Localization of Central Noradrenergic Mechanisms in Cardiovascular Regulation in Rats

1974 ◽  
Vol 48 (s2) ◽  
pp. 277s-278s ◽  
Author(s):  
H. Struyker Boudier ◽  
G. Smeets ◽  
G. Brouwer ◽  
J. Van Rossum
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Brain Stem ◽  
Cardiovascular Regulation ◽  
Anterior Hypothalamus ◽  
Anaesthetized Rats ◽  
Lower Brain Stem ◽  
The Brain

1. Various drugs were injected stereotactically into the brain of anaesthetized rats. 2. Noradrenaline injected into the area of the nucleus of the tractus solitarius in the lower brain stem or into the far anterior hypothalamus/pre-optic region induced a fall in blood pressure and in heart rate related to the administered dose. 3. When injected into the anterior hypothalamus/pre-optic region, clonidine and alpha-methyl-noradrenaline induced a long-lasting decrease in blood pressure and heart rate.

Cardiovascular actions of microinjections of angiotensin II in the brain stem of rats

1984 ◽  
Vol 246 (5) ◽  
pp. R811-R816 ◽  
Author(s):  
R. Casto ◽  
M. I. Phillips
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Brain Stem ◽  
Nucleus Tractus Solitarius ◽  
Area Postrema ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Ang Ii ◽  
The Brain

The blood pressure and heart rate responses to microinjection of angiotensin II (ANG II) into the brain stem of urethan-anesthetized rats were studied. Microinjection of ANG II into the area postrema (AP) resulted in significant elevation of blood pressure and significant reduction of heart rate. Microinjection into the region of the nucleus tractus solitarius (NTS) yielded a significant dose-dependent elevation in blood pressure and consistent increases in heart rate. The response to microinjection of ANG II into the region of the NTS was not due to leakage into the peripheral circulation, since intravenous administration of the ANG II antagonist, saralasin, did not attenuate the response. In fact, the cardiovascular response was increased after peripheral ANG II blockade, and the heart rate, which was consistently but not significantly elevated by NTS injection alone, was significantly elevated after saralasin pretreatment. Thermal ablation of the AP did not change the heart rate or the pressor response to microinjection of ANG II into the region of the NTS, indicating that the response was not mediated through the AP.

Brain stem augmentation of cardiovascular activity

1960 ◽  
Vol 198 (2) ◽  
pp. 421-423 ◽  
Author(s):  
Richard L. Glasser
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Brain Stem ◽  
Cardiovascular Activity ◽  
Rostral Portion ◽  
The Brain ◽  
Pontomedullary Junction

Midpontile ischemic decerebration in vagotomized mesencephalic cats produced marked tachycardia and hypertension. Subsequent transection of the brain stem at or above the midpontile level did not affect the cardiovascular hyperactivity. Transection at the pontomedullary junction abolished the brain stem augmentation of heart rate and blood pressure. The results suggest the existence of a cardiovascular augmenter area in the caudal half of the pons and a cardiovascular depressor area in a more rostral portion of the brain stem.

Caffeine and Placebo Expectation

2007 ◽  
Vol 21 (2) ◽  
pp. 91-99 ◽  
Author(s):  
Yunfeng Sun ◽  
Yinling Zhang ◽  
Ning He ◽  
Xufeng Liu ◽  
Danmin Miao
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Sleep Deprivation ◽  
Cognitive Performance ◽  
Cognitive Functions ◽  
Cardiovascular Regulation ◽  
Double Blind ◽  
Positive Effects ◽  
Pressure Tests ◽  
Healthy Males

Abstract. Caffeine placebo expectation seems to improve vigilance and cognitive performance. This study investigated the effect of caffeine and placebo expectation on vigilance and cognitive performance during 28 h sleep deprivation. Ten healthy males volunteered to take part in the double-blind, cross-over study, which required participants to complete five treatment periods of 28 h separated by 1-week wash-out intervals. The treatments were no substance (Control); caffeine 200 mg at 00:00 (C200); placebo 200 mg at 00:00 (P200); twice caffeine 200 mg at 00:00 and 04:00 (C200-C200); caffeine 200 mg at 00:00 and placebo 200 mg at 04:00 (C200-P200). Participants were told that all capsules were caffeine and given information about the effects of caffeine to increase expectation. Vigilance was assessed by a three-letter cancellation test, cognitive functions by the continuous addition test and Stroop test, and cardiovascular regulation by heart rate and blood pressure. Tests were performed bihourly from 00:00 to 10:00 of the second day. Results indicated that C200-P200 and C200-C200 were more alert (p < .05) than Control and P200. Their cognitive functions were higher (p < .05) than Control and P200. Also, C200-P200 scored higher than C200 in the letter cancellation task (p < .05). No test showed any significant differences between C200-P200 and C200-C200. The results demonstrated that the combination of caffeine 200 mg and placebo 200 mg expectation exerted prolonged positive effects on vigilance and cognitive performance.

Variability of the haemodynamic responses to laboratory tests employed in assessment of neural cardiovascular regulation in man

1985 ◽  
Vol 69 (5) ◽  
pp. 533-540 ◽  
Author(s):  
Gianfranco Parati ◽  
Guido Pomidossi ◽  
Agustin Ramirez ◽  
Bruno Cesana ◽  
Giuseppe Mancia
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Test Performance ◽  
Blood Pressure Response ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Cardiovascular Regulation ◽  
Pressor Test ◽  
Carotid Baroreceptor ◽  
Baroreceptor Stimulation

1. In man evaluation of neural cardiovascular regulation makes use of a variety of tests which address the excitatory and reflex inhibitory neural influences that control circulation. Because interpretation of these tests is largely based on the magnitude of the elicited haemodynamic responses, their reproducibility in any given subject is critical. 2. In 39 subjects with continuous blood pressure (intra-arterial catheter) and heart rate monitoring we measured (i) the blood pressure and heart rate rises during hand-grip and cold-pressor test, (ii) the heart rate changes occurring during baroreceptor stimulation and deactivation by injection of phenylephrine and trinitroglycerine, and (iii) the heart rate and blood pressure changes occurring with alteration in carotid baroreceptor activity by a neck chamber. Each test was carefully standardized and performed at 30 min intervals for a total of six times in each subject. 3. The results showed that the responses to any test were clearly different from one another and that this occurred in all subjects studied. For the group as a whole the average response variability (coefficient of variation) ranged from 10.2% for the blood pressure response to carotid baroreceptor stimulation to 44.2% for the heart rate response to cold-pressor test. The variability of the responses was not related to basal blood pressure or heart rate, nor to the temporal sequence of the test performance. 4. Thus tests employed for studying neural cardiovascular control in man produce responses whose reproducibility is limited. This phenomenon may make it more difficult to define the response magnitude typical of each subject, as well as its comparison in different conditions and diseases.

scholarly journals Acute Changes in Blood Pressure Following Vascular Diseases in the Brain Stem

Stroke ◽  
1973 ◽  
Vol 4 (1) ◽  
pp. 80-84 ◽  
Author(s):  
AKIRA ITO ◽  
TERUO OMAE ◽  
SHIBANOSUKE KATSUKI
Keyword(s):  
Blood Pressure ◽  
Brain Stem ◽  
Vascular Diseases ◽  
Acute Changes ◽  
The Brain

Abstract P059: A A Role of Aminopeptidase A in the Brain on Cardiovascular Regulation of Conscious Rat

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Takuto Nakamura ◽  
Masanobu Yamazato ◽  
Akio Ishida ◽  
Yusuke Ohya
Keyword(s):  
Blood Pressure ◽  
Protein Expression ◽  
Drinking Behavior ◽  
Cardiovascular Regulation ◽  
Ang Ii ◽  
Hypertensive Rats ◽  
Aminopeptidase A ◽  
The Brain

Objective: Aminopeptidase A (APA) have important role in conversion of Ang II to Ang III. Intravenous APA administration lowers blood pressure in hypertensive rats. In contrast, APA inhibition in the brain lowers blood pressure in hypertensive rats. Therefore APA might have different role on cardiovascular regulation. However, a role of APA and Ang III on cardiovascular regulation especially in the brain has not been fully understood. Our purpose of present study was to investigate a role of APA and Ang III in the brain on cardiovascular regulation in conscious state. Method: 12-13 weeks old Wistar Kyoto rat (WKY) and 12-16 weeks old spontaneously hypertensive rat (SHR) were used. i) APA distribution in the brain was evaluated by immunohistochemistry. Protein expression of APA was evaluated by Western blotting. Enzymatic activity of APA was evaluated using L-glutamic acid γ-(4-nitroanilide) as a substrate. ii) WKY received icv administration of Ang II 25ng/2μL and Ang III 25ng/2μL. We recorded change in mean arterial pressure (MAP) in conscious and unrestraied state and measured induced drinking time. iii) SHR received icv administeration of recombinant APA 400ng/4μL. We recorded change in MAP in conscious and unrestraied state and measured induced drinking time. Result: i) APA was diffusely immunostained in the cells of brain stem including cardiovascular regulatory area such as rostral ventrolateral medulla. Protein expression and APA activity in the brain were similar between WKY (n=3) and SHR (n=3).ii) Icv administration of Ang II increased MAP by 33.8±3.8 mmHg and induced drinking behavior for 405±90 seconds (n=4). Icv administration of Ang III also increased MAP by 24.7±2.4 mmHg and induced drinking behavior for 258±62 seconds (n=3). These vasopressor activity and induced drinking behavior was completely blocked by pretretment of angiotensin receptor type 1 blocker.iii) Icv administration of APA increased MAP by 10.0±1.7 mmHg (n=3). Conclusion: These results suggested that Ang III in the brain increase blood pressure by Angiotensin type 1 receptor dependent mechanism and APA in the brain may involved in blood pressure regulation as a vasopressor enzyme.

Effect of Baroreceptor Deafferentation on Central Catecholamines in the Rat

1979 ◽  
Vol 57 (s5) ◽  
pp. 221s-223s ◽  
Author(s):  
Margaret A. Petty ◽  
J. P. Chalmers ◽  
M. Brown ◽  
J. L. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Tyrosine Hydroxylase ◽  
Brain Stem ◽  
Hydroxylase Activity ◽  
Methyltransferase Activity ◽  
Neurogenic Hypertension ◽  
Noradrenaline Synthesis ◽  
Noradrenaline And Adrenaline ◽  
Sympathetic Efferent Activity

1. Sinoaortic deafferentation in the rat leads to increased blood pressure and heart rate. 2. Early increases in tyrosine hydroxylase activity both in brain stem and hypothalamus suggest that increased noradrenaline synthesis may contribute to the development of neurogenic hypertension. 3. After 4 weeks, phenylethanolamine-N-methyltransferase activity was reduced in the hypothalamus. 4. Noradrenaline- and adrenaline, but not dopamine-containing neurones may participate in regulation of sympathetic efferent activity.

scholarly journals Methane, a gut bacteria-produced gas, does not affect arterial blood pressure in normotensive anaesthetized rats.

2021 ◽  
Author(s):  
Ewelina Zaorska ◽  
Marta Gawrys-Kopczynska ◽  
Ryszard Ostaszewski ◽  
Dominik Koszelewski ◽  
Marcin Ufnal
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Acute Administration ◽  
Hemodynamic Effects ◽  
Arterial Blood ◽  
Anaesthetized Rats ◽  
Carbohydrate Fermentation ◽  
Oxidative Effects ◽  
Lines Of Evidence

Methane is produced by carbohydrate fermentation in the gastrointestinal tract through the metabolism of methanogenic microbiota. Several lines of evidence suggest that methane exerts anti-inflammatory, anti-apoptotic and anti-oxidative effects. The effect of methane on cardiovascular system is obscure. The objective of the present study was to evaluate the hemodynamic response to methane. A vehicle or methane-rich saline were administered intravenously or intraperitoneally in normotensive anaesthetized rats. We have found no significant effect of the acute administration of methane-rich saline on arterial blood pressure and heart rate in anaesthetized rats. Our study suggests that methane does not influence the control of arterial blood pressure. However, further chronic studies may be needed to fully understand hemodynamic effects of the gas.

Abstract P152: Aminopeptidase A in the Brain Exerts Cardiovascular Action via Degradation of Kallidin to Bradykinin

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Takuto Nakamura ◽  
Masanobu Yamazato ◽  
Yusuke Ohya
Keyword(s):  
Blood Pressure ◽  
Pressor Response ◽  
Cardiovascular Regulation ◽  
Receptor Blocker ◽  
Ang Ii ◽  
Aminopeptidase A ◽  
Hoe 140 ◽  
Wistar Kyoto ◽  
The Brain

Objective: Aminopeptidase A (APA) degrades of various sympathomodulatory peptides such as angiotensin (Ang) II, cholecystkinin-8, neurokinin B and kallidin. APA activity is increased in the brain of hypertensive rats. A centrally acting APA inhibitor prodrug is currently under investigation in clinical trial for treatment of hypertension. In previous reports, a role of APA in the brain on cardiovascular regulation was researched focus on only renin-angiotensin system. We previously reported that intracerebroventricular(icv) administration of APA increased blood pressure and that this pressor response was partially blocked by angiotensin receptor blocker. In this study, we evaluated a role of APA on cardiovascular regulation focusing on peptides other than Ang II. Method: Eleven weeks old Wistar Kyoto rats were used. We icv administrated 800 ng/8 μL of APA after pretreatment of following drugs, i) 8μL of artificial cerebrospinal fluid (aCSF) as a control, ii) 80 nmol/8 μL of amastatin which is a non-specific aminopeptidase inhibitor, iii) 1 nmol/8 μL of HOE-140 which is a bradykinin receptor blocker to evaluate the involvement of degradation of kallidin to bradykinin by APA. Result: i) Icv administration of APA after pretreatment of aCSF increased blood pressure rapidly. Blood pressure reached a peak within 1 minute. The elevated blood pressure decreased gradually and reached baseline blood pressure in 10 minutes. A peak pressor response is 25.5±1.4 mmHg (n=5). ii) Icv pretreatment of amastatin or HOE-140 did not change the blood pressure. A peak pressor response induced by APA is 13.1±4.1 mmHg (n=6, p<0.05 vs aCSF). iii) Icv pretreatment of HOE-140 did not change the blood pressure. A peak pressor response induced by APA is 21.2±1.8 mmHg (n=4, p<0.05 vs aCSF). Conclusion: 1) Icv administration of APA increased blood pressure by APA enzymatic activity. 2) Cardiovascular regulation of APA in the brain is due to not only degradation of Ang II to Ang III but also degradation of kallidin to bradykinin. Clinical implication: We think inhibition of APA in the brain may be a unique therapeutic target which affects several cardiovascular peptides in the brain.

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