Central Administration of H2S Donors for Studying Cardiovascular Effects of H2S in Rats

2019 ◽  
pp. 167-172
Author(s):  
Marcin Ufnal ◽  
Artur Nowinski
Keyword(s):  
Cardiovascular Effects ◽  
Central Administration

Evidence that centrally released arginine vasopressin is involved in central pressor action of angiotensin II

1996 ◽  
Vol 270 (1) ◽  
pp. H167-H173 ◽  
Author(s):  
S. Lon ◽  
E. Szczepanska-Sadowska ◽  
M. Szczypaczewska
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arginine Vasopressin ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Pressor Effect ◽  
Ang Ii ◽  
Central Administration ◽  
Hypotensive Action ◽  
Series Of Experiments

Five series of experiments were performed on conscious trained dogs to find out whether intracranially released arginine vasopressin (AVP) is involved in mediation of central cardiovascular effects of angiotensin II (ANG II). The dogs were implanted with guide tubes leading to the third cerebral ventricle (ICV) and implanted with the intra-arterial catheters. Blood pressure and heart rate were continuously monitored during intracerebroventricular administration of 1) ANG II alone (250 ng), 2) AVP alone (0.01 ng/min during 10 min), 3) ANG II together with AVP, 4) AVP together with AVP V1-receptor antagonist 1(1-mercapto-4-methylcyclohexaneacetic acid)-8-AVP [MeCAAVP, V1ANT,100 ng/min], and 5) ANG II together with V1ANT. The results revealed that 1) ANG II and AVP applied separately elicited significant, long-lasting increases of blood pressure; 2) the maximum pressor effect after ANG II and AVP applied together did not differ from that after separate application of either of these peptides, but the duration of the pressor response was significantly shorter; 3) pretreatment with V1ANT effectively prevented blood pressure increases elicited by central administration of AVP and ANG II; and 4) after blockade of V1 receptors administration of AVP resulted in a significantly delayed decrease of blood pressure below baseline. The results strongly suggest that 1) centrally released AVP mediates the pressor effect of intracerebroventricularly applied ANG II by means of V1 receptors; 2) intracerebroventricularly applied ANG II and AVP interact to activate the mechanism involved in extinction of their pressor effect; and 3) blockade of central V1 receptors uncovers the hypotensive action of centrally applied AVP.

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 < 0.01) and a small increase in mean arterial pressure (MAP) (P < 0.05). CRF infused icv or iv progressively increased MAP (P < 0.05) but had no effect on HR. Central administration of ACTH had no effect, whereas systemic infusion increased MAP and HR (P < 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.

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.

Role of sympathetic nervous system in cardiovascular effects of centrally administered endothelin-1 in rats

1997 ◽  
Vol 273 (3) ◽  
pp. H1177-H1186 ◽  
Author(s):  
A. Gulati ◽  
S. Rebello ◽  
A. Kumar
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Portal System ◽  
Central Administration ◽  
Endothelin 1 ◽  
Circulatory Effects ◽  
Sympathetic Nervous

Centrally administered endothelin-1 (ET-1) produces a biphasic response, an initial increase followed by a decrease in blood pressure (BP). The pressor effect is due to stimulation of the sympathetic nervous system and/or release of vasopressin. The mechanism responsible for the depressor effect after central administration of ET-1 is still not known. Systemic and regional circulatory effects of intracerebroventricular (i.c.v.) administration of ET-1 (100 ng) were determined in anesthetized rats, using a radioactive microsphere technique. BP, cardiac output, and stroke volume were significantly decreased 30, 60, and 120 min after central administration of ET-1. Heart rate and total peripheral resistance were not altered. ET-1 produced a reduction in blood flow to the brain (83%), heart (62%), kidneys (53%), gastrointestinal tract (43%), portal system (46%), and musculoskeletal system (55%). To determine the role of the central nervous system in cardiovascular effects of centrally administered ET-1, experiments were performed in cervical-sectioned rats. The changes in systemic and regional blood circulation induced by centrally administered ET-1 in normal rats were not observed in cervical-sectioned rats. Pretreatment with a specific antagonist of ETA receptors, BQ-123 (10 micrograms i.c.v.), antagonized systemic and regional circulatory effects of ET-1. Centrally administered clonidine (1 microgram i.c.v.) produced hypotension and bradycardia, known to be mediated through the sympathetic nervous system. Pretreatment with an ETA receptor antagonist, BMS-182874 (50 micrograms/kg iv), blocked clonidine-induced hypotension and bradycardia. We conclude that centrally administered ET-1 stimulates ETA receptors to produce systemic and regional circulatory changes mediated by the sympathetic nervous system.

Cardiovascular effects elicited by central administration of physostigmine via M2 muscarinic receptors in conscious cats

1995 ◽  
Vol 677 (2) ◽  
pp. 268-276 ◽  
Author(s):  
Ahmmed Ally ◽  
L. Britt Wilson ◽  
Antonio C.L. Nóbrega ◽  
Jere H. Mitchell
Keyword(s):  
Muscarinic Receptors ◽  
Cardiovascular Effects ◽  
Central Administration ◽  
M2 Muscarinic Receptors

Cardiovascular activation by serotonergic stimulation: role of corticotropin-releasing factor

1994 ◽  
Vol 267 (3) ◽  
pp. R859-R864 ◽  
Author(s):  
A. Dedeoglu ◽  
L. A. Fisher
Keyword(s):  
Receptor Agonist ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Corticotropin Releasing Factor ◽  
High Dose ◽  
Low Doses ◽  
Intracerebroventricular Administration ◽  
Central Administration ◽  
Pituitary Adrenal Axis

Serotonin (5-HT) and serotonergic agonists stimulate the release of corticotropin-releasing factor (CRF) from hypophysiotropic neurons and thereby activate the pituitary-adrenal axis. Studies were performed to test the hypothesis that the release of CRF into central nervous system (CNS) sites where it influences cardiovascular function is likewise stimulated by serotonergic mechanisms. Experiments were thus designed to examine whether the cardiovascular effects of central administration of low doses of 5-HT and the 5-HT1A receptor agonist, 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT), are secondary to the release of CRF. Intracerebroventricular administration of 5-HT (1 nmol) and 8-OH-DPAT (3 nmol) produced cardiovascular responses similar to those evoked by CRF (0.15 nmol), i.e., simultaneous elevations of arterial pressure and heart rate, in conscious unrestrained rats. Coadministration of the CRF receptor antagonist, alpha-helical CRF-(9-41) (9 nmol), significantly attenuated the pressor and tachycardic responses to 5-HT and 8-OH-DPAT as well as those to injection of CRF. In contrast, coadministration of alpha-helical CRF-(9-41) did not alter the pressor and bradycardic responses to a high dose (100 nmol) of serotonin. It is concluded that the cardiovascular effects of low doses of 5-HT and 8-OH-DPAT are mediated in part through the release of CRF within the CNS.

Mechanisms involved in central cardiovascular effects of prostaglandin F2 alpha

1982 ◽  
Vol 242 (5) ◽  
pp. R545-R551 ◽  
Author(s):  
G. Feuerstein ◽  
C. J. Helke ◽  
R. L. Zerbe ◽  
D. M. Jacobowitz ◽  
I. J. Kopin
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Rectal Temperature ◽  
Cardiovascular Effects ◽  
Plasma Norepinephrine ◽  
Central Administration ◽  
Prostaglandin F2 Alpha ◽  
Arterial Blood ◽  
Norepinephrine Concentration ◽  
Bilateral Vagotomy

Prostaglandin F2 alpha (PGF2 alpha) injected into the cerebroventricular system (icv) of halothane-anesthetized rats increased the arterial blood pressure, heart rate, and rectal temperature. These effects were accompanied by a preferential increase in plasma norepinephrine concentration. Plasma levels of epinephrine, renin, and vasopressin were not changed in the PGF2 alpha-icv-treated rats. Bilateral vagotomy did not affect the PGF2 alpha-induced hypertension and tachycardia nor was there any change in the selective increase in plasma norepinephrine concentration. Hexamethonium pretreatment suppressed, in a dose-response manner, the increases in blood pressure, heart rate, and rectal temperature in response to PGF2 alpha-icv. Plasma norepinephrine and epinephrine levels were not altered by PGF2 alpha-icv in hexamethonium-treated rats, but plasma vasopressin concentration was markedly elevated in all hexamethonium-infused rats. These results suggest that selective central activation of the sympathetic nervous system underlies the profound cardiovascular and temperature responses elicited by central administration of PGF2 alpha.

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