Implications of Prostacyclin Generation for Modulation of Vascular Tone

1978 ◽  
Vol 55 (s4) ◽  
pp. 195s-198s ◽  
Author(s):  
G. J. Dusting ◽  
S. Moncada ◽  
K. M. Mullane ◽  
J. R. Vane
Keyword(s):  
Blood Pressure ◽  
Prostaglandin E2 ◽  
Vascular Tone ◽  
Thromboxane A2 ◽  
Cardiovascular Effects ◽  
Peripheral Vascular ◽  
Arterial Blood ◽  
Vascular Beds ◽  
Organ Technique

1. The biotransformation of arachidonic acid and prostacyclin in the circulation was studied in anaesthetized dogs, using the blood-bathed organ technique. 2. In passage through the lungs, arachidonate (50–800 μg kg−1 min−1) was transformed into prostacyclin. No thromboxane A2 or prostaglandin E2 could be detected in arterial blood. 3. In dogs treated with indomethacin (5 mg/kg), intravenous infusions of arachidonate had no cardiovascular effects and no prostacyclin was produced. Therefore, the vasodilator effects of arachidonate in vivo may be attributable to prostacyclin formation. 4. Prostacyclin, unlike prostaglandin E2, is not inactivated by passage across the lungs, and only about 50% disappears in one passage through peripheral vascular beds. 5. Thus prostacyclin released from the lungs could function as a circulating vasodilator and contribute to the regulation of blood vessel tone and blood pressure.

Chronic regulation of arterial blood pressure by ANP: role of endogenous vasoactive endothelial factors

1998 ◽  
Vol 275 (5) ◽  
pp. H1826-H1833 ◽  
Author(s):  
L. G. Melo ◽  
A. T. Veress ◽  
U. Ackermann ◽  
H. Sonnenberg
Keyword(s):  
Blood Pressure ◽  
Enzyme Activity ◽  
Arterial Blood Pressure ◽  
Natriuretic Peptide ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Hypotensive Effect ◽  
Synthetic Activity ◽  
Arterial Blood

Atrial natriuretic peptide (ANP) exerts a chronic hypotensive effect due to a decrease in total peripheral resistance (TPR). This study examines if chronic ANP-dependent vasodilation is attributable to differences in the cardiovascular regulatory activity of vascular endothelium (VE), based on evidence that ANP affects synthesis/release and target cardiovascular effects of endothelin-1 (ET-1), C-type natriuretic peptide (CNP), and nitric oxide (NO). To determine if the synthetic activity of resistance vasculature VE is chronically altered by plasma ANP activity, we measured ET-1, CNP, and endothelial constitutive NO synthase (ecNOS) concentration and total NOS enzyme activity in homogenates of kidney, heart, lung, hindquarter skeletal muscle, and brain from hypotensive transgenic mice with elevated plasma ANP, hypertensive knockout mice (−/−) characterized by the absence of ANP, and the corresponding normotensive wild-type (NT, +/+) mice. Tissue distribution and abundance patterns of ET-1, CNP, ecNOS, and NOS enzyme activity were comparable between the different genotypes and did not differ significantly between mutant and control mice. Antagonism of ETA/B receptors in −/− and +/+ mice in vivo with SB-209670 reduced arterial blood pressure (ABP) significantly and comparably in both genotypes (−27 ± 4 and −25 ± 2% change for −/− and +/+ mice, respectively) independent of any significant changes in heart rate (HR) (−6 ± 8 and −4 ± 4% change for −/− and +/+ mice, respectively). Immunoneutralization of CNP-specific guanylate cyclase-linked receptors (GC-B) with monoclonal antibodies (3G12) increased ABP slightly, but not significantly, by similar relative amounts in both −/− (10 ± 6% change) and +/+ mice (8 ± 3% change), without changing HR significantly (4 ± 1% change for both +/+ and −/− mice). Inhibition of NOS activity (by N G-nitro-l-arginine methyl ester) significantly increased ABP, but the changes were comparable between −/− (53 ± 5% change) and +/+ mice (50 ± 6% change) and occurred in the absence of significant changes in HR (−1 ± 5 and 7 ± 5% change for −/− and +/+ mice, respectively). We conclude that the differences in ABP associated with chronic variations in endogenous ANP activity are not due to alterations in synthesis or responsiveness of the cardiovascular system to the effects of ET-1, CNP, or NO.

Cardiovascular Effects of Chlorpromazine in the Dog

1956 ◽  
Vol 186 (3) ◽  
pp. 525-528 ◽  
Author(s):  
G. B. Spurr ◽  
Steven M. Horvath ◽  
Enid Allbaugh Farrand
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Effects ◽  
Peripheral Vascular Resistance ◽  
Peripheral Vascular ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
The Mean

Chlorpromazine in doses of 2 and 5 mg/kg has been found to produce an initial hypotension in anesthetized dogs which was followed by return of the mean arterial blood pressure to near control levels. During the next 60–65 minutes there was a secondary decline in the pressure to hypotensive levels. Both an initial and secondary hypotension were the result of a decrease in peripheral vascular resistance.

Cardiovascular Effects of Micromeria graeca (L.) Benth. ex Rchb in Normotensive and Hypertensive Rats

2020 ◽  
Vol 20 (8) ◽  
pp. 1253-1261
Author(s):  
Mourad Akdad ◽  
Mohamed Eddouks
Keyword(s):  
Blood Pressure ◽  
Cardiovascular System ◽  
Arterial Blood Pressure ◽  
Antihypertensive Activity ◽  
Computer Assisted ◽  
Hypertensive Rats ◽  
Vasorelaxant Effect ◽  
Arterial Blood

Aims: The present study was performed in order to analyze the antihypertensive activity of Micromeria graeca (L.) Benth. ex Rchb. Background: Micromeria graeca (L.) Benth. ex Rchb is an aromatic and medicinal plant belonging to the Lamiaceae family. This herb is used to treat various pathologies such as cardiovascular disorders. Meanwhile, its pharmacological effects on the cardiovascular system have not been studied. Objective: The present study aimed to evaluate the effect of aqueous extract of aerial parts of Micromeria graeca (AEMG) on the cardiovascular system in normotensive and hypertensive rats. Methods: In this study, the cardiovascular effect of AEMG was evaluated using in vivo and in vitro investigations. In order to assess the acute effect of AEMG on the cardiovascular system, anesthetized L-NAME-hypertensive and normotensive rats received AEMG (100 mg/kg) orally and arterial blood pressure parameters were monitored during six hours. In the sub-chronic study, rats were orally treated for one week, followed by blood pressure assessment during one week of treatment. Blood pressure was measured using a tail-cuff and a computer-assisted monitoring device. In the second experiment, isolated rat aortic ring pre-contracted with Epinephrine (EP) or KCl was used to assess the vasorelaxant effect of AEMG. Results: Oral administration of AEMG (100 mg/kg) provoked a decrease of arterial blood pressure parameters in hypertensive rats. In addition, AEMG induced a vasorelaxant effect in thoracic aortic rings pre-contracted with EP (10 μM) or KCl (80 mM). This effect was attenuated in the presence of propranolol and methylene blue. While in the presence of glibenclamide, L-NAME, nifedipine or Indomethacin, the vasorelaxant effect was not affected. Conclusion: This study showed that Micromeria graeca possesses a potent antihypertensive effect and relaxes the vascular smooth muscle through β-adrenergic and cGMP pathways.

Vasorelaxant and Antihypertensive Effects of Mentha pulegium L. in Rats: An in vitro and in vivo Approach

2020 ◽  
Vol 20 ◽  
Author(s):  
Mohammed Ajebli ◽  
Mohamed Eddouks
Keyword(s):  
Blood Pressure ◽  
Acute Experiment ◽  
Antihypertensive Activity ◽  
Mentha Pulegium ◽  
In Vitro Experiment ◽  
Arterial Blood ◽  
Dose Dependent ◽  
Ca2 Channels

Aims and objective: The aim of the study was to investigate the effect of aqueous aerial part extract of Mentha pulegium L. (Pennyrile) (MPAE) on arterial pressure parameters in rats. Background: Mentha pulegium is a medicinal plant used to treat hypertension in Morocco. Material and methods: In the current study, MPAE was prepared and its antihypertensive activity was pharmacologically investigated. L-NAME-hypertensive and normotensive rats have received orally MPAE (180 and 300 mg/kg) during six hours for the acute experiment and during seven days for the sub-chronic treatment. Thereafter, systolic, diastolic, mean arterial blood pressure and heart rate were evaluated. While, in the in vitro experiment, isolated denuded and intact thoracic aortic rings were suspended in a tissue bath system and the tension changes were recorded. Results: A fall in blood pressure was observed in L-NAME-induced hypertensive treated with MPAE. The extract also produced a dose-dependent relaxation of aorta pre-contracted with NE and KCl. The study showed that the vasorelaxant ability of MPAE seems to be exerted through the blockage of extracellular Ca2+ entry. Conclusion: The results demonstrate that the extract of pennyrile exhibits antihypertensive activity. In addition, the effect may be, at least in part, due to dilation of blood vessels via blockage of Ca2+ channels.

Central indomethacin enhances volume-dependent vasopressin release

1984 ◽  
Vol 247 (6) ◽  
pp. R1017-R1021
Author(s):  
D. P. Brooks ◽  
L. Share ◽  
J. T. Crofton ◽  
A. Nasjletti
Keyword(s):  
Blood Pressure ◽  
Prostaglandin E2 ◽  
Mean Arterial Blood Pressure ◽  
Inhibitory Effect ◽  
Volume Depletion ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Ventriculocisternal Perfusion ◽  
Severe Hemorrhage ◽  
Vasopressin Secretion

The effect of centrally administered indomethacin on hemorrhage-induced vasopressin release was studied in the morphine-sedated, urethan/chloralose-anesthetized dog. Ventriculocisternal perfusion of indomethacin 1) significantly reduced the amount of prostaglandin E2 in the effluent from the cisterna magna, 2) significantly enhanced the vasopressin response to volume depletion, and led to a greater fall in mean arterial blood pressure during severe hemorrhage. The results suggest that central prostaglandins may have an inhibitory effect on vasopressin secretion during volume depletion.

HAEMODYNAMIC CHANGES AND ADRENAL FUNCTION IN MAN DURING INDUCED HYPOGLYCAEMIA

1963 ◽  
Vol 44 (3) ◽  
pp. 430-442 ◽  
Author(s):  
B. Arner ◽  
P. Hedner ◽  
T. Karlefors ◽  
H. Westling
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Mean Arterial Blood Pressure ◽  
Peripheral Vascular ◽  
Adrenocortical Activity ◽  
Arterial Blood ◽  
Haemodynamic Changes ◽  
The Mean ◽  
Temporary Rise ◽  
Catechol Amines

ABSTRACT Observations were made on healthy volunteers during insulin induced hypoglycaemia (10 cases) and infusion of adrenaline (3 cases) or cortisol (1 case). In all cases a rise in the cardiac output was registered during insulin hypoglycaemia. The mean arterial blood pressure was relatively unchanged and the calculated peripheral vascular resistance decreased in all cases. A temporary rise in plasma corticosteroids was observed. After infusion of adrenaline similar circulatory changes were observed but no rise in plasma corticosteroids was found. Infusion of cortisol caused an increased plasma corticosteroid level but no circulatory changes. It is concluded that liberation of catechol amines and increased adrenocortical activity following hypoglycaemia are not necessarily interdependent.

Abstract 17638: Systemic Cardiovascular Effects of Intravenous Urocortin 2 and Urocortin 3 in Patients with Heart Failure and Healthy Volunteers

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Colin G Stirrat ◽  
Sowmya Venkatasubramanian ◽  
Tania Pawade ◽  
Andrew Mitchell ◽  
Anoop Shah ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Cardiac Index ◽  
Healthy Volunteers ◽  
Diastolic Blood Pressure ◽  
Cardiovascular Effects ◽  
Peripheral Vascular ◽  
Patients With Heart Failure ◽  
Group A ◽  
Urocortin 3

Introduction: Urocortin 2 (UCN 2) and urocortin 3 (UCN 3) are endogenous peptide hormones with an emerging role in the pathophysiology and treatment of heart failure. For the first time, we examined the systemic cardiovascular effects of both UCN 2 and UCN 3 in healthy volunteers and patients with heart failure. Methods: Seven healthy volunteers (Group A) and nine patients with stable chronic heart failure (Group B, New York Heart Association class II and III, left ventricular ejection fraction <35%) on optimal medical therapy underwent non-invasive oscillometric sphygmomanometry and impedance cardiography during incremental intravenous infusions of sodium nitroprusside (0.15/0.5/1.5 μg/kg/min), UCN 2 (0.16/0.48/1.6 μg/min), UCN 3 (5/15/50 μg/min) and saline placebo in a randomised double blind two-way cross over study. Results: Other than diastolic blood pressure (78 vs 72 mmHg for Group A and B respectively, p<0.05), haemodynamic variables were similar at baseline of each infusion and were unchanged by saline placebo infusion (p>0.05 for all). SNP, UCN2 and UCN 3 infusions increased heart rate and cardiac index, and reduced systolic and diastolic blood pressure and peripheral vascular resistance index (PVRI) in both healthy volunteers and patients with heart failure (p<0.05 for all; see Figure 1). There were no significant differences in the changes in cardiac index or PVRI between healthy volunteers and patients with heart failure during either UCN 2 or UCN 3 infusions (p>0.05). Conclusion: Intravenous UCN 2 and especially UCN 3 increase cardiac output and reduce peripheral vascular resistance. This favourable haemodynamic profile suggests that UCN 2 and UCN 3 hold exciting therapeutic potential for the treatment of acute heart failure.

scholarly journals Cardiovascular effects of lumbar epidural anaesthesia in isoflurane-anaesthetised pigs during surgical removal of the liver

2009 ◽  
Vol 80 (1) ◽  
Author(s):  
G.F. Stegmann
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Abdominal Surgery ◽  
Epidural Anaesthesia ◽  
Cardiovascular Effects ◽  
Surgical Removal ◽  
Arterial Blood ◽  
Combined Administration ◽  
Lumbar Epidural Anaesthesia ◽  
Surgical Preparation

In humans the combined administration of epidural anaesthesia and inhalation anaesthesia may result in cardiovascular instability associated with decreases in heart rate and blood pressure. Anaesthesia was induced with a combination of midazolam / ketamine in 18 female pigs with a mean body weight of 24.9±5.9 kg scheduled for surgical removal of the liver. After tracheal intubation, anaesthesia was maintained on a circle rebreathing circuit with isoflurane. Epidural anaesthesia was administered with ropivacaine (AL-group, n=8) at 0.2 mℓ / kg of a 7.5 mg / mℓ solution to the anaesthetised animals. The A-group (n = 10) received isoflurane anaesthesia only. The vaporiser was set at 2.5 % for the A-group and 1.5 % for the AL-group. Heart rate, invasive systolic, diastolic, and mean arterial blood pressure were monitored. Comparisons were made between treatments and within treatments comparing variables during surgical preparation and abdominal surgery. Differences between treatments were not statistically significant (P > 0.05) during surgical preparation or during abdominal surgery. For within treatment groups, the differences between surgical preparation and abdominal surgery were statistically significant (P < 0.05) for heart rate in the A-group, but not statistically significant (P > 0.05) for the other variables. It is concluded that abdominal surgery may be associated with statistically significant changes in heart rate in isoflurane-anaesthetised pigs and that the combined administration of epidural ropivacaine may prevent statistically significant changes in HR during abdominal surgery.

The Generation of Kinins in the Blood of Dogs during Hypotension Due to Haemorrhage

1970 ◽  
Vol 39 (3) ◽  
pp. 349-365 ◽  
Author(s):  
H. E. Berry ◽  
J. G. Collier ◽  
J. R. Vane
Keyword(s):  
Blood Pressure ◽  
Time Course ◽  
Venous Pressure ◽  
Venous Blood ◽  
Systemic Circulation ◽  
Substantial Effect ◽  
Mixed Venous Blood ◽  
Shed Blood ◽  
Arterial Blood ◽  
Organ Technique

1. Circulating kinins were detected and continuously assayed during hypotension due to haemorrhage in dogs, using the blood-bathed organ technique and isolated strips of cat jejunum as the assay tissue. 2. In arterial blood kinin concentrations of 1–5 ng/ml were attained after a hypotension of 35–65 mmHg had been maintained for 10–190 min. When portal venous blood was simultaneously assayed kinins appeared earlier and in concentrations 1–2 ng/ml higher than in arterial blood. No differences in time course of kinin generation or in concentration were found when mixed venous blood and arterial blood were compared. In those instances in which the blood pressure was restored to normal by returning the shed blood, kinin formation stopped. 3. Kinin generation was due to the presence in the circulation of a kinin-forming enzyme, such as kallikrein. When kallikrein was infused into the portal vein, it was partially inactivated by the liver. 4. Prolonged intravenous infusions of kallikrein (20–60 mu kg−1 min−1) generated kinins in the circulation in concentrations (1–5 ng/ml) which were well maintained throughout the infusion, demonstrating that kinin generation is not limited by depletion of the precursor kininogen; nevertheless, the effects of kallikrein infusions on the blood pressure and central venous pressure waned. 5. It is concluded that in hypotension due to haemorrhage, an active kallikrein appears in the portal circulation. Delay in the appearance of kallikrein in the systemic circulation may be due to the kallikrein inactivating mechanism of the liver. This inactivating mechanism may fail during shock. Kinins are generated in amounts sufficient to have a substantial effect on the circulation and an influence on the course of events in shock.

Inotropes and Vasopressors for Shock

2019 ◽  
Author(s):  
Amour B U Patel ◽  
Gareth L Ackland
Keyword(s):  
Blood Pressure ◽  
Animal Studies ◽  
Cardiac Contractility ◽  
Clinical Trial Data ◽  
Cardiovascular Effects ◽  
Evidence Base ◽  
End Points ◽  
Arterial Blood ◽  
End Stage ◽  
The Impact

Inotropes and vasopressors play a key role in the management of shock. The goal of therapy is to restore end-organ perfusion by augmenting cardiac output (CO) and vascular tone. Clinical trial data have thus far failed to identify precise hemodynamic end points associated with better outcomes; in any event, such end points are highly likely to be determined on an individualized basis, reflecting patients’ chronic arterial blood pressure, baseline cardiac function, and other pathophysiologic factors (e.g., end-stage renal failure, cardiac ischemia).1 Inotropes enhance cardiac contractility and CO; vasopressors raise blood pressure. The impact of these drugs in restoring hemodynamic parameters to “normal” values has principally been used to evaluate their effectiveness, with clinical practice guided by extrapolation from animal studies and pharmacologic trials.2 However, these drugs have important extra-cardiovascular effects on metabolic, neurohormonal, and autonomic regulation that are also injurious. This review discusses the mechanisms and evidence base for inotropes and vasopressors in various types of shock. This review contains 3 figures, and 39 references. Keywords: inotropes, vasopressors, catecholamines, monitoring, shock states, cardiogenic, hemorrhagic, septic, neurogenic

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