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.

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.

scholarly journals Role of the endothelium-dependent relaxing factor nitric oxide on renal function.

1992 ◽  
Vol 2 (9) ◽  
pp. 1371-1387 ◽  
Author(s):  
J C Romero ◽  
V Lahera ◽  
M G Salom ◽  
M L Biondi
Keyword(s):  
Nitric Oxide ◽  
Renal Function ◽  
Perfusion Pressure ◽  
Sodium Intake ◽  
Systemic Circulation ◽  
Renal Perfusion ◽  
Renin Release ◽  
High Sodium ◽  
Renal Perfusion Pressure

The role of nitric oxide in renal function has been assessed with pharmacologic and physiologic interventions. Pharmacologically, the renal vasodilation and, to some extent, the natriuresis produced by endothelium-dependent vasodilators such as acetylcholine and bradykinin are mediated by nitric oxide and also by prostaglandins. However, prostaglandins and nitric oxide do not participate in the renal effects produced by endothelium-independent vasodilators such as atrial natriuretic peptide, prostaglandin I2, and nitroprusside. Physiologically, nitric oxide and prostaglandins exert a strong regulation on the effects produced by changes in renal perfusion pressure. Increments in renal perfusion pressure within the range of RBF autoregulation appear to inhibit prostaglandin synthesis while simultaneously enhancing the formation of nitric oxide. Nitric oxide modulates autoregulatory vasoconstriction and at the same time inhibits renin release. Conversely, a decrease of renal perfusion pressure to the limit of or below RBF autoregulation may inhibit the synthesis of nitric oxide but may trigger the release of prostaglandins, whose vasodilator action ameliorates the fall in RBF and stimulates renin release. Nitric oxide and prostaglandins are also largely responsible for mediating pressure-induced natriuresis. However, unlike prostaglandins, mild impairment of the synthesis of nitric oxide in systemic circulation produces a sustained decrease in sodium excretion, which renders blood pressure susceptible to be increased during high-sodium intake. This effect suggests that a deficiency in the synthesis of nitric oxide could constitute the most effective single disturbance to foster the development of a syndrome similar to that seen in salt-sensitive hypertension.

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.

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.

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.

Renin release in rats during blockade of nitric oxide synthesis

1994 ◽  
Vol 266 (6) ◽  
pp. R1723-R1729 ◽  
Author(s):  
R. A. Johnson ◽  
R. H. Freeman
Keyword(s):  
Nitric Oxide ◽  
Plasma Renin Activity ◽  
Perfusion Pressure ◽  
Plasma Renin ◽  
Treated Group ◽  
Renal Perfusion ◽  
Renin Activity ◽  
Renin Release ◽  
Nitric Oxide Synthesis ◽  
Renal Perfusion Pressure

The influence of renal perfusion pressure on renin release was examined in rats administered the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME). Compared with the control plasma renin of 6.0 +/- 0.7 ng angiotensin I (ANG I).ml-1.h-1, plasma renin activity was suppressed (1.8 +/- 0.2 ng ANG I.ml-1.h-1, P < 0.05) in L-NAME-treated animals in which the renal perfusion pressure was permitted to increase and reached 141 +/- 8 mmHg. Plasma renin activity also was suppressed (2.5 +/- 0.4 ng ANG I.ml-1.h-1, P < 0.05) in a second L-NAME-treated group in which the renal perfusion pressure was controlled to a level of 105 +/- 5 mmHg via tightening of a suprarenal aortic snare. Plasma renin activity was increased (12.0 +/- 1.4 ng ANG I.ml-1.h-1, P < 0.05) in a third L-NAME-treated group in which renal perfusion pressure was reduced to 59 +/- 1 mmHg. Overall, these findings suggest that the intrarenal pressure-sensing mechanism for renin release does not stringently require nitric oxide synthesis. In a second experimental series, bilaterally renal-denervated rats were administered L-NAME, and again plasma renin activity was suppressed significantly whether renal perfusion pressure was permitted to increase or was controlled. Thus L-NAME also suppressed plasma renin activity independently of reflex reductions in renal neuroadrenergic activity even when renal perfusion pressure was controlled. Infusions of sodium nitroprusside completely inhibited L-NAME-induced suppression of plasma renin activity in these renal-denervated rats. Nitric oxide may function as a paracrine stimulatory mechanism for the local regulation of renin release.

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.

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 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.

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