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.

Decreased hexokinase activity in paraventricular nucleus of adult SHR and renal hypertensive rats

1988 ◽  
Vol 254 (3) ◽  
pp. R508-R512 ◽  
Author(s):  
T. L. Krukoff
Keyword(s):  
Arterial Pressure ◽  
Paraventricular Nucleus ◽  
Metabolic Activity ◽  
Central Nucleus ◽  
Hypothalamic Nucleus ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Medial Nucleus ◽  
Wistar Kyoto ◽  
Renal Hypertensive Rats

Metabolic activity was assessed in the brains of spontaneously hypertensive rats (SHR) using the histochemical hexokinase (HK) technique and photodensitometric analysis. Of eight regions known to play a role in cardiovascular regulation, only the paraventricular nucleus of the hypothalamus (PVH) exhibited alterations in HK activity. Significantly lower levels of HK activity in SHR than in control Sprague-Dawley and Wistar-Kyoto rats were measured in both the parvo- and magnocellular divisions of the PVH. No differences in HK activity were found in the anterior hypothalamic nucleus, posterior hypothalamic nucleus, supraoptic nucleus, subfornical organ, central nucleus of the amygdala, or the medial nucleus of the tractus solitarius of SHR. Similar results were obtained in renal hypertensive rats; furthermore, a positive correlation was found between levels of arterial pressure and densitometric readings. These latter results strongly suggest that metabolic alterations in the PVH of SHR are directly related to the increases in arterial pressure and are not due to the genetic makeup of SHR. In light of studies by others, the data from the present study have been interpreted to suggest that the decreases in metabolic activity in the PVH of the adult SHR are the result of a central attempt to bring the level of the arterial pressure down to normal levels and not to the altered activity of a region that might be acting to keep arterial pressure elevated.

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 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.

Inhibition of nitric oxide causes exaggerated natriuresis in spontaneously hypertensive rats

1994 ◽  
Vol 266 (5) ◽  
pp. F762-F766 ◽  
Author(s):  
A. A. Khraibi
Keyword(s):  
Nitric Oxide ◽  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Competitive Inhibition ◽  
High Dose ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Fractional Excretion Of Sodium

Competitive inhibition of the conversion of L-arginine to nitric oxide by a high dose of NG-monomethyl-L-arginine (L-NMMA) leads to significant increases in arterial pressure, natriuresis, and diuresis in Sprague-Dawley rats. The purpose of this study was to determine the extent of the natriuretic and diuretic responses and the possible role of arterial pressure and renal interstitial hydrostatic pressure (RIHP) elevations with the infusion of L-NMMA in anesthetized spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Intravenous infusion of L-NMMA (15 mg/kg bolus followed by 500 micrograms.kg-1.min-1 continuous infusion) in WKY rats (n = 8) resulted in a significant increase in mean arterial pressure (MAP, 122 +/- 3 to 152 +/- 2 mmHg), RIHP (4.7 +/- 0.4 to 6.7 +/- 0.5 mmHg), fractional excretion of sodium (FENa, 0.76 +/- 0.21 to 4.74 +/- 0.70%), and urine flow rate (V, 27.7 +/- 5.0 to 161.3 +/- 19.6 microliters/min). Increases in RIHP and sodium and water excretions are abolished when renal perfusion pressure is prevented from increasing with L-NMMA infusion in a group of WKY rats (n = 6). In SHR (n = 6) administration of the same dose of L-NMMA resulted in no significant changes in MAP (172 +/- 3 to 178 +/- 2 mmHg) or RIHP (3.3 +/- 0.4 to 3.5 +/- 0.6 mmHg), but significantly higher increases in FENa (1.19 +/- 0.26 to 7.52 +/- 0.68%) and V (47.1 +/- 10.0 to 248.3 +/- 25.7 microliters/min) compared with WKY rat.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

GABA-A Function and Receptor Binding in the Paraventricular Nucleus in Chronic Renal Wrap Hypertension

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 701-701
Author(s):  
Joseph R Haywood ◽  
Teresa Craig ◽  
Julie Hensler ◽  
Carmen Hinojosa-Laborde
Keyword(s):  
Arterial Pressure ◽  
Paraventricular Nucleus ◽  
Receptor Binding ◽  
Binding Sites ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Gaba A ◽  
Gaba Binding ◽  
In Vivo Autoradiography

P48 The onset of renal wrap hypertension is associated with a reduced tonic GABA inhibition in the paraventricular nucleus (PVN) on the sympathetic nervous system. This reduced functional inhibition occurs without a change in GABA-A receptor binding in the PVN. The goal of the present study was to determine if GABAergic transmission and GABA binding is altered in chronic renal wrap hypertensive rats. Sprague-Dawley rats were made hypertensive or sham-operated. Four weeks later, animals were prepared with femoral artery catheters for the measurement of arterial pressure. Subgroups were also prepared with bilateral cannulae directed at the PVN. The renal wrap rats had higher mean arterial pressure (MAP): 139±4 mmHg vs.113±2 mmHg, but heart rate (HR) was not different (354±12 bpm vs. 369±6 bpm) as compared to control animals. Administration of the GABA-A antagonist, bicuculline, into the PVN caused a greater increase in MAP and HR in wrap animals (25±2 mmHg and 150±30 bpm) compared to sham operated rats (16±2 mmHg and 89±12 bpm). GABA-A binding sites in the PVN were estimated using in vivo autoradiography. [3H]-Flunitrazepam was used as the receptor ligand. Magnocellular neurons of the PVN showed a higher density of receptors than other areas of the nucleus. However, the number of binding sites was not different between normotensive and hypertensive rats in either the high density (1825±56 vs. 1756±41 fmol/mg protein) or low density (1454±26 vs. 1433±57 fmol/mg protein) regions of PVN. These data indicate that the inhibition by GABA in the PVN is augmented in the chronic stage of hypertension, and appears to be unrelated to a change in the number of GABA binding sites. The increased GABAergic inhibition is in contrast to the reduced inhibition that has been observed during the onset of hypertension.

Circadian rhythm of plasma sodium is disrupted in spontaneously hypertensive rats fed a high-NaCl diet

2000 ◽  
Vol 278 (6) ◽  
pp. R1490-R1495 ◽  
Author(s):  
Zhiwu Fang ◽  
Scott H. Carlson ◽  
Ning Peng ◽  
J. Michael Wyss
Keyword(s):  
Circadian Rhythm ◽  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Plasma Sodium Concentration ◽  
And Control

High-NaCl diets elevate arterial pressure in NaCl-sensitive individuals, and increases in plasma sodium may trigger this effect. The present study tests the hypotheses that 1) plasma sodium displays a circadian rhythm in rats, 2) the plasma sodium rhythm is disturbed in spontaneously hypertensive rats (SHR), and 3) excess dietary NaCl elevates plasma sodium concentration in SHR. The results demonstrate that plasma sodium has a circadian rhythm that is inversely related to the circadian rhythm of arterial pressure. Although the plasma sodium rhythms of SHR and control rats are nearly identical, the plasma sodium concentrations are significantly higher in SHR throughout the 24-h cycle. Maintenance on a high-NaCl diet increases plasma sodium concentration similarly in both SHR and control rats, but it blunts the plasma sodium rhythm only in SHR. These results demonstrate that in rats, plasma sodium has a circadian rhythm and that high-NaCl diets increase plasma sodium concentration.

Rat brainstem neurons responsive to changes in portal blood sodium concentration

1984 ◽  
Vol 247 (5) ◽  
pp. R792-R799 ◽  
Author(s):  
P. J. Kahrilas ◽  
R. C. Rogers
Keyword(s):  
Hypertonic Saline ◽  
Choline Chloride ◽  
Vena Cava ◽  
Sodium Concentration ◽  
Portal Blood ◽  
Solitary Tract ◽  
Sprague Dawley ◽  
Response Characteristics ◽  
Medial Nucleus ◽  
Rat Brainstem

Studies were performed to identify the response characteristics of nucleus of the solitary tract neurons receiving afferent projections from the hepatic branch of the vagus nerve. Thirty Sprague-Dawley rats under pentobarbital anesthesia had catheters placed in the ileocolic vein and the inferior vena cava. Neuronal recordings were made in the left medial nucleus of the solitary tract (NST), in the area where hepatic vagal fibers terminate. Sixteen NST cells were identified that responded selectively to the portal infusion of water or hypertonic saline. Two patterns of response were seen: 1) 12 neurons were persistently stimulated by portal hypertonic saline and persistently inhibited by portal water, and 2) four neurons were either transiently excited (n = 3) or transiently inhibited (n = 1) by portal hypertonic saline with no water effect. All units recorded responded to changes of 1% or less in portal blood sodium concentration. Hypertonic mannitol was an ineffective stimulus but choline chloride was as effective as sodium chloride. This suggests that the hepatic receptors utilize an Na+-K+-ATPase electrogenic pump in the transduction process.

scholarly journals Open-loop analysis on sympathetically mediated arterial pressure and urine output responses in spontaneously hypertensive rats: effect of renal denervation

2021 ◽  
Vol 71 (1) ◽  
Author(s):  
Toru Kawada ◽  
Takuya Nishikawa ◽  
Satoru Suehara ◽  
Satoshi Sawada ◽  
Tetsuo Tanaka ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Urine Output ◽  
Spontaneously Hypertensive Rats ◽  
Renal Denervation ◽  
Sympathetic Innervation ◽  
Urine Flow ◽  
Hypertensive Rats ◽  
Loop Analysis ◽  
Intact Side ◽  
Spontaneously Hypertensive

AbstractPrimary acute sympathetic activation (PASA) causes a subsequent arterial pressure (AP) elevation. In this case, an antidiuretic effect via the renal innervation and pressure diuresis can act antagonistically on the kidneys. We examined the effect of PASA on urine output in spontaneously hypertensive rats (SHR) 4–7 days after unilateral renal denervation (RDN) (n = 9). The slope of the plot of urine flow versus AP was positive (0.120 ± 0.031 μL min−1 kg−1 mmHg−1) on the intact side, but it was less than 1/3 of the slope observed previously in normotensive Wistar–Kyoto rats (WKY). RDN did not normalize the slope of urine flow versus AP (0.179 ± 0.025 μL min−1 kg−1 mmHg−1, P = 0.098 versus the intact side). The urine flow at the operating point of the AP tended to be greater on the denervated than the intact side (29.0 ± 1.8 vs. 25.3 ± 1.9 μL min−1 kg−1, P = 0.055). The percent increase (17.2 ± 7.2%) was not different from that observed previously in WKY. Although high-resting sympathetic nerve activity is prerequisite for maintaining hypertension in SHR, the effect of sympathetic innervation on the urine output function was not greater than that in WKY.

scholarly journals Different blood pressure responses in hypertensive rats following chemerin mRNA inhibition in dietary high fat compared to dietary high-salt conditions

2019 ◽  
Vol 51 (11) ◽  
pp. 553-561 ◽  
Author(s):  
David J. Ferland ◽  
Emma D. Flood ◽  
Hannah Garver ◽  
Steve T. Yeh ◽  
Stanley Riney ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Antisense Oligonucleotides ◽  
Reduce Blood Pressure ◽  
High Salt ◽  
Whole Body ◽  
Sprague Dawley ◽  
High Fat ◽  
Hypertensive Rats ◽  
Blood Pressure Responses ◽  
Antihypertensive Treatments

Chemerin is a contractile adipokine, produced in liver and fat, and removal of the protein by antisense oligonucleotides (ASO) lowers blood pressure in the normal Sprague Dawley rat. In humans, chemerin is positively associated with blood pressure and obesity so we hypothesized that in a model of hypertension derived from high-fat (HF) feeding, the chemerin ASO would reduce blood pressure more than a high-salt (HS) model. Male Dahl S rats were given a HF (60% kcal fat; age 3–24 wk) or HS diet (4% salt; age 20–24 wk to match age and blood pressure of HF animals). Scrambled control, whole body, or liver-specific ASOs that knock down chemerin were delivered subcutaneously once per week for 4 wk with tissue and blood collected 2 days after the last injection. Conscious blood pressure was measured 24 h/day by radiotelemetry. By the end of whole body ASO administration, blood pressure of HF animals had fallen 29 ± 2 mmHg below baseline, while blood pressure of HS-diet animals fell by only 12 ± 4 mmHg below baseline. Administration of a liver-specific ASO to HF Dahl S resulted in a 6 ± 2 mmHg fall in blood pressure below baseline. Successful knockdown of chemerin in both the whole body and liver-specific administration was confirmed by Western and PCR. These results suggest that chemerin, not derived from liver but potentially from adipose tissue, is an important driver of hypertension associated with high fat. This knowledge could lead to the development of antihypertensive treatments specifically targeted to obesity-associated hypertension.

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