ANG II-induced downregulation of RBF after a prolonged reduction of renal perfusion pressure is due to pre- and postglomerular constriction

2004 ◽  
Vol 286 (5) ◽  
pp. R865-R873 ◽  
Author(s):  
Charlotte Mehlin Sorensen ◽  
Paul Peter Leyssac ◽  
Max Salomonsson ◽  
Ole Skott ◽  
Niels-Henrik Holstein-Rathlou
Keyword(s):  
Perfusion Pressure ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Renal Perfusion Pressure ◽  
Sprague Dawley Rats ◽  
Proximal Tubular ◽  
Tubular Flow ◽  
Over Time

Previous experiments from our laboratory showed that longer-lasting reductions in renal perfusion pressure (RPP) are associated with a gradual decrease in renal blood flow (RBF) that can be abolished by clamping plasma ANG II concentration ([ANG II]). The aim of the present study was to investigate the mechanisms behind the RBF downregulation in halothane-anesthetized Sprague-Dawley rats during a 30-min reduction in RPP to 88 mmHg. During the 30 min of reduced RPP we also measured glomerular filtration rate (GFR), proximal tubular pressure (Pprox), and proximal tubular flow rate (QLP). Early distal tubular fluid conductivity was measured as an estimate of early distal [NaCl] ([NaCl]ED), and changes in plasma renin concentration (PRC) over time were measured. During 30 min of reduced RPP, RBF decreased gradually from 6.5 ± 0.3 to 6.0 ± 0.3 ml/min after 5 min (NS) to 5.2 ± 0.2 ml/min after 30 min ( P < 0.05). This decrease occurred in parallel with a gradual increase in PRC from 38.2 ± 11.0 × 10-5 to 87.1 ± 25.1 × 10-5 Goldblatt units (GU)/ml after 5 min ( P < 0.05) to 158.5 ± 42.9 × 10-5 GU/ml after 30 min ( P < 0.01). GFR, Pprox, and [NaCl]ED all decreased significantly after 5 min and remained low. Estimates of pre- and postglomerular resistances showed that the autoregulatory mechanisms initially dilated preglomerular vessels to maintain RBF and GFR. However, after 30 min of reduced RPP, both pre- and postglomerular resistance had increased. We conclude that the decrease in RBF over time is caused by increases in both pre- and postglomerular resistance due to rising plasma renin and ANG II concentrations.

Atrial appendectomy reduces ANF but not sodium excretion in acute vasopressin hypertension

1990 ◽  
Vol 258 (1) ◽  
pp. R77-R81
Author(s):  
R. S. Zimmerman ◽  
R. W. Barbee ◽  
A. Martinez ◽  
A. A. MacPhee ◽  
N. C. Trippodo
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Sprague Dawley ◽  
Renal Perfusion Pressure ◽  
Sprague Dawley Rats ◽  
Circulating Levels

The present study was designed to determine whether atrial appendectomy would decrease the sodium excretion associated with pressor doses of arginine vasopressin (AVP) infusion in rats by decreasing circulating levels of atrial natriuretic factor (ANF). Ten to 21 days after either sham (n = 9) or bilateral atrial appendectomy (n = 13) AVP (19 ng.kg-1.min-1) was infused for 90 min in anesthetized Sprague-Dawley rats. Atrial appendectomy decreased circulating ANF levels from 469 +/- 70 pg/ml in sham-operated animals to 259 +/- 50 pg/ml (P less than 0.05) in atrial-appendectomized animals after 90 min of AVP infusion. Despite a reduction in circulating levels of ANF, sodium excretion, potassium excretion, and urine flow increased and were not affected by bilateral atrial appendectomy. Glomerular filtration rate and mean arterial pressure significantly increased in both groups of rats. The present study supports non-ANF factors such as increases in renal perfusion pressure and/or glomerular filtration rate as potential mechanisms in AVP-induced natriuresis.

beta-Adrenoceptor modulation of renin response to short-term reductions in pressure in young SHR

1992 ◽  
Vol 263 (2) ◽  
pp. R405-R411
Author(s):  
J. P. Porter
Keyword(s):  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Sprague Dawley ◽  
Short Term ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Beta Adrenoceptor ◽  
Renal Perfusion Pressure ◽  
Sprague Dawley Rats ◽  
Renal Nerve Activity

The increase in renin secretion in response to short-term (5 min) reductions in arterial pressure has recently been shown to be similar in young spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto (WKY) animals. This was puzzling, since tonic renal nerve activity is thought to be elevated in the young SHR, and this has the potential to enhance the renin response. The purpose of the present investigation was to determine whether beta-adrenoceptor modulation of pressure-dependent renin release is diminished in the SHR. In conscious, age-matched SHR, WKY, and Sprague-Dawley rats, the effect on arterial plasma renin activity of 5-min reductions in renal perfusion pressure to 90 and 50 mmHg was determined before and during beta-adrenoceptor activation with isoproterenol or beta-adrenoceptor blockade with propranolol. Isoproterenol augmented the renin response at 50 mmHg in all three strains, with the greatest effect occurring in the Sprague-Dawley rats. The response at 90 mmHg was also enhanced in the SHR and Sprague-Dawley rats, but not the WKY rats. Propranolol had no effect in the SHR and WKY animals, but significantly reduced the renin response at 50 mmHg in the Sprague-Dawley rats. Thus, under the conditions of the present investigation (i.e., short-term reductions in pressure), tonic renal nerve activity does not affect pressure-dependent renin release through a beta-adrenergic receptor mechanism in either the SHR or WKY rats. However, under conditions of acute beta-adrenoceptor activation, the renin response is enhanced at a higher renal perfusion pressure in the SHR than in the WKY rat.

Abstract P111: Renal Perfusion Pressure Determines Renal Leukocyte Infiltration During Angiotensin II-Induced Hypertension in Sprague Dawley Rats

Hypertension ◽  
2019 ◽  
Vol 74 (Suppl_1) ◽  
Author(s):  
Satoshi Shimada ◽  
Justine M Abais-Battad ◽  
Ammar J Alsheikh ◽  
Megan Stumpf ◽  
Theresa Kurth ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Leukocyte Infiltration ◽  
Sprague Dawley ◽  
Renal Perfusion Pressure ◽  
Sprague Dawley Rats ◽  
Induced Hypertension

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.

Identification of a Delivery-Related Influence on Proximal Tubular Reabsorption during Expansion with Hyperoncotic Albumin in the Rat

1978 ◽  
Vol 55 (4) ◽  
pp. 369-376
Author(s):  
J. F. Donohoe ◽  
Gertrude S. Lefavour ◽  
S. Cortell ◽  
F. J. Gennari
Keyword(s):  
Fluid Flow ◽  
Flow Rate ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Tubular Reabsorption ◽  
Renal Perfusion Pressure ◽  
Proximal Tubular ◽  
Tubular Flow ◽  
Proximal Tubular Reabsorption

1. Proximal tubular fluid flow rate was deliberately reduced to control values in rats after acute volume expansion with hyperoncotic albumin, to determine if the depression of reabsorption by albumin-induced expansion could be uncovered by preventing the associated increase in filtrate delivery. Tubular fluid flow was reduced either by reducing renal perfusion pressures or by diverting fluid from early proximal tubular sites. 2. In the absence of controlled delivery, expansion with hyperoncotic albumin increased nephron filtration rate, reduced the TF/P inulin ratio, but had no effect on absolute reabsorptive rate. When proximal tubular flow rate was returned to control values by a simultaneous early collection, fractional reabsorption remained depressed. By contrast, when tubular flow was maintained at control values by reducing renal perfusion pressure, the large fall in fractional reabsorption was blocked. 3. The results indicate that expansion with hyperoncotic albumin depresses proximal tubular reabsorption independently of delivery rate into the proximal tubule, but that this effect can be reversed by a reduction in renal perfusion pressure. These observations unify the results of previous studies and indicate the presence of a delivery-related influence on proximal reabsorption. The inability to detect a reduction in absolute reabsorption when nephron filtration rate is increased during expansion with hyperoncotic albumin is probably due to the countervailing influence of increased delivery rate, which raised reabsorptive rate.

scholarly journals Resetting of exaggerated tubuloglomerular feedback activity in acutely volume-expanded young SHR

1999 ◽  
Vol 276 (3) ◽  
pp. F409-F416 ◽  
Author(s):  
Kristina Brännström ◽  
William J. Arendshorst
Keyword(s):  
Turning Point ◽  
Tubuloglomerular Feedback ◽  
Maximal Response ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Spontaneously Hypertensive ◽  
Sprague Dawley Rats ◽  
Proximal Tubular ◽  
Wistar Kyoto ◽  
Tubular Flow

One purpose of the present study was to evaluate the ability of 7-wk-old spontaneously hypertensive rats (SHR) to reset tubuloglomerular feedback (TGF) activity in response to acute volume expansion (VE). Second, we evaluated the contribution of ANG II, via its action on AT1 receptors, to TGF control of glomerular function during VE. TGF was assessed by micropuncture methods and proximal tubular stop-flow pressure (SFP) determinations in SHR, Wistar-Kyoto rats (WKY), and Sprague-Dawley rats (SD). During euvolemia SHR exhibited enhanced TGF activity. In the same animals acute VE was achieved by infusion of saline (5 ml ⋅ h−1 ⋅ 100 g body wt−1). VE led to resetting of TGF in all three strains. Maximal SFP responses, elicited by a 30–40 nl/min loop of Henle perfusion rate, decreased from 19 to 12 mmHg in SHR and, on average, from 11 to 5 mmHg in WKY and SD ( P < 0.001). Tubular flow rate producing a half-maximal response (turning point) shifted to higher flow rates during VE, from 12 to 14 nl/min in SHR and from 15 to 19 nl/min in WKY. Administration of the AT1 receptor blocker candesartan (0.05 mg/kg iv) during sustained VE decreased TGF-mediated reductions in SFP in SHR and slightly increased the turning point in WKY. Nevertheless, other parameters of TGF activity were unaffected by AT1 receptor blockade. In conclusion, young SHR possess the ability to reset TGF activity in response to VE to a degree similar to compensatory adjustments in WKY. However, TGF remains enhanced in SHR during VE. ANG II and its action on AT1 receptors are in part responsible for the exaggerated SFP responses in young SHR during VE.

Mechanisms compensating Na and water retention induced by long-term reduction of renal perfusion pressure

1997 ◽  
Vol 273 (2) ◽  
pp. R646-R654 ◽  
Author(s):  
E. Seeliger ◽  
W. Boemke ◽  
M. Corea ◽  
T. Encke ◽  
H. W. Reinhardt
Keyword(s):  
Water Retention ◽  
Perfusion Pressure ◽  
Daily Intake ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Compensatory Mechanism ◽  
Ang Ii ◽  
Renal Perfusion Pressure ◽  
Water Balances

Endogenous downregulation of plasma aldosterone (Aldo) concentration, despite increased plasma renin activity (PRA), has been suggested to compensate Na and water retention, which is induced by long-term reduction of renal perfusion pressure (rRPP). To determine whether fixed plasma Aldo concentration would prevent equilibration of 24-h Na and water balances during rRPP, chronically instrumented, freely moving beagle dogs were kept under standardized conditions (daily intake 5.5 mmol Na/kg body wt) and studied for 4 consecutive days under the following conditions: control without rRPP (protocol 1) and rRPP + infusion of Aldo (rRPP + Aldo, protocol 2). Because Aldo administration reduces PRA and, thereby, angiotensin II (ANG II) levels ANG II was additionally infused in protocol 3 (rRPP + ANG II + Aldo). During rRPP + Aldo, 24-h Na balances were never equilibrated. Daily Na retention was approximately 3.5 mmol/kg body wt on day 1 and decreased to approximately 1.6 mmol/kg body wt on day 4; 24-h water balances changed in a similar manner. PRA decreased stepwise. On all rRPP + ANG II + Aldo days, Na and water retentions were more extensive than during rRPP + Aldo. Daily Na retention decreased from approximately 4.4 mmol/kg body wt on day 1 to approximately 3.0 mmol/kg body wt on day 4. Plasma atrial natriuretic peptide increased during both protocols. It is concluded that 1) endogenous downregulation of components of the renin-angiotensin-aldosterone system is a pivotal compensatory mechanism to reduce Na and water retention and 2) natriuretic and diuretic factors seem to be of minor potency, because not even the sum of all could counterbalances the Na- and water-retaining effects of Aldo and ANG II.

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.

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.

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