined in the isolated perfused rat kidney. These substances are potential renal vasodilators with opposite effects on urine sodium excretion. 2. Both agents significantly increased renin secretion rate above control values. In the case of frusemide this was not altered by ureteric occlusion and presumed absence of urine flow. 3. Mean renal perfusion pressure decreased to the same extent with diazoxide and frusemide infusion as in the control experiments and no additional vasodilatory effect was observed on the basis of changes in flow rate of perfusate. 4. These observations identify an intrarenal site of action for diazoxide and frusemide on renin secretion. The apparent independence of this stimulatory action on renal vasodilatation and urine flow suggests a direct effect on the renin-producing cell.

Dose-dependent effect of cyclosporin on renal arterial resistance in dogs

1991 ◽  
Vol 261 (6) ◽  
pp. H1791-H1796
Author(s):  
M. Carrier ◽  
F. Tronc ◽  
D. Stewart ◽  
L. C. Pelletier
Keyword(s):  
Perfusion Pressure ◽  
Autologous Blood ◽  
Venous Blood ◽  
Renal Perfusion ◽  
Blood Levels ◽  
Renal Vasoconstriction ◽  
Alpha Adrenergic Receptors ◽  
Renal Perfusion Pressure ◽  
Arterial Resistance ◽  
Dose Dependent

Important side effects of cyclosporin (CSA) are renal insufficiency and hypertension. They might be related to a renal vasoconstrictive effect of CSA, and this vascular response might be due to a local mechanism. CSA was injected in isolated renal artery perfused at constant flow in dogs. Changes in renal perfusion pressure reflected variations in vascular resistance. Pure CSA was dissolved in autologous blood and injected at doses of 0.5, 1, 5, and 10 mg. The infusion of 0.5 and 1 mg caused averaged renal perfusion pressure increases of 8 +/- 4 mmHg and 15 +/- 8 mmHg. Renal venous CSA levels averaged 32 +/- 3 and 49 +/- 9 nmol/l, respectively, at the end of injections. Infusion of 5 and 10 mg of CSA caused averaged renal perfusion pressure increases of 32 +/- 12 mmHg and 81 +/- 21 mmHg. Renal venous CSA levels at the end of injections averaged 142 +/- 30 and 382 +/- 82 nmol/l, respectively. A positive correlation was found between the changes in renal perfusion pressure and renal venous CSA levels. Blockade of alpha-adrenergic receptors, surgical renal sympathectomy, administration of thromboxane receptor antagonist, and endothelial-dependent vasodilation by acetylcholine infusion did not affect the renal vasoconstriction effect of CSA; renal response to CSA was prevented by blockade of the Ca channels with diltiazem, and the plasma endothelin concentration in renal venous blood increased significantly after injection of CSA. A dose-dependent increase in renal arterial resistance occurs with therapeutic blood levels of CSA. Renal vasoconstriction is induced by a local effect at the arterial wall, which is independent of neurogenic, adrenergic, and prostaglandin mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Inhibition of Renin Secretion in the Isolated Rat Kidney by Antidiuretic Hormone

1975 ◽  
Vol 49 (1) ◽  
pp. 73-76 ◽  
Author(s):  
R. Vandongen
Keyword(s):  
Antidiuretic Hormone ◽  
Calcium Ions ◽  
Perfusion Pressure ◽  
Direct Action ◽  
Rat Kidney ◽  
Renal Perfusion ◽  
Renin Secretion ◽  
Renal Perfusion Pressure ◽  
Isolated Rat Kidney ◽  
Isolated Rat

1. The effect of antidiuretic hormone (ADH) on isoprenaline-stimulated renin secretion was examined in the isolated rat kidney perfused with modified Krebs-Ringer saline. 2. Intrarenal infusion of ADH effectively prevented stimulation of renin secretion by isoprenaline whilst increasing renal perfusion pressure. 3. The exclusion of calcium ions from the perfusion medium abolished the vasoconstrictor effect of ADH and attenuated the inhibitory effect of ADH on isoprenaline-stimulated renin secretion. However, significant suppression of renin secretion was still apparent compared with experiments where isoprenaline was infused alone. 4. These observations indicate that ADH inhibits renin secretion and that this is effected by a direct action on the kidney. Although this may be partly mediated by the rise in renal perfusion pressure, an additional direct effect of ADH on the renin-producing cell, which is dependent on the availability of calcium ions, is proposed.

Atrial natriuretic peptide blocks renin response to renal hypotension

1987 ◽  
Vol 252 (2) ◽  
pp. R423-R427 ◽  
Author(s):  
D. A. Scheuer ◽  
T. N. Thrasher ◽  
E. W. Quillen ◽  
C. H. Metzler ◽  
D. J. Ramsay
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Perfusion Pressure ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Atrial Pressure ◽  
Renal Perfusion Pressure ◽  
Endogenous Release ◽  
Stimulation Of ◽  
Atrial Natriuretic

We have reported that the renin response to systemic hypotension is inhibited in the presence of elevated atrial pressure and that elevations in atrial pressure of similar or larger magnitude cause graded increases in plasma atrial natriuretic peptide (ANP). Therefore we tested the hypothesis that comparable increments in plasma ANP can inhibit renal hypotension-induced increases in plasma renin activity (PRA) in conscious dogs. Renal perfusion pressure was controlled using cuffs implanted around the abdominal aorta just above the renal arteries. Reducing renal perfusion pressure by 10 or 30% of control caused graded increases in PRA (P less than 0.01). Infusion of 1-28 rat ANP (5 ng X kg-1 X min-1), which increased plasma ANP by 34.8 +/- 7.5 (SE) pg/ml, eliminated increases in PRA in response to a 10% reduction in renal perfusion pressure and markedly inhibited the response to a 30% pressure reduction (P less than 0.01). These results indicate that increments in plasma ANP which reproduce endogenous release inhibit renal hypotension-induced stimulation of PRA. Furthermore, the results provide an explanation for the inhibition of the renin response to renal hypotension during elevated atrial pressure.

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