Enhanced pressor responses to ICV vasopressin after pretreatment with oxytocin

1994 ◽  
Vol 266 (2) ◽  
pp. R592-R598 ◽  
Author(s):  
P. Poulin ◽  
A. Komulainen ◽  
Y. Takahashi ◽  
Q. J. Pittman
Keyword(s):  
Skeletal Muscle ◽  
Cardiovascular Effects ◽  
Intracerebroventricular Injection ◽  
Central Administration ◽  
Cardiovascular Actions ◽  
Pressor Responses ◽  
The Central Nervous System ◽  
Dose Dependent ◽  
Higher Doses

The role of oxytocin (OT) in the modulation of arginine vasopressin (AVP)-induced cardiovascular effects within the central nervous system was investigated in urethan-anesthetized rats. Intracerebroventricular injection of AVP (1-10 pmol) produced dose-dependent increases in mean arterial pressure (MAP) and heart rate (HR). These responses were enhanced in rats pretreated 24 h earlier with OT (10 pmol icv). The enhanced cardiovascular effects of AVP in OT-pretreated animals were dose dependent, blocked by the V1 antagonist d(CH2)5Tyr(Me)AVP, not evoked by OT alone, and occurred in the absence of changes in basal (nonstimulated) MAP and HR. In addition, central administration of AVP in OT-pretreated rats, but not in saline-pretreated controls, caused dose-dependent oscillations of the MAP and HR responses and, at higher doses, death of the animals. The enhanced cardiovascular actions of centrally injected AVP in OT-pretreated rats do not appear to be secondary to skeletal muscle contractions or the result of cerebral ischemia. Our data point to an interaction between the central oxytocinergic and vasopressinergic systems in cardiovascular control.

Central administration of atrial peptide decreases sympathetic outflow in rats

1990 ◽  
Vol 258 (5) ◽  
pp. R1250-R1256 ◽  
Author(s):  
H. D. Schultz ◽  
M. K. Steele ◽  
D. G. Gardner
Keyword(s):  
Heart Rate ◽  
Third Ventricle ◽  
Cardiovascular Effects ◽  
Afferent Input ◽  
Sympathetic Outflow ◽  
Central Administration ◽  
C Fibers ◽  
Afferent Vagal ◽  
Dose Dependent

Previously, we reported that intravenous (iv) administration of atrial natriuretic peptide (ANP) evokes a decrease in sympathetic outflow. This effect requires an afferent input from vagal C-fibers. Here, we examined the effect of intracerebroventricular (icv) administration of ANP on sympathetic outflow, as well as the potential role of central mechanisms in mediating the sympathoinhibitory effects evoked by systemic administration of the peptide. In anesthetized rats with arterial baroreceptors intact, injection of ANP (100-500 ng) into the third ventricle did not affect renal and least-splanchnic sympathetic nerve activities, heart rate, and mean arterial pressure. After sinoaortic denervation, however, icv injection of ANP (100 ng) decreased these variables by 8 +/- 1 and 9 +/- 2% of control nerve activity, 9 +/- 3 beats/min, and 13 +/- 2 mmHg, respectively (P less than 0.05). The inhibitory sympathetic and cardiovascular effects of icv ANP were dose dependent, with responses seen after doses too small to produce systemic effects (less than 100 ng). Vagal blockade did not abolish the effects evoked by icv ANP. In addition, iv administration of ANP did not alter reflex responses to graded electrical stimulation of afferent vagal C-fibers. Furthermore, central administration of an antiserum directed against rat ANP did not alter the inhibitory sympathetic responses evoked by iv administration of the peptide. Taken together, these results indicate that centrally administered ANP, like systemic ANP, decreases sympathetic outflow, heart rate, and blood pressure; however, the central and peripheral actions of the peptide can be distinguished and appear to be independent.

The role of oxidative stress in the cardiovascular actions of particulate air pollution

2014 ◽  
Vol 42 (4) ◽  
pp. 1006-1011 ◽  
Author(s):  
Mark R. Miller
Keyword(s):  
Oxidative Stress ◽  
Air Pollution ◽  
Diesel Exhaust ◽  
Vascular Function ◽  
Cardiovascular Effects ◽  
Increase Blood Pressure ◽  
Potential Mechanism ◽  
Particulate Air Pollution ◽  
Cardiovascular Actions

Air pollution has been estimated to be responsible for several millions of deaths worldwide per year, the majority of which have been attributed to cardiovascular causes. The particulate matter in air pollution has been shown impair vascular function, increase blood pressure, promote thrombosis and impair fibrinolysis, accelerate the development of atherosclerosis, increase the extent of myocardial ischaemia, and increase susceptibility to myocardial infarction. The pathways underlying these effects are complex and poorly understood; however, particulate-induced oxidative stress repeatedly emerges as a potential mechanism in all of these detrimental cardiovascular actions. The present mini-review will use diesel exhaust as an example of a pollutant rich in combustion-derived nanoparticles, to describe the potential by which oxidative stress could drive the cardiovascular effects of air pollution.

Release of nitric oxide and prostaglandin H2 to acetylcholine in skeletal muscle venules

1997 ◽  
Vol 272 (6) ◽  
pp. H2541-H2546 ◽  
Author(s):  
G. Dornyei ◽  
G. Kaley ◽  
A. Koller
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Perfusion Pressure ◽  
Thromboxane A2 ◽  
No Synthase ◽  
Gracilis Muscle ◽  
Vasoactive Agents ◽  
Before And After ◽  
Higher Doses

The role of endothelium in regulating venular resistance is not well characterized. Thus we aimed to elucidate the endothelium-derived factors involved in the mediation of responses of rat gracilis muscle venules to acetylcholine (ACh) and other vasoactive agents. Changes in diameter of perfusion pressure (7.5 mmHg)- and norepinephrine (10(-6) M)-constricted venules (approximately 225 microns in diam) to cumulative doses of ACh (10(-9) to 10(-4) M) and sodium nitroprusside (SNP, 10(-9) to 10(-4) M), before and after endothelium removal or application of various inhibitors, were measured. Lower doses of ACh elicited dilations (up to 42.1 +/- 4.7%), whereas higher doses of ACh resulted in smaller dilations or even constrictions. Endothelium removal abolished both ACh-induced dilation and constriction. In the presence of indomethacin (2.8 x 10(-5) M), a cyclooxygenase blocker, or SQ-29548 (10(-6) M), a thromboxane A2-prostaglandin H2 (PGH2) receptor antagonist, higher doses of ACh caused further dilation (up to 72.7 +/- 7%) instead of constriction. Similarly, lower doses of arachidonic acid (10(-9) to 10(-6) M) elicited dilations that were diminished at higher doses. These reduced responses were, however, reversed to substantial dilation by SQ-29548. The nitric oxide (NO) synthase blocker, N omega-nitro-L-arginine (L-NNA, 10(-4) M), significantly reduced the dilation to ACh (from 30.6 +/- 5.5 to 5.4 +/- 1.4% at 10(-6) M ACh). In contrast, L-NNA did not affect dilation to SNP. Thus ACh elicits the release of both NO and PGH2 from the venular endothelium.

scholarly journals Silymarin: Friend or Foe of UV Exposed Keratinocytes?

Molecules ◽  
2019 ◽  
Vol 24 (9) ◽  
pp. 1652 ◽  
Author(s):  
Fidrus ◽  
Ujhelyi ◽  
Fehér ◽  
Hegedűs ◽  
Janka ◽  
...  
Keyword(s):  
Pyrimidine Dimer ◽  
Ros Generation ◽  
Keratinocyte Cell ◽  
Pre Treatment ◽  
Different Origins ◽  
Apoptotic Effects ◽  
Dose Dependent ◽  
Higher Doses

The application of natural plant extracts in UV-protection is popular and intensively studied. Silymarin (from Silibum marianum), a naturally occurring polyphenol, has recently received attention due to its antioxidant, anti-inflammatory and anti-apoptotic effects. However, its role in the UV-mediated keratinocyte cell response is still controversial. In this study, we investigated the effects of Silibum marianum extracts with different origins and formulations on UVA-exposed HaCaT keratinocytes in vitro. Our results show, that silymarin treatment caused an inverse dose-dependent photosensitivity relationship (at higher doses, a decrease in cell viability and ROS production) after UVA exposure. The attenuation of the UVA-induced ROS generation after silymarin treatment was also observed. Moreover, silymarin pre-treatment increased the cyclobutane pyrimidine dimer photolesions in keratinocytes after UVA exposure. These results indicated the dual role of silymarin in UVA-exposed keratinocytes. It scavenges ROS but still induces phototoxicity. Based on our results dermatological applications of silymarin and related compounds should be considered very carefully.

Neuroendocrine and cardiovascular effects of serotonin: selective role of brain angiotensin on vasopressin

1996 ◽  
Vol 270 (3) ◽  
pp. E513-E521 ◽  
Author(s):  
J. A. Saydoff ◽  
P. A. Rittenhouse ◽  
M. Carnes ◽  
J. Armstrong ◽  
L. D. Van De Kar ◽  
...  
Keyword(s):  
Enzyme Inhibitor ◽  
Cardiovascular Effects ◽  
Intraventricular Injection ◽  
Intracerebroventricular Injection ◽  
Ang Ii ◽  
Acth Secretion ◽  
At1 Antagonist ◽  
Neuroendocrine Activation ◽  
Ly 53857

Central serotonin (5-HT) and angiotensin (ANG II) stimulate arginine vasopressin (AVP), oxytocin (OT), and adrenocorticotropin (ACTH) secretion and increase blood pressure. Studies were conducted in conscious rats to determine whether neuroendocrine activation by 5-HT requires a brain angiotensinergic intermediate pathway. In the first study, ANG II formation was inhibited by the angiotensin-converting enzyme inhibitor enalapril before injection of the 5-HT releaser/uptake inhibitor d-fenfluramine. Fenfluramine (2 mg/kg ip) stimulated AVP, OT, corticosterone, and prolactin (PRL) secretion (P<0.01). Enalapril (60 mg/l in drinking water for 4 days and 10 mg/kg ip 2 h before the rats were killed) inhibited only the AVP response (P<0.01) to d-fenfluramine. In the second study, the effect of intracerebroventricular injection of the 5-HT2A/2C antagonist LY-53857 (10 microgram), or the ANG II AT1 antagonist DuP-753 (10 microgram), on intracerebroventricular 5-HT (10 microgram)-stimulated AVP, OT, ACTH, PRL, renin secretion, mean arterial pressure (MAP) and heart rate (HR) was tested. LY-53857 inhibited the AVP, OT, and ACTH responses to 5-HT (P<0.01), whereas DuP-753 inhibited only the AVP response (P<0.01). Intraventricular injection of 5-HT increased MAP and decreased HR. The MAP response was not affected by LY-53857 or DuP-753, and at no time did MAP decline below starting levels. The decreased HR was inhibited by LY-53857 but not by DuP-753. These results demonstrate that 5-HT-induced AVP secretion is mediated selectively via brain angiotensinergic mechanisms by way of the AT1 receptor.

scholarly journals Cardiovascular Effects of Long-Term Central and Peripheral Administration of Urocortin, Corticotropin-Releasing Factor, and Adrenocorticotropin in Sheep

Endocrinology ◽  
2004 ◽  
Vol 145 (12) ◽  
pp. 5598-5604 ◽  
Author(s):  
R. S. Weisinger ◽  
J. R. Blair-West ◽  
P. Burns ◽  
D. A. Denton ◽  
B. Purcell ◽  
...  
Keyword(s):  
Stress Response ◽  
Arterial Pressure ◽  
Cardiovascular Effects ◽  
Corticotropin Releasing Factor ◽  
Central Administration ◽  
Long Term Effects ◽  
Cardiovascular Actions ◽  
Term Administration

Abstract The neuroendocrine hormones ACTH and corticotropin- releasing factor (CRF), which are involved in the stress response, have acute effects on arterial pressure. New evidence indicates that urocortin (UCN), the putative agonist for the CRF type 2 receptor, has selective cardiovascular actions. The responses to long-term infusions of these hormones, both peripherally and centrally, in conscious animals have not been studied. Knowledge of the long-term effects is important because they may differ considerably from their acute actions, and stress is frequently a chronic stimulus. The present experiments investigated the cardiovascular effects of CRF, UCN, and ACTH in conscious sheep. Infusions were made either into the lateral cerebral ventricles (icv) or iv over 4 d at 5 μg/h. UCN infused icv or iv caused a prolonged increase in heart rate (HR) (P &lt; 0.01) and a small increase in mean arterial pressure (MAP) (P &lt; 0.05). CRF infused icv or iv progressively increased MAP (P &lt; 0.05) but had no effect on HR. Central administration of ACTH had no effect, whereas systemic infusion increased MAP and HR (P &lt; 0.001). In conclusion, long-term administration of these three peptides associated with the stress response had prolonged, selective cardiovascular actions. The striking finding was the large and sustained increase in HR with icv and iv infusions of UCN. These responses are probably mediated by CRF type 2 receptors because they were not reproduced by infusions of CRF.

Neuromodulatory role of angiotensin-(1–7) in the central nervous system

2013 ◽  
Vol 125 (2) ◽  
pp. 57-65 ◽  
Author(s):  
Mariela M. Gironacci ◽  
Nadia A. Longo Carbajosa ◽  
Jorge Goldstein ◽  
Bruno D. Cerrato
Keyword(s):  
Renin Angiotensin System ◽  
Cardiovascular Effects ◽  
Synaptic Cleft ◽  
Neutral Endopeptidase ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
The Central Nervous System ◽  
Release Characteristic ◽  
Transporter Expression

Ang-(1–7) [angiotensin-(1–7)] constitutes an important functional end-product of the RAS (renin–angiotensin system) endogenously formed from AngI (angiotensin I) or AngII (angiotensin II) through the catalytic activity of ACE2 (angiotensin-converting enzyme 2), prolyl carboxypeptidase, neutral endopeptidase or other endopeptidases. Ang-(1–7) lacks the pressor, dipsogenic or stimulatory effect on aldosterone release characteristic of AngII. In contrast, it produces vasodilation, natriuresis and diuresis, and inhibits angiogenesis and cell growth. At the central level, Ang-(1–7) acts at sites involved in the control of cardiovascular function, thus contributing to blood pressure regulation. This action may result from its inhibitory neuromodulatory action on NE [noradrenaline (norepinephrine)] levels at the synaptic cleft, i.e. Ang-(1–7) reduces NE release and synthesis, whereas it causes an increase in NE transporter expression, contributing in this way to central NE neuromodulation. Thus, by selective neurotransmitter release, Ang-(1–7) may contribute to the overall central cardiovascular effects. In the present review, we summarize the central effects of Ang-(1–7) and the mechanism by which the peptide modulates NE levels in the synaptic cleft. We also provide new evidences of its cerebroprotective role.

Reserpine-induced central effects: pharmacological evidence for the lack of central effects of reserpine methiodide

2005 ◽  
Vol 83 (6) ◽  
pp. 509-515 ◽  
Author(s):  
Srinivas Nammi ◽  
Krishna Murthy Boini ◽  
Sushruta Koppula ◽  
Satyanarayana Sreemantula
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Target Tissue ◽  
Central Effects ◽  
Anaesthetized Rats ◽  
The Central Nervous System ◽  
Rats And Mice ◽  
Dose Dependent ◽  
Higher Doses

Reserpine, an alkaloid from Rauwolfia serpentina, was widely used for its antihypertensive action. However, its use has been reduced because of its sedative and extra pyramidal symptoms. In the present investigation, reserpine methiodide (RMI), a quaternary analogue of reserpine, was synthesized and pharmacologically evaluated in rats and mice for its central (barbiturate hypnosis, spontaneous motor activity, body temperature, and avoidance of conditioned response) and peripheral actions (blood pressure) in comparison with reserpine. The results indicate that reserpine produced a dose-dependent depression of the central nervous system. RMI at doses equal to and double the equimolar doses of reserpine did not produce any behavioural changes compared with control animals. Nevertheless, both reserpine and RMI were found to produce dose-dependent reduction in the blood pressure of anaesthetized rats, although only at higher doses of RMI, indicating that quaternization of reserpine not only attenuated the entry of RMI into the central nervous system, but also reduced its access to the target tissue in the periphery. It is speculated that the hypotensive actions of RMI may also be due to peripheral depletion of catecholamines. Key words: resperine methiodide (RMI), reserpine, behaviour, blood pressure, mice, rats.

Regional differences in constitutive and induced ICAM-1 expression in vivo

1995 ◽  
Vol 269 (6) ◽  
pp. H1955-H1964 ◽  
Author(s):  
J. Panes ◽  
M. A. Perry ◽  
D. C. Anderson ◽  
A. Manning ◽  
B. Leone ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Regional Differences ◽  
Time Course ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Fourfold Increase ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Higher Doses

The aim of the present study was to characterize and compare the expression of intercellular adhesion molecule 1 (ICAM-1) on unstimulated and endotoxin-challenged endothelial cells in different tissues of the rat. ICAM-1 expression was measured using 125I-labeled anti-rat ICAM-1 monoclonal antibody (MAb) and an isotype-matched control MAb labeled with 131I (to correct for nonspecific accumulation of the binding MAb). Under baseline conditions, ICAM-1 MAb binding was observed in all organs. The binding of 125I-ICAM-1 MAb varied widely among organs, with the largest accumulation (per g tissue) in the lung, followed by heart (1/30th of lung activity), splanchnic organs (1/50th of lung activity), thymus (1/100th of lung activity), testes (1/300th of lung activity), and skeletal muscle (1/800th of lung activity). Endotoxin induced an increase in ICAM-1 MAb binding in all organs except the spleen. Endotoxin-induced upregulation of ICAM-1 was greatest in heart and skeletal muscle (5- to 10-fold), whereas the remaining organs exhibited a two- to fourfold increase in ICAM-1 expression. Maximal upregulation of ICAM-1 occurred at 9-12 h after endotoxin administration. A dose-dependent increase in ICAM-1 expression was elicited by 0.1-10 microgram/kg, with higher doses (up to 5 mg/kg) producing no further increment. Induction of ICAM-1 mRNA after endotoxin was observed in all tissues examined (lung, heart, intestine), peaked at 3 h, and then rapidly returned to control levels. These findings indicate that ICAM-1 is constitutively expressed on vascular endothelium in all organs of the rat and that there are significant regional differences in the magnitude and time course of endotoxin-induced ICAM-1 expression.

The Role of Endogenous Opiates in the Area Postrema Pressor Pathway

1980 ◽  
Vol 59 (s6) ◽  
pp. 267s-269s ◽  
Author(s):  
Julianna E. Szilagyi ◽  
C. M. Ferrario
Keyword(s):  
Angiotensin Ii ◽  
Vertebral Artery ◽  
Area Postrema ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Endogenous Opiates ◽  
Pressor Responses ◽  
Vasomotor Activity ◽  
The Brain

1. Intra-vertebral artery-administered angiotensin II acts at the area postrema to facilitate central sympathetic vasomotor activity. Recent evidence suggests a possible role of the opiate system in the mechanism of action of angiotensin II at the level of the brain stem. 2. In these experiments, we show that the morphine antagonist naloxone reduces significantly the magnitude of the pressor response to vertebral artery-infused angiotensin II. 3. Morphine, in contrast, doubled the peak of the vertebral response to identical doses of the peptide. Neither naloxone nor morphine affected the pressor responses to intravenously administered angiotensin II. 4. The data suggest that the endogenous opiate system in the medulla modulates the cardiovascular effects of angiotensin II at the level of the area postrema.

Sign in / Sign up

Export Citation Format

Share Document