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.

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.

Role of vasopressin in blood pressure regulation in conscious water-deprived dogs

1983 ◽  
Vol 244 (1) ◽  
pp. R74-R77 ◽  
Author(s):  
J. Schwartz ◽  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Water Deprivation ◽  
Plasma Renin ◽  
Renin Activity ◽  
Pressure Regulation

The role of vasopressin in the regulation of blood pressure during water deprivation was assessed in conscious dogs with two antagonists of the vasoconstrictor activity of vasopressin. In water-replete dogs, vasopressin blockade caused no significant changes in mean arterial pressure, heart rate, plasma renin activity (PRA), or plasma corticosteroid concentration. In the same dogs following 48-h water deprivation, vasopressin blockade increased heart rate from 85 +/- 6 to 134 +/- 15 beats/min (P less than 0.0001), increased cardiac output from 2.0 +/- 0.1 to 3.1 +/- 0.1 1/min (P less than 0.005), and decreased total peripheral resistance from 46.6 +/- 3.1 to 26.9 +/- 3.1 U (P less than 0.001). Plasma renin activity increased from 12.4 +/- 2.2 to 25.9 +/- 3.4 ng ANG I X ml-1 X 3 h-1 (P less than 0.0001) and plasma corticosteroid concentration increased from 3.2 +/- 0.7 to 4.9 +/- 1.2 micrograms/dl (P less than 0.05). Mean arterial pressure did not change significantly. When the same dogs were again deprived of water and pretreated with the beta-adrenoceptor antagonist propranolol, the heart rate and PRA responses to the antagonists were attenuated and mean arterial pressure decreased from 103 +/- 2 to 91 +/- 3 mmHg (P less than 0.001). These data demonstrate that vasopressin plays an important role in blood pressure regulation during water deprivation in conscious dogs.

Renal memory after potassium adaptation: role of Na+-K+-ATPase

1988 ◽  
Vol 254 (6) ◽  
pp. F845-F850 ◽  
Author(s):  
S. K. Mujais
Keyword(s):  
Atpase Activity ◽  
Time Course ◽  
Base Line ◽  
Sprague Dawley ◽  
Membrane Transport Proteins ◽  
Sprague Dawley Rats ◽  
Potassium Adaptation ◽  
Collecting Tubule ◽  
Cortical Collecting Tubule

The present study was designed to explore the time course of the resolution of enhanced Na+-K+-ATPase activity in the cortical collecting tubule (CCT) and the parallel changes in renal K excretion that are characteristic of potassium adaptation. Potassium-adapted male Sprague-Dawley rats manifested an enhanced kaliuretic response to an acute intravenous load of KCl and a doubling of Na+-K+-ATPase activity in the CCT. Withdrawal of dietary K loading from these adapted rats was associated with a gradual resolution of these adaptive biochemical (t1/2 of Na+-K+-ATPase return to base line 48 h) and excretory changes. During this resolution phase, however, a temporal discrepancy was uncovered between the change in dietary K and the slower changes in enzyme activity and renal K excretion with a persistence of the enhanced kaliuresis leading to a negative K balance. We conclude that the slow inactivation, after withdrawal of K loading, of the increased membrane transport proteins of K adaptation, will manifest as a renal memory of the antecedent excretory requirements.

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

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.

Effect of circulating vasopressin on arterial pressure regulation in rats

1989 ◽  
Vol 257 (1) ◽  
pp. H209-H218 ◽  
Author(s):  
C. M. Pawloski ◽  
N. M. Eicker ◽  
L. M. Ball ◽  
M. L. Mangiapane ◽  
G. D. Fink
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Body Fluid ◽  
Area Postrema ◽  
Sodium Intake ◽  
Blood Levels ◽  
Fluid Composition ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Autonomic Cardiovascular Control

It has been hypothesized that moderately increased blood levels of arginine vasopressin (AVP) contribute to the development and/or maintenance of hypertension. In this study, male Sprague-Dawley rats on a fixed 1 meq daily sodium intake received 10-day intravenous infusions of 0.2 and 2.0 ng.kg-1.min-1 AVP. The higher infusion rate was above the acute vasoconstrictor threshold for AVP administration and also produced a maximal antidiuretic effect. During chronic AVP administration, however, daily mean arterial pressure, heart rate, and body fluid composition were not changed, despite a maintained antidiuresis. To test the hypothesis that circulating AVP failed to cause hypertension as a result of sensitization of the baroreflex or a direct sympathoinhibitory effect of the peptide, additional experiments were performed in rats subjected to sinoaortic denervation (SAD) or ablation of the area postrema (APX). Infusion of AVP for 10 days into SAD or APX rats caused a sustained antidiuresis but did not change arterial pressure, heart rate, or body fluid composition. In all groups of rats, the depressor response to ganglionic blockade (20 mg/kg hexamethonium) was used to estimate the autonomic component of resting arterial pressure; no change in autonomic cardiovascular control was found using this method in any of the groups during AVP infusion. Long-term elevation of plasma AVP in rats, therefore, does not cause hypertension or significantly affect autonomic regulation of arterial pressure.

Abstract P616: Evidence That The Extracellular Domain Of Na + /K + Atpase Is The Receptor For Cyclic Gmp-Induced Natriuresis

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Brandon A Kemp ◽  
John J Gildea ◽  
Nancy L Howell ◽  
Susanna R Keller ◽  
Robert M Carey
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Control Period ◽  
Extracellular Domain ◽  
Sprague Dawley ◽  
Binding Studies ◽  
Urine Sodium ◽  
Sprague Dawley Rats ◽  
Normal Rat ◽  
Change In Mean

Previous studies from our laboratory have shown that extracellular renal interstitial (RI) cyclic guanosine 3’5’-monophosphate (cGMP) increases urine sodium (Na + ) excretion (U Na V) at the renal proximal tubule (RPT) in rats via activation of Src family kinase. Extracellular cGMP engenders this response through an unknown receptor. We hypothesized that cGMP binds to the extracellular domain of Na + /K + -ATPase (NKA) on basolateral membranes of RPT cells inhibiting Na + transport. In the present study, we evaluated the effect of RI infusion of rostafuroxin (RF), a digitoxigenin derivative that specifically displaces oubain (OUA) binding from NKA, on U Na V in the presence of RI cGMP infusion. Volume expanded, uninephrectomized, 12-week-old female Sprague-Dawley rats received RI infusions of vehicle (D 5 W) (N=8), RI cGMP (18, 36, and 72 μg/kg/min; each dose for 30 min; N=10), or RI cGMP + RF (0.012 μg/kg/min; N=5) for 90 min following a 30 min control period with RI infusion of vehicle D 5 W. RI cGMP infusion induced a significant natriuresis from 0.39 ± 0.06 μmol/min to 1.03 ± 0.21 (P<0.05), 1.17 ± 0.19 (P<0.01), and 1.94 ± 0.16 (P<0.001) μmol/min at 18, 36, and 72 μg/kg/min cGMP, respectively. RI co-infusion of cGMP + RF abolished the cGMP-induced natriuresis at all doses (F=16.05, P<0.001). There was no change in mean arterial pressure during any infusion. To further demonstrate that cGMP binds to NKA, we performed a series of competitive binding studies in isolated RPTs from normal rat kidneys (N=4 for each) with bodipy-OUA (2 μM) + cGMP (10 μM) and 8-[Biotin]-AET-cGMP (2 μM) + OUA (10 μM). In the presence of cGMP, bodipy-OUA fluorescence intensity was reduced from 1422.1 ± 63 to 1072.5 ± 64 relative fluorescent units (RFU, P<0.01). In the presence of OUA, 8-[Biotin]-AET-cGMP staining was reduced from 1916.3 ± 144 to 1492.2 ± 84 RFU (P<0.05). Serving as control, biotinylated cAMP (N=2) did not demonstrate any fluorescence above background. Together, these data suggest that cGMP may compete with RF for binding on NKA and that the extracellular domain of NKA may serve as the receptor for cGMP-induced natriuresis.

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.

Role of the vasoconstrictor and antidiuretic activities of vasopressin in inhibition of renin secretion in conscious dogs

1986 ◽  
Vol 250 (1) ◽  
pp. F92-F96 ◽  
Author(s):  
J. Schwartz ◽  
I. A. Reid
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Arginine Vasopressin ◽  
Plasma Renin ◽  
Renin Secretion ◽  
Conscious Dogs ◽  
Specific Antagonist

The nature of the activity of vasopressin that is responsible for the inhibition of renin secretion was studied in normally hydrated conscious dogs using intravenous infusions of vasopressin and analogues of vasopressin with selective antidiuretic and vasoconstrictor activity. Vasopressin (1.0 ng . kg-1 . min-1) increased mean arterial pressure (MAP) from 106 +/- 2 to 115 +/- 3 mmHg (P less than 0.05) and decreased heart rate (HR) from 81 +/- 6 to 56 +/- 5 beats/min (P less than 0.001). Plasma renin activity (PRA) decreased from 4.4 +/- 1.1 to 2.4 +/- 0.8 ng . ml-1 . 3 h-1 (P less than 0.05). A specific antagonist of the vasoconstrictor activity of vasopressin, d(CH2)5MeTyrAVP (10 micrograms/kg), completely blocked the cardiovascular and renin responses to vasopressin. A selective vasoconstrictor agonist, 2-phenylalanine-8-ornithine oxytocin (1.0 ng . kg-1 . min-1), increased MAP from 112 +/- 4 to 128 +/- 6 mmHg (P less than 0.001) and decreased HR from 69 +/- 3 to 47 +/- 4 beats/min (P less than 0.001). PRA decreased from 5.5 +/- 1.1 to 2.7 +/- 0.2 ng . ml-1 X 3 h-1 (P less than 0.001). In contrast, a selective antidiuretic agonist, 1-deamino-8-D-arginine vasopressin (1.0 ng . kg-1 . min-1) did not alter PRA, MAP, or HR. These results demonstrate that the acute inhibition of renin secretion by vasopressin in normally hydrated conscious dogs is due to vasoconstrictor rather than antidiuretic activity.

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