A C TYPE NATRIURETIC PEPTIDE IS A VASODILATOR IN VIVO AND IN VITRO IN THE COMMON DOGFISH

1992 ◽  
Vol 133 (2) ◽  
pp. R1-R4 ◽  
Author(s):  
C. Bjenning ◽  
Y. Takei ◽  
T.X. Watanabe ◽  
K. Nakajima ◽  
S. Sakakibara ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Natriuretic Peptide ◽  
Natriuretic Peptides ◽  
Physiological Role ◽  
Arterial Blood ◽  
Brain Natriuretic Peptides ◽  
Dose Dependent

ABSTRACT The effects of an elasmbranch cardiac C-type natriuretic peptide (dogfish CNP-22) on arterial blood pressure were investigated in vivo in chronically cannulated dogfish Scyliorhinus canicula and in vitro by a myographic technique using the distal part of the first branchial artery. In-vivo dogfish CNP-22 caused a dose-dependent reduction in mean arterial blood pressure which was much more potent than that of α-human ANP. In-vitro dogfish CNP-22 also caused a dose-dependent relaxation which was independent of the endothelium. These results are in marked contrast to those obtained in similar studies on other vertebrate species in which CNP exhibited only mild hypotensive effects compared to both atrial and brain natriuretic peptides. This study indicates the importance of using homologous peptides in determing the physiological role of natriuretic peptides in non-mammalian vertebrates.

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.

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.

PROSTACYCLIN (PGI2) FORMATION IN RELATION TO ANAPHYLATOXIN C5a GENERATION DURING RABBIT ENDOTOXIN SHOCK

1987 ◽  
Author(s):  
M Rampart ◽  
H Bult ◽  
A G Herman ◽  
P J Jose ◽  
T J Williams
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Endotoxin Shock ◽  
Rabbit Serum ◽  
Classical Pathway ◽  
E Coli ◽  
Arterial Blood ◽  
Anaphylatoxin C5a

Injection of endotoxin (LPS) in animals, a model for gram-negative septic shock, leads to intravascular activation of the complement system, and is one of the few conditions in which 6-oxo-PGF]CX and thromboxane (TX) B2 (non-enzymic metabolites of PGI2 and TXA2) can be detected in arterial blood. Previously we reported associations between complement activation, PGI2 biosynthesis and LPS-induced hypotension in rabbits. As C5a and C5adesArg trigger endothelial PGI2 formation in vitro, we have now measured the plasma levels of immunoreactive (ir) C5a in relation to generation of PGI2 and changes in arterial blood pressure in LPS shock. Pentobarbitone anaesthethized rabbits received LPS (E. coli 0111:B4, 0.5 mg/kg) or saline via the marginal ear vein. A catheter in the left carotid artery was used to collect blood and to monitor mean arterial blood pressure (MABP). Platelet and leukocyte numbers, haemolytic complement titre (CH50), and plasma ir6-oxo-PGFioc , irTXB2 and irC5a were measured 15 min before and at different times after saline or LPS injection. LPS caused a dose- and time-dependent formation of irC5a in rabbit serum in vitro, predominantly via the classical pathway. LPS also activated complement in vivo, as indicated by about 20 % reduction of CH50 titre (measured after 3h) and a marked increase of arterial irC5a (20-120 ng/ml) in the first 2 to 5 min. After 30 min, irC5a had returned to baseline levels (< 2-5 ng/ml) and remained so up to 3h after injection of LPS. This irC5a peak correlated with a shortlasting initiation of PGI2 release (from < 20 pg/ml up to 550 pg/ml) and a drop in MABP (from about 95 mmHg to 50 mmHg) 2-5 min after LPS. None of these changes occurred after saline injection.In conclusion, LPS activates complement in vivo with concomitant formation of C5a. This peptide may trigger -either directly or after phagocyte activation - endothelial PGI2 biosynthesis, leading to arterial hypotension. This is supported by the suppression of the initial rise of arterial ir6-oxo-PGF1α and hypotension in complement-depleted rabbits. Inhibition of C5a formation or activity may prove to be a meaningful approach to the treatment of septic circulatory shock.

IN VIVO SELECTIVITY BETWEEN HYPOTENSIVE AND PLATELET ANTIAGGREGATING ACTIONS OF ILOPROST AND PGI2 IN BEAGLE DOGS

1987 ◽  
Author(s):  
F Hermán ◽  
P Hadházy ◽  
K Magyar
Keyword(s):  
Blood Pressure ◽  
Platelet Aggregation ◽  
Arterial Blood Pressure ◽  
Bolus Administration ◽  
Beagle Dogs ◽  
Duration Of Action ◽  
Arterial Blood ◽  
Level Of Significance

Iloprost (Schering A.G.) is a chemically stable derivative of prostacyclin. We compared the hypotensive and antiaggregatory effects of PGI2 and Iloprost. The concentration producing 50% inhibition (IC50) of ADP-induced platelet aggregation in vitro was 0.35±0.15 nmol/1 for PGI2 and 0.56±0.2 nmol/1 for Iloprost (n=5). The in vivo antiaggregatory activity was measured with a modified filtration pressure technique (F.Hermán et al.Thromb. Res.44 /1986/, 575) in anaesthetized beagle dogs; the change in arterial blood pressure was recorded simultaneously. Using this technique, the dose-response relationship and the duration of action of prostacyclin and Iloprost following bolus administration have been determined. PGI2 was equipotent with Iloprost in inhibiting platelet aggregation in vivo (ED25: 0.25±0.04 nmol/kg; 0.28±0.05 respectively). At the same time PGI2 was two times as potent as Iloprost in decreasing the mean arterial blood pressure (ED25: 0.41±0.12 nmol/kg; 0.87±0.14 nmol/kg respectively). The antiaggregatory and hypotensive effects of Iloprost last longer in each experiment than that of PGI2, but did not reach the level of significance probably due to the considerable interindividual differences. The in vivo selectivity ratios (hypotensive potency/antiaggregatory potency) of Iloprost and PGI2 were 0.32 and 0.6 respectively. These results show that in anesthetized beagles Iloprost is somewhat more selective than PGI2 in inhibiting platelet aggregation.

Human vascular smooth muscle responses mediated by α2 mechanisms in vivo and in vitro

1985 ◽  
Vol 68 (s10) ◽  
pp. 147s-150s ◽  
Author(s):  
S. Thom ◽  
J. Calvete ◽  
R. Hayes ◽  
G. Martin ◽  
P. Sever
Keyword(s):  
Smooth Muscle ◽  
Physiological Role ◽  
Smooth Muscle Contraction ◽  
Α1 Receptors ◽  
Dose Dependent ◽  
Higher Doses ◽  
Α2 Receptors ◽  
Autoregulatory Mechanism

1. The effects of compounds with α2-agonist and α2-antagonist properties on human forearm blood flow and on isolated human arterial segments have been studied. 2. The findings from these studies in vivo and in vitro did not provide evidence in support of the hypothesis that postsynaptic α2-receptors mediate smooth muscle contraction in the tissues under investigation. 3. The constriction of the forearm vascular bed in response to low intra-arterial doses of idazoxan (RX 781094), an α2-antagonist, provides evidence for a physiological role for a presynaptic α2 autoregulatory mechanism. 4. The variability of the forearm vascular responses to higher doses of idazoxan highlights the pitfalls that may have misled previous authors in their interpretation of the results of similar studies. A U-shaped dose-response curve to compounds with mixed α2-and α1-antagonist properties may be constructed, which emphasizes the importance of the dose-dependent selectivity of these antagonists at α2- and α1-receptors. 5. The effect of idazoxan on the responses of arterial segments in vitro to exogenous catecholamines was dependent on the integrity of the endothelium, and provides evidence that α2-receptors may mediate release of the endothelium-derived relaxing factor.

Effects of natriuretic peptides and nitroprusside on venous function in trout

1997 ◽  
Vol 273 (2) ◽  
pp. R527-R539 ◽  
Author(s):  
K. R. Olson ◽  
D. J. Conklin ◽  
A. P. Farrell ◽  
J. E. Keen ◽  
Y. Takei ◽  
...  
Keyword(s):  
Natriuretic Peptide ◽  
Natriuretic Peptides ◽  
Aortic Pressure ◽  
Systemic Resistance ◽  
Venous Compliance ◽  
Venous Capacitance ◽  
Unstressed Volume ◽  
Ventral Aorta

Active venous regulation of cardiovascular function is well known in mammals but has not been demonstrated in fish. In the present studies, the natriuretic peptides (NP) rat atrial natriuretic peptide (ANP) and trout ventricular natriuretic peptide (VNP), clearance receptor inhibitor SC-46542, and sodium nitroprusside (SNP) were infused into unanesthetized trout fitted with pressure cannulas in the ventral aorta, dorsal aorta, and ductus Cuvier, and a ventral aorta (VA) flow probe was used to measure cardiac output (CO). In another group, in vivo vascular (venous) capacitance curves were obtained during ANP or SNP infusion. The in vitro effects of NP on vessels and the heart were also examined. ANP, VNP, and SC-46542 decreased central venous pressure (PVen), CO, stroke volume (SV), and gill resistance (RG), whereas systemic resistance (RS) and heart rate (HR) increased. Dorsal aortic pressure (PDA) transiently increased and then fell even though RS remained elevated. ANP decreased mean circulatory filling pressure (MCFP), increased vascular compliance at all blood volumes, and increased unstressed volume in hypovolemic fish. ANP had no direct effect on the heart. ANP responses in vivo were not altered in trout made hypotensive by prior treatment with the angiotensin-converting enzyme inhibitor lisinopril. SNP reduced ventral aortic pressure (PVA), PDA, and RS, increased CO and HR, but did not affect PVen, SV, or RG. SNP slightly decreased MCFP but did not affect compliance or unstressed volume. In vitro, large systemic arteries were more responsive than veins to NP, whereas SNP relaxed both. These results show that, in vivo, NP decrease venous compliance, thereby decreasing venous return, CO, and arterial pressure. Conversely, SNP hypotension is due to decreased RS. This is the first evidence for active regulation of venous capacitance in fish, which probably occurs in small veins or venules. The presence of venous baroreceptors is also suggested.

Vasodilation of cat cerebral arterioles by prostaglandins D2, E2, G2, and I2

1979 ◽  
Vol 237 (3) ◽  
pp. H381-H385 ◽  
Author(s):  
E. F. Ellis ◽  
E. P. Wei ◽  
H. A. Kontos
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Blood Pressure ◽  
Standard Error ◽  
Arterial Blood ◽  
Cerebral Arterioles ◽  
The Mean ◽  
Dose Dependent ◽  
The Brain

To determine the possible role that endogenously produced prostaglandins may play in the regulation of cerebral blood flow, the responses of cerebral precapillary vessels to prostaglandins (PG) D2, E2, G2, and I2 (8.1 X 10(-8) to 2.7 X 10(-5) M) were studied in cats equipped with cranial windows for direct observation of the microvasculature. Local application of PGs induced a dose-dependent dilation of large (greater than or equal to 100 microns) and small (less than 100 microns) arterioles with no effect on arterial blood pressure. The relative vasodilator potency was PGG2 greater than PGE2 greater than PGI2 greater than PGD2. With all PGs, except D2, the percent dilation of small arterioles was greater than the dilation of large arterioles. After application of prostaglandins in a concentration of 2.7 X 10(-5) M, the mean +/- standard error of the percent dilation of large and small arterioles was, respectively, 47.6 +/- 2.7 and 65.3 +/- 6.1 for G2, 34.1 +/- 2.0, and 53.6 +/- 5.5 for E2, 25.4 +/- 1.8, and 40.2 +/- 4.6 for I2, and 20.3 +/- 2.5 and 11.0 +/- 2.2 for D2. Because brain arterioles are strongly responsive to prostaglandins and the brain can synthesize prostaglandins from its large endogenous pool of prostaglandin precursor, prostaglandins may be important mediators of changes in cerebral blood flow under normal and abnormal conditions.

Sign in / Sign up

Export Citation Format

Share Document