Chronic Lability of Arterial Pressure in the Rat Does Not Evolve into Hypertension

1980 ◽  
Vol 59 (s6) ◽  
pp. 405s-407s ◽  
Author(s):  
W. T. Talman ◽  
D. R. Alonso ◽  
D. J. Reis
Keyword(s):  
Heart Rate ◽  
Standard Deviation ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Histopathological Changes ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Electrolytic Lesions ◽  
The Mean ◽  
Catecholamine Neurons

1. In rats, electrolytic lesions of the A2 group of catecholamine neurons result in lability of arterial pressure without hypertension. 2. To establish whether labile arterial pressure, when chronic, will lead to fixed hypertension, we placed lesions in the A2 area of adult male Sprague-Dawley rats and measured mean arterial pressure, heart rate and their variability (expressed as the standard deviation) 11 months later. Controls were age-matched, unoperated or sham-operated rats. 3. In rats with A2 lesions: (a) the mean arterial pressure was lower (103 ± 7.5 mmHg; n = 6; P<0.05) than in sham-operated (123 ± 4.7 mmHg; n = 4) or unoperated (120 ± 3.1 mmHg; n = 9) controls; (b) the standard deviation of mean arterial pressure was higher (16 ± 1.8 mmHg; P<0.001) than in sham-operated (5 ± 0.7 mmHg) or unoperated controls (7 ± 0.6 mmHg); (c) the mean and standard deviation of heart rate did not differ between groups. No histopathological changes were detected in the A2 group. 4. Chronic lability of arterial pressure does not evolve into sustained hypertension nor does it induce systemic lesions.

Responses of the Systemic Circulation and of the Renin—Angiotensin—Aldosterone System to Ketanserin at Rest and Exercise in Normal Man

1984 ◽  
Vol 66 (1) ◽  
pp. 17-25 ◽  
Author(s):  
Robert Fagard ◽  
Anne Cattaert ◽  
Paul Lijnen ◽  
Jan Staessen ◽  
Luc Vanhees ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Catecholamines ◽  
Plasma Renin ◽  
Systemic Circulation ◽  
Work Rate ◽  
Plasma Aldosterone ◽  
Sitting Position ◽  
The Mean

1. The systemic circulation at rest and during exercise was studied in ten normal male volunteers, after placebo on one occasion and after acute intravenous administration of the serotonergic antagonist ketanserin on another occasion. The effects of ketanserin on the components of the renin—angiotensin—aldosterone system, on plasma catecholamines and on exercise capacity for graded uninterrupted exercise were also investigated. 2. At rest in recumbency rapid intravenous injection of 10 mg of ketanserin, followed by a continuous infusion of 2 mg/h, produced an acute but transient fall in mean intra-arterial pressure of 6 mmHg compared with placebo. After 15 min the mean arterial pressure with ketanserin was within 2 mmHg of the mean pressure with placebo. In the sitting position both at rest and up to 30% of maximal work rate, the mean arterial pressure during ketanserin did not differ from the pressure on placebo. However, at higher levels of physical activity the rise in mean arterial pressure was lower with ketanserin; the pressure achieved with placebo was 7.5 mmHg higher at maximal work rate. Heart rate and cardiac output were significantly higher during ketanserin. 3. When the subjects were lying down and resting, plasma noradrenaline and adrenaline levels, plasma renin activity and angiotensin II concentration were not affected by ketanserin; however, these values were higher in the sitting position both at rest and during exercise. Plasma aldosterone was reduced by ketanserin during exercise and also when the subject was resting in the recumbent position. 4. Exercise capacity as measured by peak oxygen uptake was similar during ketanserin (3.09 ± se 0.12 litres/min) and during placebo (3.11 ± 0.13). 5. The data suggest that 5-hydroxytryptamine can have only a small role, if any, in pressure homoeostasis in sodium replete man at rest in recumbency. At moderate and heavy levels of exercise, the results are compatible with a role for 5-hydroxytryptamine in pressure regulation. Activation of the sympathetic nervous system by ketanserin is suggested by increases of plasma catecholamines, heart rate, cardiac output and plasma renin. The suppression of plasma aldosterone suggests that 5-hydroxytryptamine may have a role in the regulation of aldosterone secretion which is independent of angiotensin II.

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

scholarly journals COMPARATIVE CHARACTERISTICS OF THE DYNAMICS OF CARDIOVASCULAR AND RESPIRATORY EFFECTS OF PNEUMOPERITONEUM BASED ON CARBON DIOXIDE AND ARGON IN LAPAROSCOPIC CHOLECYSTECTOMY

2021 ◽  
pp. 90-95
Author(s):  
O. L. Tkachuk ◽  
R. L. Parakhoniak ◽  
S. V. Melnyk ◽  
O. O. Tkachuk-Hryhorchuk
Keyword(s):  
Carbon Dioxide ◽  
Heart Rate ◽  
Cardiac Output ◽  
Laparoscopic Cholecystectomy ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Negative Impact ◽  
Abdominal Pressure ◽  
The Mean ◽  
Respiratory Systems

Pneumoperitoneum is one of the most critical components of laparoscopic surgery, which has a negative effect on gas exchange and stress to circulatory buffering system. One of the top priorities of laparoscopic technologies is to minimize the impact on the respiratory and cardiovascular systems, metabolic dynamics and compensatory abilities of homeostasis. The main goal of this research work is to compare the effects of carboxyperitoneum and argonoperitoneum on the intraoperative dynamics of CO2 concentration as well as cardiovascular and respiratory characteristics in patients undergoing laparoscopic cholecystectomy for various forms of cholelithiasis. Materials and methods. Four experimental groups involved patients based on their nosological form of cholelithiasis and the gas used to induce pneumoperitoneum. All patients underwent laparoscopic cholecystectomy by means of standard procedure. Either medical carbon dioxide or medical argon was used to induce pneumoperitoneum. Intraoperative monitoring of blood carbon dioxide levels PaCO2 was performed by taking venous blood every 15 minutes. Capnometry was performed by means of mainstream analysis using “BIOMED” BM1000C modular patient monitor by recording the discrete values of PetCO2 every 15 minutes, as well as by analyzing photocopies of capnography curves every 15 minutes. Intraoperative echocardiography was performed to identify the mean arterial pressure (MAP), heart rate (HR) and cardiac output (CO) in order to assess the effects of different types of pneumoperitoneum on the cardiovascular system. Results. The obtained data confirm the expected difference in the indices of cardiorespiratory functions between patients with acute cholecystitis and cholelithiasis without signs of inflammation. The investigation revealed that under the influence of pneumoperitoneum, heart rate and mean arterial pressure increase, while the cardiac output decreases. The respiratory pressure marker depends more on the intra-abdominal pressure and presumably the patient’s body type than on the presence of inflammatory syndrome. Argon insufflation has a slight negative impact on the cardiovascular system. Particularly, the mean arterial pressure and heart rate increase, while the cardiac output marker is less decreased as compared to the use of carbon dioxide. Abdominal pressure has a significant effect on the cardiovascular and respiratory systems regardless of the used type of gas. The combination of high intra-abdominal pressure with the elevated head end of the operating table, which is a common practise during cholecystectomy, has especially great influence on cardiovascular and respiratory functions. Operation which is carried out at decreased pressure allows reducing the deviations of practically all indices. Conclusions. Thus, the cardiovascular and respiratory systems adapt under the influence of pneumoperitoneum, providing compensation for the negative effects of mechanical and resorptive-metabolic character. Compensatory-adaptive abilities of the cardiovascular and respiratory systems increase with the decrease of intra-abdominal pressure. The use of argon as a working gas for insufflation into the abdominal cavity during laparoscopy reduces the negative impact of pneumoperitoneum on the cardiovascular and respiratory systems, providing a greater reserve of homeostatic and buffer systems of the body.

Effect of carotid or aortic baroreceptor denervation on arterial pressure during hemorrhage in conscious dogs

2001 ◽  
Vol 280 (6) ◽  
pp. R1642-R1649 ◽  
Author(s):  
Terry N. Thrasher ◽  
Cassandra Shifflett
Keyword(s):  
Heart Rate ◽  
Standard Deviation ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Conscious Dogs ◽  
Carotid Baroreceptors ◽  
Intact Condition ◽  
Aortic Baroreceptors

We studied the effect of chronically denervating aortic baroreceptors (ABR; n = 6) or carotid baroreceptors (CBR; n= 7) on mean arterial pressure (MAP) and heart rate (HR) responses to hemorrhage in the dog. Neither denervation had a significant effect on basal MAP, the variability (standard deviation) of MAP, or resting HR. However, the breakpoint of MAP (defined as the volume of blood removed when MAP fell more than 10% below control and declined monotonically thereafter) was significantly reduced in dogs with only ABR functional (12.4 ± 1.4 ml/kg) compared with the volume in the intact condition (18.9 ± 1.8 ml/kg). In contrast, there was no difference in the breakpoint or the MAP at any time during hemorrhage in dogs with both CBR functional compared with their intact responses. In a different group of dogs ( n = 6), responses were determined with both CBR operating and again after unilateral denervation, leaving only one CBR (1CBR) functional. Basal MAP and the variability of MAP were not altered in dogs with only 1CBR functional, but the breakpoint (11.7 ± 1.4 ml/kg) during hemorrhage was significantly different compared with responses with two CBR (21.2 ± 2.3 ml/kg), and MAP fell to much lower levels. These results indicate that the CBR can compensate fully for loss of ABR during hemorrhage but not vice versa; and bilateral CBR inputs are required for normal responses to hemorrhage.

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.

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.

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 Glucocorticoids act in the dorsal hindbrain to modulate baroreflex control of heart rate

2006 ◽  
Vol 290 (4) ◽  
pp. R1003-R1011 ◽  
Author(s):  
Andrea G. Bechtold ◽  
Deborah A. Scheuer
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Logistic Function ◽  
Receptor Expression ◽  
Arterial Baroreflex ◽  
Sprague Dawley ◽  
Baroreflex Control ◽  
Sprague Dawley Rats ◽  
Corticosteroid Receptor ◽  
Dorsal Hindbrain

Systemic corticosterone (Cort) modulates arterial baroreflex control of both heart rate and renal sympathetic nerve activity. Because baroreceptor afferents terminate in the dorsal hindbrain (DHB), an area with dense corticosteroid receptor expression, we tested the hypothesis that prolonged activation of DHB Cort receptors increases the midpoint and reduces the gain of arterial baroreflex control of heart rate in conscious rats. Small (3–4 mg) pellets of Cort (DHB Cort) or Silastic (DHB Sham) were placed on the surface of the DHB, or Cort was administered systemically by placing a Cort pellet on the surface of the dura (Dura Cort). Baroreflex control of heart rate was determined in conscious male Sprague Dawley rats on each of 4 days after initiation of treatment. Plots of arterial pressure vs. heart rate were analyzed using a four-parameter logistic function. After 3 days of treatment, the arterial pressure midpoint for baroreflex control of heart rate was increased in DHB Cort rats (123 ± 2 mmHg) relative to both DHB Sham (108 ± 3 mmHg) and Dura Cort rats (109 ± 2 mmHg, P < 0.05). On day 4, baseline arterial pressure was greater in DHB Cort (112 ± 2 mmHg) compared with DHB Sham (105 ± 2 mmHg) and Dura Cort animals (106 ± 2 mmHg, P < 0.05), and the arterial pressure midpoint was significantly greater than mean arterial pressure in the DHB Cort group only. Also on day 4, maximum baroreflex gain was reduced in DHB Cort (2.72 ± 0.12 beats·min−1·mmHg−1) relative to DHB Sham and Dura Cort rats (3.51 ± 0.28 and 3.37 ± 0.27 beats·min−1·mmHg−1, P < 0.05). We conclude that Cort acts in the DHB to increase the midpoint and reduce the gain of the heart rate baroreflex function.

scholarly journals Comparison between esmolol and verapamil in attenuation of cardiovascular stress response to laryngoscopy and endotracheal intubation in elective surgery

2021 ◽  
Vol 12 (7) ◽  
pp. 64-68
Author(s):  
Nitisha Chakraborty ◽  
Sankar Roy ◽  
Debajyoti Sur ◽  
Arunava Biswas ◽  
Dipasri Bhattacharya ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Body Weight ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Diastolic Blood Pressure ◽  
Endotracheal Intubation ◽  
Efficacy And Safety ◽  
Cardiovascular Stress ◽  
The Mean

Background: Cardiovascular stress due to reflex sympathetic over activity is a great concern during laryngoscopy and endotracheal intubation. Aims and Objectives: To compare the efficacy and safety of esmolol and verapamil for attenuation of hemodynamic effects (heart rate, systolic blood pressure, diastolic blood pressure and mean arterial pressure) due to laryngoscopy and endotracheal intubation in elective surgical cases. Materials and Methods: A prospective, randomized, double blinded, controlled study was conducted on 60 patients divided equally into 30 each receiving esmolol (2 mg/kg body weight) and verapamil (0.1 mg/kg body weight) respectively. Heart rate, systolic and diastolic blood pressure and mean arterial pressure were recordedat pre-operative stage, after administration of the study drugs, immediately after intubation and at 1 ,3 ,5 minutes after intubation. Data collected were statistically analyzed. Results: The mean systolic blood pressure was lower in the esmolol group at all times of estimation compared with the verapamil group and the difference was at the time of intubation (p value <0.001).The mean diastolic blood pressure was lower in the esmolol group at all times of estimation compared to the verapamil group which was not statistically significant at any time of estimation. The mean arterial pressure was significantly lower at the time of immediately after intubation (p<0.001) in esmolol as compared to verapamil group. Adverse effects in both the study groups were insignificant. Conclusion: Esmololand Verapamil can effectively attenuate the cardiovascular stress to laryngoscopy and endotracheal intubation with the former appears to be a better alternative from efficacy and safety perspectives.

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