scholarly journals Upregulation of endothelin B receptors in kidneys of DOCA-salt hypertensive rats

2000 ◽  
Vol 278 (2) ◽  
pp. F279-F286 ◽  
Author(s):  
David M. Pollock ◽  
Graham H. Allcock ◽  
Arthi Krishnan ◽  
Brian D. Dayton ◽  
Jennifer S. Pollock
Keyword(s):  
Arterial Pressure ◽  
Renal Medulla ◽  
Systolic Arterial Pressure ◽  
Receptor Subtypes ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Water Excretion ◽  
Sprague Dawley Rats ◽  
The Difference ◽  
Endothelin B

Experiments were designed to elucidate the role of endothelin B receptors (ETB) on arterial pressure and renal function in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Male Sprague-Dawley rats underwent uninephrectomy and were treated with either DOCA and salt (0.9% NaCl to drink) or placebo. DOCA-salt rats given the ETB-selective antagonist, A-192621, for 1 wk (10 mg ⋅ kg− 1 ⋅ day− 1in the food) had significantly greater systolic arterial pressure compared with untreated DOCA-salt rats (208 ± 7 vs. 182 ± 4 mmHg) whereas pressure in placebo rats was unchanged. In DOCA-salt, but not placebo rats, A-192621 significantly decreased sodium and water excretion along with parallel decreases in food and water intake. To determine whether the response in DOCA-salt rats was due to increased expression of ETB receptors, endothelin receptor binding was performed by using membranes from renal medulla. Maximum binding (Bmax) of [125I]ET-1, [125I]ET-3, and [125I]IRL-1620 increased from 227 ± 42, 146 ± 28, and 21 ± 1 fmol/mg protein, respectively, in placebo rats to 335 ± 27, 300 ± 38, and 61 ± 6 fmol/mg protein, respectively, in DOCA-salt hypertensive rats. The fraction of receptors that are the ETB subtype was significantly increased in DOCA-salt (0.88 ± 0.07) compared with placebo (0.64 ± 0.01). The difference between [125I]ET-3 and [125I]IRL-1620 binding is consistent with possible ETB receptor subtypes in the kidney. These results indicate that ETB receptors in the renal medulla are up-regulated in the DOCA-salt hypertensive rat and may serve to maintain a lower arterial pressure by promoting salt and water excretion.

Arginine vasopressin-induced natriuresis in the anaesthetized rat: involvement of V1 and V2 receptors

1993 ◽  
Vol 136 (2) ◽  
pp. 283-288 ◽  
Author(s):  
C. P. Smith ◽  
R. J. Balment
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arginine Vasopressin ◽  
Plasma Concentrations ◽  
Receptor Subtypes ◽  
Vasopressin Receptor ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Anaesthetized Rat

ABSTRACT The present study was undertaken to determine the involvement of the two established vasopressin receptor subtypes (V1 and V2) in arginine vasopressin (AVP)-induced natriuresis and also to determine whether changes in mean arterial pressure (MAP) and/or the renally active hormones atrial natriuretic peptide (ANP), angiotensin II (AII) and aldosterone are a prerequisite for the expression of AVP-induced natriuresis. In Sprague–Dawley rats which were anaesthetized with Inactin (5-ethyl-5-(1′-methylpropyl)-2-thiobarbiturate) and infused with 0·077 mol NaCl/l, infusion of 63 fmol AVP/min was found to be natriuretic whereas an approximately equipotent dose of the specific V2 agonist [deamino-cis1, d-Arg8]-vasopressin (dDAVP) did not induce natriuresis. The specific V1 antagonist [β-mercapto-β,β-cyclopenta-methylene-propionyl1, O-Me-Tyr2, Arg8]-vasopressin when administered prior to infusion of 63 fmol AVP/min did not inhibit AVP-induced natriuresis. AVP-induced natriuresis was not accompanied by changes in MAP or in the plasma concentrations of the renally active hormones ANP, AII or aldosterone. These results suggest that neither the V1 nor the V2 receptor subtypes are involved in AVP-induced natriuresis. In addition, it was found that changes in MAP, plasma ANP, All or aldosterone concentrations were not a prerequisite for AVP-induced natriuresis. Journal of Endocrinology (1993) 136, 283–288

Abstract 334: Selective Renal Deafferentation Attenuates the Development of Genetic and Renal Hypertension

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Mark M Knuepfer ◽  
Nathan E Billington ◽  
Laura A Willingham ◽  
Julie E Langasek ◽  
Willis K Samson ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
G Protein ◽  
Left Kidney ◽  
Renal Hypertension ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Afferent Nerves ◽  
Sprague Dawley Rats ◽  
Direct Recording ◽  
Tail Cuff

Renal denervation decreases arterial pressure (AP) in hypertensive rats and humans. This procedure destroys both afferent and efferent nerves. Several investigators have proposed that renal afferent nerves contribute to the elevated AP. We developed a procedure to selectively remove renal afferent nerves with capsaicin (1-100 mM) both topically on the nerve and in the renal pelvis. We examined the effects of renal deafferentation on the development of genetic and renal hypertension. We studied spontaneously hypertensive rats (SHR), and a model of renal hypertension, two kidney-one clip (2K1C) in Sprague-Dawley rats. SHR were treated at 3-4 weeks of age with capsaicin. Mean arterial pressure was recorded by tail cuff through 16 weeks of age. On week 17, rats were cannulated, allowed 3 days to recover then had their AP measured directly for 3 days (3 hrs/day). Rats with renal deafferentation (n=11) had lower arterial pressure weeks 9-16 (average reduction AP=10.1±1.4 mmHg, ANOVA, p=0.0049) compared to control (saline treated, n=6) although the final direct recording was not significantly different on week 17 (control AP=184.1±3.4 mmHg vs deafferented AP=173.9±4.3 mmHg, p=0.07). Substance P levels from the kidneys were reduced in deafferented rats compared to control (6.9±1.0 vs 17.3±5.2 pg/g protein, p=0.0009). In contrast, renal NE levels were not altered (307±19 vs 313±20 pg/g protein, p=0.428). In the second study, the left kidney in weanling Sprague-Dawley rats was exposed to capsaicin or saline. Rats were allowed to mature (>250 g BW) then subjected to left renal artery clipping (0.2mm) or sham clip. AP was recorded by tail cuff during development of 2K1C for 6 weeks before direct cannulation to record AP on week 7. Renal deafferentation prevented the development of hypertension in 13 rats compared to 9 saline treated rats (average reduction AP=16.9±2.7 mmHg, ANOVA, p=0.0031). Saline treated rats had a higher AP 7 weeks after clipping (147.1±10.2 vs 130.5±4.2 mmHg direct recording, p=0.02). The left kidney contained 48% SP compared to the right kidney (p=0.04). These data suggest that increased afferent renal nerve activity contributes to the elevation in AP in hypertension and contributes to essential hypertension in humans. Supported by USPHS DA017371.

scholarly journals Renal medullary ETB receptors produce diuresis and natriuresis via NOS1

2008 ◽  
Vol 294 (5) ◽  
pp. F1205-F1211 ◽  
Author(s):  
Daisuke Nakano ◽  
Jennifer S. Pollock ◽  
David M. Pollock
Keyword(s):  
Renal Medulla ◽  
Urinary Sodium Excretion ◽  
Receptor Activation ◽  
No Production ◽  
Sprague Dawley ◽  
Receptor Stimulation ◽  
Water Excretion ◽  
Sprague Dawley Rats

Endothelin-1 (ET-1) plays an important role in the regulation of salt and water excretion in the kidney. Considerable in vitro evidence suggests that the renal medullary ETB receptor mediates ET-1-induced inhibition of electrolyte reabsorption by stimulating nitric oxide (NO) production. The present study was conducted to test the hypothesis that NO synthase 1 (NOS1) and protein kinase G (PKG) mediate the diuretic and natriuretic effects of ETB receptor stimulation in vivo. Infusion of the ETB receptor agonist sarafotoxin S6c (S6c: 0.45 μg·kg−1·h−1) in the renal medulla of anesthetized, male Sprague-Dawley rats markedly increased the urine flow (UV) and urinary sodium excretion (UNaV) by 67 and 120%, respectively. This was associated with an increase in medullary cGMP content but did not affect blood pressure. In addition, S6c-induced diuretic and natriuretic responses were absent in ETB receptor-deficient rats. Coinfusion of NG-propyl-l-arginine (10 μg·kg−1·h−1), a selective NOS1 inhibitor, suppressed S6c-induced increases in UV, UNaV, and medullary cGMP concentrations. Rp-8-Br-PET-cGMPS (10 μg·kg−1·h−1) or RQIKIWFQNRRMKWKK-LRK5H-amide (18 μg·kg−1·h−1), a PKG inhibitor, also inhibited S6c-induced increases in UV and UNaV. These results demonstrate that renal medullary ETB receptor activation induces diuretic and natriuretic responses through a NOS1, cGMP, and PKG pathway.

Contrasting effects of vasopressin on baroreflex inhibition of lumbar sympathetic nerve activity

1985 ◽  
Vol 249 (5) ◽  
pp. H922-H928 ◽  
Author(s):  
F. M. Sharabi ◽  
G. B. Guo ◽  
F. M. Abboud ◽  
M. D. Thames ◽  
P. G. Schmid
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Urinary Osmolality ◽  
Arterial Baroreceptors ◽  
Sprague Dawley Rats ◽  
The Difference ◽  
High Level

Baroreflex inhibition of lumbar sympathetic nerve activity (LSNA) during intravenous infusions of phenylephrine and vasopressin is contrasted in rats and rabbits. In rabbits, vasopressin caused smaller increases in arterial pressure and greater inhibition of LSNA than phenylephrine. In Sprague-Dawley rats, however, both vasopressin and phenylephrine caused equivalent increases in arterial pressure and reflex reductions in LSNA. The inhibition of LSNA was mediated through the arterial baroreceptors in both species because it was abolished by sinoaortic denervation. In rats, the possibility that a high level of endogenous vasopressin may have prevented the demonstration of a facilitated baroreflex with the infusion of exogenous vasopressin is unlikely since vasopressin also did not facilitate the reflex in Brattleboro rats, which lack circulating vasopressin. Further, Sprague-Dawley rats were responsive to exogenous vasopressin since infusion of increasing doses of vasopressin caused significant increases in urinary osmolality as well as progressive increments in arterial pressure. The results indicate that intravenous vasopressin given for a period of 6 min facilitates the reflex inhibition of LSNA mediated through arterial baroreceptors in rabbits, but not in rats. Vasopressin given for a period of up to 45 min to rats also fails to facilitate baroreflexes, emphasizing the difference from rabbits. In rabbits, this facilitation appears to involve a central mechanism.

scholarly journals Increased angiotensinogen expression, urinary angiotensinogen excretion, and tissue injury in nonclipped kidneys of two-kidney, one-clip hypertensive rats

2016 ◽  
Vol 311 (2) ◽  
pp. F278-F290 ◽  
Author(s):  
Weijian Shao ◽  
Kayoko Miyata ◽  
Akemi Katsurada ◽  
Ryousuke Satou ◽  
Dale M. Seth ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Sodium Excretion ◽  
Cellular Proliferation ◽  
Immune Cell ◽  
Tissue Injury ◽  
Renal Plasma Flow ◽  
Systolic Arterial Pressure ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Hypertensive Rats

In angiotensin II (ANG II)-dependent hypertension, there is an angiotensin type 1 receptor-dependent amplification mechanism enhancing intrarenal angiotensinogen (AGT) formation and secretion in the tubular fluid. To evaluate the role of increased arterial pressure, AGT mRNA, protein expression, and urinary AGT (uAGT) excretion and tissue injury were assessed in both kidneys of two-kidney, one-clip Sprague-Dawley hypertensive rats subjected to left renal arterial clipping (0.25-mm gap). By 18–21 days, systolic arterial pressure increased to 180 ± 3 mmHg, and uAGT increased. Water intake, body weights, 24-h urine volumes, and sodium excretion were similar. In separate measurements of renal function in anesthetized rats, renal plasma flow and glomerular filtration rate were similar in clipped and nonclipped kidneys and not different from those in sham rats, indicating that the perfusion pressure to the clipped kidneys remained within the autoregulatory range. The nonclipped kidneys exhibited increased urine flow and sodium excretion. The uAGT excretion was significantly greater in nonclipped kidneys compared with clipped and sham kidneys. AGT mRNA was 2.15-fold greater in the nonclipped kidneys compared with sham (1.0 ± 0.1) or clipped (0.98 ± 0.15) kidneys. AGT protein levels were also greater in the nonclipped kidneys. The nonclipped kidneys exhibited greater glomerular expansion and immune cell infiltration, medullary fibrosis, and cellular proliferation than the clipped kidneys. Because both kidneys have elevated ANG II levels, the greater tissue injury in the nonclipped kidneys indicates that an increased arterial pressure synergizes with increased intrarenal ANG II to stimulate AGT production and exert greater renal injury.

Adrenalectomy eliminates both fiber-type differences and starvation effects on denervated muscle

1988 ◽  
Vol 255 (6) ◽  
pp. E850-E856 ◽  
Author(s):  
R. R. Almon ◽  
D. C. Dubois
Keyword(s):  
Muscle Mass ◽  
Extensor Digitorum Longus ◽  
Fiber Type ◽  
Sprague Dawley ◽  
Denervated Muscle ◽  
Adrenalectomized Animal ◽  
Sprague Dawley Rats ◽  
Starvation Effects ◽  
The Difference ◽  
Denervated Muscles

This report describes changes in muscle mass of innervated and denervated pairs of muscles taken from intact and adrenalectomized 250-g male Sprague-Dawley rats provided with different diets. Diets ranged from a nutritionally complete liquid diet to starvation (water only). In the intact animals, muscles with a more tonic character (soleus) are less sensitive to starvation than are muscles with a more phasic character (extensor digitorum longus), whereas the opposite is true of denervation. In the intact animals, starvation greatly increased the amount of atrophy following denervation. In the adrenalectomized animals, starvation had no effect on the amounts of atrophy following denervation. Furthermore, adrenalectomy virtually eliminated the fiber-type differences in the amount of atrophy following denervation. In addition, a comparison between denervated muscles from intact animals and adrenalectomized animals subjected to starvation demonstrates that all denervated muscles from the adrenalectomized animals atrophy less. Finally, it was observed that although an adrenalectomized animal can tolerate 6 days of starvation, an adrenalectomized-castrated animal cannot tolerate even short periods of starvation. The difference appears to be due to low amounts of corticosterone of testicular origin.

scholarly journals Further evidence against the role renal medullary perfusion in short-term control of arterial pressure in normotensive and mildly or overtly hypertensive rats

2021 ◽  
Vol 473 (4) ◽  
pp. 623-631
Author(s):  
Bożena Bądzyńska ◽  
Iwona Baranowska ◽  
Janusz Sadowski
Keyword(s):  
Arterial Pressure ◽  
Renal Excretion ◽  
Sodium Concentration ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Critical Determinant ◽  
Human Hypertension ◽  
Pressure Elevation ◽  
Doppler Probe ◽  
Medullary Tissue

AbstractEarlier evidence from studies of rat hypertension models undermines the widespread view that the rate of renal medullary blood flow (MBF) is critical in control of arterial pressure (MAP). Here, we examined the role of MBF in rats that were normotensive, with modest short-lasting pressure elevation, or with overt established hypertension. The groups studied were anaesthetised Sprague-Dawley rats: (1) normotensive, (2) with acute i.v. norepinephrine-induced MAP elevation, and (3) with hypertension induced by unilateral nephrectomy followed by administration of deoxycorticosterone-acetate (DOCA) and 1% NaCl drinking fluid for 3 weeks. MBF was measured (laser-Doppler probe) and selectively increased using 4-h renal medullary infusion of bradykinin. MAP, renal excretion parameters and post-experiment medullary tissue osmolality and sodium concentration were determined. In the three experimental groups, baseline MAP was 117, 151 and 171 mmHg, respectively. Intramedullary bradykinin increased MBF by 45%, 65% and 70%, respectively, but this was not associated with a change in MAP. In normotensive rats a significant decrease in medullary tissue sodium was seen. The intramedullary bradykinin specifically increased renal excretion of water, sodium and total solutes in norepinephrine-treated rats but not in the two other groups. As previously shown in models of rat hypertension, in the normotensive rats and those with acute mild pressure elevation (resembling labile borderline human hypertension), 4-h renal medullary hyperperfusion failed to decrease MAP. Nor did it decrease in DOCA-salt model mimicking low-renin human hypertension. Evidently, within the 4-h observation, medullary perfusion was not a critical determinant of MAP in normotensive and hypertensive rats.

scholarly journals Renal haemodynamic and tubular actions of urotensin II in the rat

2008 ◽  
Vol 198 (3) ◽  
pp. 617-624 ◽  
Author(s):  
Alaa E S Abdel-Razik ◽  
Ellen J Forty ◽  
Richard J Balment ◽  
Nick Ashton
Keyword(s):  
Body Weight ◽  
Renal Medulla ◽  
Fractional Excretion ◽  
Haemodynamic Effects ◽  
Urotensin Ii ◽  
Sprague Dawley ◽  
Minimal Impact ◽  
Sprague Dawley Rats ◽  
Fractional Excretion Of Sodium ◽  
Excretion Rates

Urotensin II (UTS) is a potent vasoactive peptide that was originally identified in teleost fish. Mammalian orthologues of UTS and its receptor (UTSR) have been described in several species, including humans and rats. We have shown previously that bolus injections of UTS caused a decrease in urine flow and sodium excretion rates in parallel with marked reductions in renal blood flow (RBF) and glomerular filtration rate (GFR). The aim of this study was to determine the effect of UTS infusion at a dose that has minimal impact upon renal haemodynamics in order to identify a potential direct tubular action of UTS. Infusion of rat UTS (rUTS) at 0.6 pmol/min per 100 g body weight in male Sprague–Dawley rats, which had no effect on RBF and caused a 30% reduction in GFR, resulted in a significant increase in the fractional excretion of sodium (vehicle 2.3±0.6 versus rUTS 0.6 pmol 4.5±0.6%, P<0.05) and potassium. At the higher dose of 6 pmol/min per 100 g body weight, haemodynamic effects dominated the response. rUTS induced a marked reduction in RBF and GFR (vehicle 1.03±0.06 versus rUTS 6 pmol 0.31±0.05 ml/min per 100 g body weight, P<0.05) resulting in an anti-diuresis and anti-natriuresis, but no change in fractional excretion of sodium or potassium. Uts2d and Uts2r mRNA expression were greater in the renal medulla compared with the cortex. Together, these data support an inhibitory action of Uts2d on renal tubule sodium and potassium reabsorption in the rat, in addition to its previously described renal haemodynamic effects.

scholarly journals Inhibition of microRNA-429 in the renal medulla increased salt sensitivity of blood pressure in Sprague Dawley rats

2017 ◽  
Vol 35 (9) ◽  
pp. 1872-1880 ◽  
Author(s):  
Qing Zhu ◽  
Junping Hu ◽  
Lei Wang ◽  
Weili Wang ◽  
Zhengchao Wang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Medulla ◽  
Salt Sensitivity ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

scholarly journals Diagnosis of sialodacryoadenitis virus infection of rats in a virulent enzootic outbreak

1981 ◽  
Vol 15 (4) ◽  
pp. 339-342 ◽  
Author(s):  
P. Carthew ◽  
R. P. Slinger
Keyword(s):  
Virus Infection ◽  
Antibody Response ◽  
Clinical Signs ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Natural Conditions ◽  
Breeding Colony ◽  
Serological Screening ◽  
Sprague Dawley Rats ◽  
Natural Outbreak

In a natural outbreak of sialodacryoadenitis virus it was observed that the incidence of clinical signs in spontaneous-hypertensive rats was 100%, and that these signs were of a severity not observed before in other strains of rats. Rats free of the virus were introduced so that the progress of the disease could be studied under natural conditions of spontaneous spread from the enzootically-affected breeding colony. The pathogenesis of the infection in these Sprague-Dawley rats has been recorded over a period of 10 days after their introduction to the colony, and the results of extensive serological screening have shown that the antibody response of the spontaneous-hypertensive rats to the virus is lower than in other strains of rat.

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