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.

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.

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.

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.

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.

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.

Urinary excretion of urodilatin is increased during pressure natriuresis in the isolated perfused rat kidney

1999 ◽  
Vol 277 (3) ◽  
pp. F347-F351
Author(s):  
Matthias Heringlake ◽  
Klaus Wagner ◽  
Jan Schumacher ◽  
Horst Pagel
Keyword(s):  
Perfusion Pressure ◽  
Rat Kidney ◽  
Renal Perfusion ◽  
Direct Relation ◽  
Renal Perfusion Pressure ◽  
Arterial Blood ◽  
Urinary Potassium ◽  
Perfused Rat Kidney ◽  
Pressure Natriuresis ◽  
Serial Measurements

The findings about mechanisms regulating production and excretion of urodilatin [ANP-(95–126)], a member of the atrial natriuretic peptide (ANP) family, are controversial. To elucidate a possible relationship between arterial blood pressure and renal urodilatin excretion, we studied the effects of different perfusion pressures on urine flow (UV), urinary sodium (UNaV), urinary potassium (UKV), and urodilatin excretion (UUROV), and the concentration of urodilatin in the perfusate (PURO) of isolated perfused rat kidneys. Kidneys were perfused for 180 min with constant perfusion pressures (80 and 120 mmHg, respectively; each, n = 4) in a closed circuit system. Samples of urine and perfusate were taken every 30 min. Mean UV, UNaV, UKV, and UUROV values were significantly higher with a perfusion pressure of 120 mmHg than with 80 mmHg, whereas PURO did not change significantly. Serial measurements revealed no direct relation of UUROV with either UNaV or UV. This suggests that renal perfusion pressure is a determinant of UUROV and that urinary and venous effluent concentrations of urodilatin (probably production) are not coupled directly and that UUROV and UNaV may dissociate during acute variations of sodium excretion and UV.

The Inhibition of Renin Secretion by Alpha-Adrenergic Stimulation in the Isolated Rat Kidney

1974 ◽  
Vol 47 (5) ◽  
pp. 471-479 ◽  
Author(s):  
R. Vandongen ◽  
W. S. Peart
Keyword(s):  
Adrenergic Receptors ◽  
Perfusion Pressure ◽  
Rat Kidney ◽  
Blocking Agent ◽  
Renal Perfusion ◽  
Renin Secretion ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Renal Perfusion Pressure ◽  
Adrenergic Activity

1. The respective role of alpha-adrenergic and beta-adrenergic receptors in mediating the effect of catecholamines on renin secretion was examined in the isolated perfused rat kidney. 2. Noradrenaline, which has combined alpha- and beta-adrenergic activity, stimulated renin secretion only in the presence of the alpha-receptor blocking agent phenoxybenzamine. This stimulatory effect was largely prevented by the addition of the beta-blocking agent, propranolol. The vasoconstrictor action of noradrenaline, and thus the rise in mean renal perfusion pressure, was abolished by phenoxybenzamine. Our previous finding that noradrenaline alone stimulated renin release was inconclusive (Vandongen, Peart & Boyd, 1973). 3. Noradrenaline stimulated renin secretion when calcium was excluded from the perfusion fluid, to which disodium EDTA (25 mmol/l) was added. The vasoconstrictor action of noradrenaline was considerably attenuated under these conditions. 4. Methoxamine, which has only alpha-adrenergic activity, did not increase renin secretion when infused alone or with phenoxybenzamine. The increase in renin secretion after beta-adrenergic stimulation with isoproterenol was significantly suppressed by methoxamine, although this was associated with an increase in mean renal perfusion pressure. 5. These findings indicate the importance of intrarenal beta-adrenergic receptors in the stimulation of renin secretion and suggest that an opposite inhibitory effect on renin secretion follows alpha-adrenergic activity. 6. Although the results do not exclude a direct effect of vascular tone and renal perfusion pressure, it is suggested that the stimulation and inhibition of renin secretion is related to smooth muscle activity by the involvement of a calcium-dependent process similar to that involved in contraction and relaxation. This would accord with the common derivation of the renin-producing and vascular smooth muscle cells

Blockade of Renin Release by Lanthanum

1974 ◽  
Vol 48 (s2) ◽  
pp. 31s-32s
Author(s):  
A. G. Logan ◽  
I. Tenyi ◽  
T. Quesada ◽  
W. S. Peart ◽  
A. S. Breathnach ◽  
...  
Keyword(s):  
Rat Kidney ◽  
Renin Secretion ◽  
Renin Release ◽  
Isolated Perfused Rat Kidney ◽  
Renal Vasoconstriction ◽  
Perfused Rat Kidney ◽  
Stimulation Of

1. The effects of lanthanum on renin release and renal vasoconstriction were studied in the isolated perfused rat kidney. 2. Lanthanum reduced noradrenaline-induced renal vasoconstriction. 3. Lanthanum prevented isoprenaline-induced and glucagon-induced stimulation of renin secretion.

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.

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