Serotonergic and noradrenergic mechanisms involved in the cardiovascular effects of angiotensin II injected into the anterior hypothalamic preoptic region of rats

1981 ◽  
Vol 20 (1) ◽  
pp. 9-13 ◽  
Author(s):  
E.E. Benarroch ◽  
C.J. Pirola ◽  
Azucena L. Alvarez ◽  
V.E. Nahmod
Keyword(s):  
Angiotensin Ii ◽  
Cardiovascular Effects ◽  
Preoptic Region

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.

Kainic acid lesions of the median preoptic nucleus: effects on angiotensin II induced drinking and pressor responses in the conscious rat

1988 ◽  
Vol 66 (8) ◽  
pp. 1082-1086 ◽  
Author(s):  
D. L. Jones
Keyword(s):  
Angiotensin Ii ◽  
Kainic Acid ◽  
Pressor Response ◽  
Cerebral Ventricle ◽  
Central Administration ◽  
Preoptic Region ◽  
Conscious Rat ◽  
Drinking Response ◽  
Pressor Responses ◽  
Lateral Cerebral Ventricle

Input to the nucleus medianus of the preoptic region has been suggested to be involved in both the drinking and pressor responses elicited by the central administration of angiotensin II. Evidence in support of this suggestion has been gained principally from electrical lesion experiments. This lesion procedure does not differentiate between the cells of the region and fibers coursing through the region. To test the hypothesis that cells in this region are involved in both the pressor and drinking responses elicited by central administration of angiotensin II, injections of kainic acid were made to induce lesions of the cells, while sparing fibers of passage. Drinking and blood pressure responses were determined pre- and post-lesion in the chronically instrumented awake rat. Injections of 50 ng angiotensin II in a 2-μL volume into a lateral cerebral ventricle of the conscious rat elicited pronounced drinking and pressor responses with a latency of 3–5 min. Lesions of the median preoptic region produced by injecting 1.0 μg of kainic acid in 0.25 μL for 15 s attenuated or blocked the drinking response and increased the latency to drink induced by central injections of angiotensin II. However, kainic acid lesions did not significantly alter the pressor responses produced by angiotensin II administration. These results suggest that cells in the median preoptic region are involved in the drinking response but do not participate in the pressor response elicited by angiotensin II administration into a lateral cerebral ventricle of the conscious rat.

Cardiovascular effects of angiotensin II and vasopressin in intact awake rats

1994 ◽  
Vol 25 (3) ◽  
pp. 527-532
Author(s):  
Isabel Hernandez ◽  
Andrés C. Inglés ◽  
Francisco Ruiz ◽  
Tomás Quesada ◽  
Luis F. Carbonell
Keyword(s):  
Angiotensin Ii ◽  
Cardiovascular Effects ◽  
Awake Rats

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.

Cardiovascular effects of angiotensin II and angiotensin-(1–7) at the RVLM of trained normotensive rats

2005 ◽  
Vol 1040 (1-2) ◽  
pp. 121-128 ◽  
Author(s):  
Lenice K. Becker ◽  
Robson A.S. Santos ◽  
Maria José Campagnole-Santos
Keyword(s):  
Angiotensin Ii ◽  
Cardiovascular Effects

scholarly journals Cardiovascular effects of chronically increasing angiotensin II type 2 receptor expression in the nucleus of the solitary tract (874.2)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Prashant Ruchaya ◽  
Graziela Blanch ◽  
Guilherme Speretta ◽  
André Freiria‐Oliveira ◽  
Colin Sumners ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Cardiovascular Effects ◽  
Receptor Expression ◽  
Solitary Tract

Forebrain control of fluid and electrolyte homeostasis and angiotensin sensitivity in rabbit

1980 ◽  
Vol 239 (5) ◽  
pp. R372-R376 ◽  
Author(s):  
G. D. Fink ◽  
W. J. Bryan
Keyword(s):  
Angiotensin Ii ◽  
Third Ventricle ◽  
Extracellular Fluid ◽  
Cardiovascular Effects ◽  
Plasma Potassium ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Electrolyte Balance ◽  
Pressor Responses ◽  
Discrete Area

A small discrete area near the optic recess of the anterior ventral third ventricle (AV3V) in the rat brain has been shown to be an important mediator of cardiovascular and dipsogenic response to angiotensin II and osmotic stimuli and to be involved in normal day-to-day regulation of water and electrolyte balance. However, no attempt has been made until now to explore the function of the AV3V in species other than the rat. In the present study, rabbits subjected to electrolytic lesion of the AV3V exhibited expanded plasma volume and plasma sodium concentration, and significantly attenuated pressor responses to angiotensin II and hypertonic sodium chloride solutions injected via the lateral ventricles. Resting arterial pressure, plasma potassium concentration, extracellular fluid volume, and pressor responses to intravenous angiotensin II were not changed by lesioning. Thus, the effects of AV3V lesions in rabbits are similar, but not identical, to those previously observed in rats. Rabbits should be a suitable species in which to carry out studies aimed at distinguishing central and peripheral cardiovascular effects of angiotensin II.

Sign in / Sign up

Export Citation Format

Share Document