Effects of naloxone on renin and pressor responses to acute renal hypotension in rats.

1990 ◽  
Vol 259 (3) ◽  
pp. E432
Author(s):  
C J Weaver ◽  
M D Johnson
Keyword(s):  
Arterial Pressure ◽  
Abdominal Aorta ◽  
Pressor Response ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Opiate Antagonist ◽  
Sprague Dawley ◽  
Aortic Constriction ◽  
Sprague Dawley Rats ◽  
Pressor Responses

Reduction of renal perfusion is followed by increases in plasma renin activity (PRA) and arterial pressure. The present experiments were designed to determine if an opiate antagonist would alter pressor or renin responses to acute reduction of renal arterial pressure (RAP) in anesthetized rats. Male Sprague-Dawley rats were anesthetized with Inactin, and an adjustable constrictor device was placed around the abdominal aorta proximal to the renal arteries. One-half of the animals were pretreated with the opiate antagonist naloxone (2 mg/kg iv), and the other one-half were pretreated with saline vehicle. The abdominal aorta was then constricted to reduce RAP by 25% (measured as femoral arterial pressure) in one-half of the animals in each pretreatment group. Compared with vehicle pretreatment, naloxone pretreatment did not alter the PRA response to aortic constriction; however, naloxone did attenuate the pressor response. We conclude that 1) the PRA response to acute reduction of renal arterial pressure is not dependent on an opiate mechanism in the rat, and 2) attenuation of the pressor response to aortic constriction by naloxone in intact rats is not secondary to a suppression of the PRA response.

Area postrema: essential for support of arterial pressure after hemorrhage in rats

1990 ◽  
Vol 258 (6) ◽  
pp. R1472-R1478 ◽  
Author(s):  
K. M. Skoog ◽  
M. L. Blair ◽  
C. D. Sladek ◽  
W. M. Williams ◽  
M. L. Mangiapane
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Data Acquisition ◽  
Area Postrema ◽  
Plasma Renin ◽  
Base Line ◽  
Sprague Dawley ◽  
Time Period ◽  
Sprague Dawley Rats

Previous studies have indicated that the area postrema (AP) of the rat is necessary for the development of chronic angiotensin-dependent hypertension. The present study assesses the role of the AP in the maintenance of arterial pressure during hemorrhage. Sprague-Dawley rats were given sham or AP lesions 1 wk before the experiment. They were instrumented with femoral arterial and venous catheters 2 days before the experiment. On the day of the experiment, base-line mean arterial pressure (MAP) was measured for 1 h before hemorrhage. During the following 45 min, each rat was subjected to one 7-ml/kg hemorrhage every 15 min for a total of three hemorrhages. MAP was monitored by computerized data acquisition. As shown previously, MAP was slightly but significantly lower in AP-lesion rats compared with sham-lesion rats before the hemorrhage procedure. In AP-lesion rats, hemorrhage resulted in a significantly greater fall in arterial pressure than in sham-lesion rats. In spite of larger drops in pressure in AP-lesion rats, hemorrhage caused equivalent increases in plasma renin and vasopressin in both groups. In AP-lesion rats compared with sham-lesion rats, significant bradycardia was present before hemorrhage. Hemorrhage caused bradycardia in both sham- and AP-lesion rats relative to the prehemorrhage heart rates, but AP-lesion rats showed greater bradycardia than did sham-lesion rats during every time period. We conclude that the AP may play an important role in the defense of arterial pressure against hemorrhage.

Angiotensin II-mediated catecholamine release during the pressor response in rats

1994 ◽  
Vol 142 (1) ◽  
pp. 19-28 ◽  
Author(s):  
D G Butler ◽  
D A Butt ◽  
D Puskas ◽  
G Y Oudit
Keyword(s):  
Angiotensin Ii ◽  
Pressor Response ◽  
Plasma Renin ◽  
Sympathetic Nerves ◽  
Catecholamine Release ◽  
Plasma Catecholamine ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Pressor Responses ◽  
Plasma Catecholamine Concentrations

Abstract Angiotensin II (ANG II)-mediated catecholamine release and its possible contribution to the pressor response was assessed in baroreceptor-denervated rats. Neonatal male Sprague-Dawley rats were injected with the sympatholytic drug, guanethidine monosulphate (50 mg/kg s.c., 6 days/week) for 40 days. Plasma catecholamine concentrations were measured using a 3H-radioenzymatic assay as follows: (a) before and 30 s after the injection of saline or ANG II (79·3 pmol/kg i.v.), at the peak of the pressor response, then 50 s and 80 s thereafter, in guanethidine-treated (GUAN) and saline-injected (SHAM) rats, and (b) before and after adrenalectomy (ADX), following the same time-sequence for ANG II as in (a). Peak pressor responses to graded doses of ANG II (6·6, 26·4, 53·0 and 79·3 pmol/kg i.v.) were measured in GUAN+ADX and ADX rats. Destruction of peripheral sympathetic nerves was confirmed by measurements of plasma noradrenaline (NA), adrenaline (AD) and dopamine (DA) concentrations and by changes in pressor responses and heart rates following i.v. doses of tyramine. ANG II induced significantly (P<0·05) greater pressor responses in GUAN+ADX rats than in ADX rats, especially after the 53·0 and 79·3 pmol/kg doses. Plasma AD concentrations increased within seconds after the pressor response to ANG II in both GUAN and SHAM rats but there was no change in plasma NA or DA concentrations (P<0·05). ANG-II-mediated AD release from the adrenal medulla may contribute to the overall pressor action of the peptide. The vasculature became more sensitive to ANG II at a time when NA and DA depletion occurred following sympathectomy and/or adrenalectomy. This heightened sensitivity to ANG II was not due to a decrease in circulating ANG II in sympathectomized rats because even though plasma renin activity fell from 6·54 ±0·52 to 3·77 ±0·26 ng ANG I/ml per h it remained within the normal range. Journal of Endocrinology (1994) 142, 19–28

scholarly journals Bilateral renal cryodenervation decreases arterial pressure and improves insulin sensitivity in fructose-fed Sprague-Dawley rats

2018 ◽  
Vol 315 (3) ◽  
pp. R529-R538 ◽  
Author(s):  
Tyler Soncrant ◽  
Dragana Komnenov ◽  
William H. Beierwaltes ◽  
Haiping Chen ◽  
Min Wu ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Arterial Pressure ◽  
Plasma Renin ◽  
Sprague Dawley ◽  
High Salt Diet ◽  
Glucose Levels ◽  
Fructose Intake ◽  
Blood Glucose Levels ◽  
Sprague Dawley Rats ◽  
High Fructose

Consumption of food high in fructose is prevalent in modern diets. One week of moderately high fructose intake combined with high salt diet has been shown to increase blood pressure and failed to suppress plasma renin activity (PRA). We tested the hypothesis that the hypertension and high PRA are consequences of elevated renal sympathetic nerve activity (RSNA). In protocol 1, we assessed RSNA by telemetry in conscious Sprague-Dawley rats given 20% fructose or 20% glucose in drinking water on a 0.4% NaCl diet (NS) for 1 wk and then transitioned to a 4% NaCl diet (HS). After an additional week, mean arterial pressure (MAP) and RSNA increased significantly in fructose-fed but not glucose-fed HS rats. In protocol 2, fructose (Fruc)- or glucose (Glu)-fed rats on NS or HS diet for 3 wk underwent sham denervation (shamDNX) or bilateral renal denervation using cryoablation (cryoDNX). MAP was higher in Fruc-HS rats compared with Glu-NS, Glu-HS, or Fruc-NS rats and decreased after cryoDNX ( P < 0.01). MAP did not change in Fruc-HS shamDNX rats. Renal norepinephrine content decreased by 85% in cryoDNX ( P < 0.01 vs. shamDNX). PRA significantly decreased after cryoDNX in both Fruc-NS and Fruc-HS rats. Nonfasting blood glucose levels were similar among the four groups. Glucose-to-insulin ratio significantly increased in Fruc-HS cryoDNX rats, consistent with greater insulin sensitivity. Taken together, these studies show that renal sympathoexcitation is, at least in part, responsible for salt-dependent increases in MAP, increased PRA, and decreased insulin sensitivity in rats fed a moderately high fructose diet for as little as 3 wk.

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.

scholarly journals Chronic renal artery insulin infusion increases mean arterial pressure in male Sprague-Dawley rats

2018 ◽  
Vol 314 (1) ◽  
pp. F81-F88 ◽  
Author(s):  
Debra L. Irsik ◽  
Jian-Kang Chen ◽  
Michael W. Brands
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Artery ◽  
Insulin Infusion ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Experimental Models ◽  
Sprague Dawley ◽  
Novel Approach ◽  
Sprague Dawley Rats

Hyperinsulinemia has been hypothesized to cause hypertension in obesity, type 2 diabetes, and metabolic syndrome through a renal mechanism. However, it has been challenging to isolate renal mechanisms in chronic experimental models due, in part, to technical difficulties. In this study, we tested the hypothesis that a renal mechanism underlies insulin hypertension. We developed a novel technique to permit continuous insulin infusion through the renal artery in conscious rats for 7 days. Mean arterial pressure increased by ~10 mmHg in rats that were infused intravenously (IV) with insulin and glucose. Renal artery doses were 20% of the intravenous doses and did not raise systemic insulin levels or cause differences in blood glucose. The increase in blood pressure was not different from the IV group. Mean arterial pressure did not change in vehicle-infused rats, and there were no differences in renal injury scoring due to the renal artery catheter. Glomerular filtration rate, plasma renin activity, and urinary sodium excretion did not differ between groups at baseline and did not change significantly with insulin infusion. Thus, by developing a novel approach for chronic, continuous renal artery insulin infusion, we provided new evidence that insulin causes hypertension in rats through actions initiated within the kidney.

mu-Opioid receptors in NTS elicit pressor responses via sympathetic pathways

1987 ◽  
Vol 252 (1) ◽  
pp. H156-H162 ◽  
Author(s):  
A. H. Hassen ◽  
G. Feuerstein
Keyword(s):  
Pressor Response ◽  
Cardiovascular Responses ◽  
Receptor Activation ◽  
Sprague Dawley ◽  
Baroreflex Function ◽  
Sprague Dawley Rats ◽  
Pressor Responses ◽  
Adrenergic Antagonist ◽  
Atropine Methyl Nitrate ◽  
Mu Receptors

We have evaluated the relative contributions of the sympathetic and parasympathetic nervous systems to the increased mean arterial pressure (MAP) and heart rate (HR) elicited by the selective mu-agonist D-Ala2, MePhe4, Gly-ol5 enkephalin (DAGO) following microinjection (100 nl) into the nucleus of tractus solitarius (NTS) of anesthetized, artificially ventilated Sprague-Dawley rats. The effects of anesthesia and central opioid-receptor activation on baroreflex function were also examined. All cardiovascular responses elicited by DAGO were eliminated by complete C1 spinal transection. Pretreatment with the alpha-adrenergic antagonist phentolamine attenuated the increase in MAP, but not the tachycardia; the beta-blocker propranolol abolished the tachycardia but not the pressor response to DAGO. Adrenalectomy, vagotomy, or pretreatment with atropine methyl nitrate were all without effect. Baroreflexes were attenuated in animals anesthetized with pentobarbital sodium, but were present in urethan-anesthetized rats. DAGO attenuated the increases in MAP and HR elicited following carotid occlusion, but not the bradycardia elicited by a phenylephrine-induced pressor response. These data indicate that mu-receptors in the NTS elicit cardiovascular responses that are mediated by increased sympathetic nerve activity, and accompanied by selective attenuation of baroreflex function.

Glucocorticoids potentiate central actions of angiotensin to increase arterial pressure

2001 ◽  
Vol 280 (6) ◽  
pp. R1719-R1726 ◽  
Author(s):  
Deborah A. Scheuer ◽  
Andrea G. Bechtold
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Guide Cannula ◽  
Intravenous Injections ◽  
Sprague Dawley Rats ◽  
And Control

Experiments were performed to determine if glucocorticoids potentiate central hypertensive actions of ANG II. Male Sprague-Dawley rats were treated for 3 days to 3 wk with corticosterone (Cort). Experiments were performed in conscious rats that had previously been instrumented with arterial and venous catheters and an intracerebroventricular guide cannula in a lateral ventricle. Baseline arterial pressure (AP) was greater in Cort-treated rats than in control rats (119 ± 2 vs. 107 ± 1 mmHg, P < 0.01). Microinjection of ANG II intracerebroventricularly produced a significantly larger increase in AP in Cort-treated rats than in control rats. For example, at 30 ng ANG II, AP increased by 23 ± 1 and 16 ± 2 mmHg in Cort-treated and control rats, respectively ( P < 0.01). Microinjection of an angiotensin type 1 receptor antagonist significantly decreased AP (−6 ± 2 mmHg) and heart rate (−26 ± 7 beats/min) in Cort-treated but not control rats. Increases in AP produced by intravenous administration of ANG II were not different between control and Cort-treated rats. Intravenous injections of ANG II antagonist had no significant effects on mean AP or heart rate in control or Cort-treated rats. Therefore, a sustained increase in plasma Cort augments the central pressor effects of ANG II without altering the pressor response to peripheral administration of the hormone.

Effect of electroacupuncture on pressor reflex during gastric distension

2002 ◽  
Vol 283 (6) ◽  
pp. R1335-R1345 ◽  
Author(s):  
Peng Li ◽  
Kasra Rowshan ◽  
Melissa Crisostomo ◽  
Stephanie C. Tjen-A-Looi ◽  
John C. Longhurst
Keyword(s):  
Peroneal Nerve ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Gastric Wall ◽  
Ventrolateral Medulla ◽  
Gastric Distension ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Stomach Meridian ◽  
Pressor Reflex

The effect of electroacupuncture (EA) on the reflex cardiovascular response induced by mechanical distension of the stomach was studied in ventilated male Sprague-Dawley rats anesthetized by ketamine and α-chloralose. Repeated balloon inflation of the stomach to produce 20 mmHg tension on the gastric wall induced a consistent rise in mean arterial pressure, while heart rate (372 ± 22 beats/min) was unchanged. This response was reversed by transection of the splanchnic nerves. Bilateral application of EA (1–2 mA, 2 Hz) at Neiguan-Jianshi acupoints (pericardial meridian, Pe 5–6) over the median nerve for 30 min significantly decreased the pressor response from 33 ± 6 to 18 ± 4 mmHg ( n = 7, P < 0.05). This effect began after 10 min of EA and continued for 40 min after termination of EA. EA at Zusanli-Shangquxu acupoints (stomach meridian, St 36–37) over the deep peroneal nerve similarly inhibited the pressor response. The effect lasted for 10 min after EA was stopped ( n = 6, P < 0.05), while EA at Guangming-Xuanzhong acupoints (gallbladder meridian, GB 37–39) over the superficial peroneal nerve did not inhibit the pressor response. Naloxone injected intravenously ( n = 6) immediately after termination of EA or administered by microinjection into the rostral ventrolateral medulla (rVLM) 25 min after initiation of EA ( n = 6) reversed the inhibition by EA, suggesting an opiate mechanism, including the rVLM, was involved.

Importance of chloride for the correction of chronic metabolic alkalosis in the rat

1987 ◽  
Vol 253 (5) ◽  
pp. F1031-F1039 ◽  
Author(s):  
B. M. Wall ◽  
G. V. Byrum ◽  
J. H. Galla ◽  
R. G. Luke
Keyword(s):  
Plasma Volume ◽  
Metabolic Alkalosis ◽  
Choline Chloride ◽  
Plasma Renin ◽  
Sodium Balance ◽  
Sprague Dawley ◽  
Volume Contraction ◽  
Chloride Depletion ◽  
Sprague Dawley Rats ◽  
Sodium And Potassium

To determine whether chloride repletion without sodium could correct chronic chloride depletion metabolic alkalosis (CDA) in Sprague-Dawley rats without volume expansion and without increasing glomerular filtration rate (GFR), CDA was generated by peritoneal dialysis (PD) against 0.15 M NaHCO3 and maintained for 7-10 days by a chloride-restricted diet supplemented with sodium and potassium salts. Control animals were dialyzed against Ringer bicarbonate. The maintenance period of chronic CDA, compared with control, was characterized by hypokalemic metabolic alkalosis (serum TCO2 31.9 +/- 0.6 vs. 23.1 +/- 0.5 meq/l, P less than 0.05), volume contraction (plasma volume 3.76 +/- 0.08 vs. 4.19 +/- 0.22 ml/100 g body wt, P less than 0.05), decreased GFR (838 +/- 84 vs. 1045 +/- 45 microliters.min-1.100 g body wt-1, P less than 0.05), increased plasma renin activity (PRA) (63 +/- 13 vs. 12 +/- 3 ng.ml-1.h-1, P less than 0.05), but unchanged plasma aldosterone concentrations (PAC) (4.1 +/- 1.0 vs. 3.4 +/- 1.6 ng/dl, P = NS). Complete correction of chronic CDA was accomplished by 24 h of ingestion of choline chloride drink, and despite negative sodium balance, neutral potassium balance, continued bicarbonate ingestion, and persistent volume contraction (plasma volume 3.76 +/- 0.08 vs. 3.73 +/- 0.12 ml/100 g body wt pre- and postcorrection, P = NS), GFR remained decreased (659 +/- 87 vs. 1,045 +/- 45 microliters.min-1.100 g body wt-1, P less than 0.05), PRA decreased (63 +/- 13 vs. 33 +/- 5 ng.ml-1.h-1, P less than 0.05), but PAC did not change (4.1 +/- 1.0 vs. 6.1 +/- 1.6 ng/dl, P = NS) after correction of CDA.(ABSTRACT TRUNCATED AT 250 WORDS)

High-NaCl diets increase natriuretic and diuretic responses in salt-resistant but not salt-sensitive SHR

1991 ◽  
Vol 260 (6) ◽  
pp. F890-F897 ◽  
Author(s):  
M. S. Mozaffari ◽  
S. Jirakulsomchok ◽  
Z. H. Shao ◽  
J. M. Wyss
Keyword(s):  
Arterial Pressure ◽  
Renal Denervation ◽  
Isotonic Saline ◽  
Renal Nerves ◽  
Sprague Dawley ◽  
Volume Loading ◽  
Spontaneously Hypertensive ◽  
Volume Load ◽  
Sprague Dawley Rats ◽  
Wistar Kyoto

This study tested the hypothesis that NaCl-sensitive spontaneously hypertensive rats (SHR-S) display a defect in natriuretic and diuretic responses to acute volume loading that contributes to the rise in arterial pressure observed when the rats are fed a high-NaCl diet. Seven-week-old SHR-S and NaCl-resistant SHR rats (SHR-R) and normotensive (Wistar-Kyoto and Sprague-Dawley rats) were fed high- or basal NaCl diets. After 2.5 wk on the diets, preinstrumented conscious rats received an intravenous infusion (5% body wt; 0.5 ml/min) of isotonic saline, and urine was collected through a bladder catheter for 90 min. Control rats on the high-NaCl diet (compared with basal) excreted a significantly greater percentage of Na+ and volume load. In contrast, SHR-S on high-NaCl diet (compared with basal) had a very small increase in natriuretic response and no increase in diuretic response to volume expansion. The effect of renal denervation on natriuretic and diuretic responses to volume load was tested. In SHR-R on 1 and 8% NaCl diets, renal denervation had little or no effect on these responses, suggesting that renal nerves do not play a prominent role in the dietary NaCl-induced increases in the natriuretic and diuretic responses to volume load. These results demonstrate that NaCl-resistant rats rapidly adapt to diets high in NaCl content with increased natriuretic and diuretic responses to acute volume loading. The failure of SHR-S to adapt to the dietary challenge may result in volume loading and a secondary increase in arterial pressure after feeding.

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