Effects of angiotensins on day-night fluctuations and stress-induced changes in blood pressure

2002 ◽  
Vol 282 (6) ◽  
pp. R1663-R1671 ◽  
Author(s):  
Aline Nardoni Gonçalves Braga ◽  
Marisa Da Silva Lemos ◽  
José Roberto Da Silva ◽  
Walkíria Ramos Peliky Fontes ◽  
Robson Augusto Souza Dos Santos
Keyword(s):  
Blood Pressure ◽  
Restraint Stress ◽  
Control Period ◽  
Circadian Variation ◽  
Cardiovascular Responses ◽  
Ang Ii ◽  
Brain Areas ◽  
Induced Changes ◽  
Infusion Period

In this study we evaluated by telemetry the effects of ANG II and ANG-(1–7) infusion on the circadian rhythms of blood pressure (BP) and heart rate (HR) and on the cardiovascular adjustment resulting from restraint stress in rats. ANG II or ANG-(1–7) or vehicle were infused subcutaneously for 7 days. Restraint stress was carried out before, during, and after infusion at 7-day intervals. Parallel with an increase in MAP, ANG II infusion produced an inversion of MAP circadian rhythm with a significant MAP acrophase inversion. It also produced bradycardia during the first 3 days of infusion. Thereafter, HR progressively increased, reaching values similar to or above those of the control period at the end of the infusion period. HR circadian variation was not changed by ANG II infusion. Strikingly, ANG II significantly attenuated the increase in MAP induced by restraint stress without altering the HR response. ANG-(1–7) infusion produced a slight but significant decrease in MAP restricted to the daytime period. No significant changes in the MAP acrophase were observed. In addition, ANG-(1–7) infusion produced a small but significant sustained bradycardia. ANG-(1–7) did not change cardiovascular responses to restraint stress. These data indicate that ANG II can influence the activity of brain areas involved in the determination of stress-induced or circadian-dependent variations of blood pressure without changing HR fluctuations. A significant modulatory influence of ANG-(1–7) on basal MAP and HR is also suggested.

Comparison of fast and slow pressor effects of angiotensin II in the conscious rat

1981 ◽  
Vol 241 (3) ◽  
pp. H381-H388 ◽  
Author(s):  
A. J. Brown ◽  
J. Casals-Stenzel ◽  
S. Gofford ◽  
A. F. Lever ◽  
J. J. Morton
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Control Period ◽  
Urinary Sodium Excretion ◽  
Sodium Balance ◽  
Pressor Effect ◽  
Ang Ii ◽  
Conscious Rat ◽  
Female Wistar Rats

Female Wistar rats were infused intravenously with 5% dextrose for 3 days, then with angiotensin II (ANG II) in 5% dextrose at 20 ng . kg-1 . min-1 for 7 days, and finally with dextrose for 2.5 days. ANG II raised mean arterial pressure (MAP) gradually; by the 7th day it was 49.7 mmHg higher than during the dextrose control period in the same rats. Control rats were infused with dextrose for 12.5 days; MAP did not change. Plasma ANG II concentration was measured during infusion. In hypertensive rats on the 7th day of ANG II infusion, it was six times higher than in control rats infused with dextrose. Changes of blood pressure and plasma ANG II concentration were compared in further rats infused with much larger doses of ANG II. Rats receiving 270 ng . kg-1 . min-1 for 1 h had an almost maximal direct pressor response, MAP rising 45.3 mmHg and plasma ANG II rising 32-fold compared with controls. Thus, infusion of ANG II at low dose without direct pressor effect gradually raises blood pressure to a level similar to the maximum direct pressor effect produced by larger doses of ANG II. Sodium balance and food and water intakes were also measured and did not change during prolonged infusion of ANG II at 20 ng . kg-1 . min-1. Thus, the slow pressure effect of ANG II develops at a lower and more nearly physiological plasma concentration of the peptide than do the direct pressor effect and the effects on drinking, eating, and urinary sodium excretion.

Interactions between ANG II, sympathetic nervous system, and baroreceptor reflexes in regulation of blood pressure

1992 ◽  
Vol 262 (6) ◽  
pp. E763-E778 ◽  
Author(s):  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Blood Pressure Control ◽  
Cardiovascular Responses ◽  
Pressure Control ◽  
Ang Ii ◽  
Arterial Blood ◽  
Baroreceptor Reflexes ◽  
Sympathetic Nervous

The renin-angiotensin system plays an important role in the regulation of arterial blood pressure and in the development of some forms of clinical and experimental hypertension. It is an important blood pressure control system in its own right but also interacts extensively with other blood pressure control systems, including the sympathetic nervous system and the baroreceptor reflexes. Angiotensin (ANG) II exerts several actions on the sympathetic nervous system. These include a central action to increase sympathetic outflow, stimulatory effects on sympathetic ganglia and the adrenal medulla, and actions at sympathetic nerve endings that serve to facilitate sympathetic neurotransmission. ANG II also interacts with baroreceptor reflexes. For example, it acts centrally to modulate the baroreflex control of heart rate, and this accounts for its ability to increase blood pressure without causing a reflex bradycardia. The physiological significance of these actions of ANG II is not fully understood. Most evidence indicates that the actions of ANG to enhance sympathetic activity do not contribute significantly to the pressor response to exogenous ANG II. On the other hand, there is considerable evidence that the actions of endogenous ANG II on the sympathetic nervous system enhance the cardiovascular responses elicited by activation of the sympathetic nervous system.

Alterations in Blood Pressure and Heart Rate Variabililty in Transgenic Rats with Low Brain Angiotensinogen

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 727-727
Author(s):  
Ovidiu Baltatu ◽  
Ben J Janssen ◽  
Ralph Plehm ◽  
Detlev Ganten ◽  
Michael Bader
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Baroreflex Sensitivity ◽  
Circadian Variation ◽  
Ang Ii ◽  
Transgenic Rats ◽  
Short Term ◽  
Baroreflex Control ◽  
Sd Rats ◽  
The Brain

P191 The brain renin-angiotensin system (RAS) system may play a functional role in the long-term and short-term control of blood pressure (BPV) and heart rate variability (HRV). To study this we recorded in transgenic rats TGR(ASrAOGEN) with low brain angiotensinogen levels the 24-h variation of BP and HR during basal and hypertensive conditions, induced by a low-dose s.c. infusion of angiotensin II (Ang II, 100 ng/kg/min) for 7 days. Cardiovascular parameters were monitored by telemetry. Short-term BPV and HRV were evaluated by spectral analysis and as a measure of baroreflex sensitivity the transfer gain between the pressure and heart rate variations was calculated. During the Ang II infusion, in SD but not TGR(ASrAOGEN) rats, the 24-h rhythm of BP was inverted (5.8 ± 2 vs. -0.4 ± 1.8 mm Hg/group of day-night differences of BP, p< 0.05, respectively). In contrast, in both the SD and TGR(ASrAOGEN) rats, the 24-h HR rhythms remained unaltered and paralleled those of locomotor activity. The increase of systolic BP was significantly reduced in TGR(ASrAOGEN) in comparison to SD rats as previously described, while the HR was not altered in TGR(ASrAOGEN) nor in SD rats. The spectral index of baroreflex sensitivity (FFT gain between 0.3-0.6 Hz) was significantly higher in TGR(ASrAOGEN) than SD rats during control (0.71 ± 0.1 vs. 0.35 ± 0.06, p<0.05), but not during Ang II infusion (0.6 ± 0.07 vs. 0.4 ± 0.1, p>0.05). These results demonstrate that the brain RAS plays an important role in mediating the effects of Ang II on the circadian variation of BP. Furthermore these data are consistent with the view that the brain RAS modulates baroreflex control of HR in rats, with AII having an inhibitory role.

scholarly journals Renal effects of oral prostaglandin supplementation after ibuprofen in diabetic subjects: a double-blind, placebo-controlled, multicenter trial.

1995 ◽  
Vol 5 (9) ◽  
pp. 1684-1688
Author(s):  
G L Bakris ◽  
U Starke ◽  
M Heifets ◽  
D Polack ◽  
M Smith ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Insufficiency ◽  
Fractional Excretion ◽  
Multicenter Trial ◽  
Common Side Effect ◽  
Double Blind ◽  
Entire Study ◽  
Fractional Excretion Of Sodium ◽  
Induced Changes

Prostaglandins of the E series (PGE) are known to contribute to the maintenance of renal hemodynamics in subjects with chronic renal insufficiency. Agents that block PGE synthesis, nonsteroidal anti-inflammatory agents (NSAID), are widely used by people with renal insufficiency. This study was undertaken in subjects with renal insufficiency secondary to diabetes to evaluate the acute effects of a PGE1 analog, misoprostol, on NSAID-induced changes in RBF, as calculated by para-aminohippurate clearance, and GFR, as calculated by inulin clearance. Sodium excretion was also assessed. Twenty-five fasting subjects with a mean age of 56 +/- 4 yr received 800 mg of ibuprofen orally. A concomitant dose of either a placebo (PL) or 200 micrograms of misoprostol was also given. This was followed in 1 h by either a placebo or an additional 200-micrograms dose of misoprostol. Measurements for the determination of RBF, GFR, blood pressure, and fractional excretion of sodium were performed every 30 min for the next 5 h. The greatest reduction in both GFR (-25 +/- 7 mL/min per 1.73 m2 PL versus -10 +/- 4 mL/min per 1.73 m2, misoprostol delta GFR; P < 0.05) and RBF (-48 +/- 21 mL/min per 1.73 m2 PL versus -15 +/- 8 mL/min per 1.73 m2, M delta RBF; P < 0.05) occurred approximately 2 h after the NSAID dose. No significant differences were noted in blood pressure, fractional excretion of sodium, or other measured parameters between groups during the entire study. Gastrointestinal upset was the most common side effect observed in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Fetal placental vascular responses to prostacyclin after angiotensin II-induced vasoconstriction

1989 ◽  
Vol 257 (1) ◽  
pp. E102-E107
Author(s):  
V. M. Parisi ◽  
S. W. Walsh
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Control Period ◽  
Vena Cava ◽  
Ang Ii ◽  
Flow Measurements ◽  
Control Value ◽  
Blood Flow Measurements ◽  
Infusion Period

The vasodilator prostacyclin is produced by many fetal tissues and may serve to protect umbilical placental blood flow. We hypothesized that prostacyclin could reverse fetoplacental vasoconstriction produced by angiotensin II (ANG II). Studies were done in eight unanesthetized near-term ovine fetuses. After a control period, ANG II was infused into the fetal inferior vena cava at a rate of 0.5 microgram/min for 40 min. Twenty minutes after starting the ANG II infusion, an infusion of prostacyclin at a rate of 5 micrograms/min was added to the ANG II infusion. Blood flows were measured by the radioactive microsphere technique. Blood flow measurements were made during the control period, 20 min after starting the ANG II infusion, and 20 min after adding prostacyclin to the ANG II infusion. ANG II produced significant fetal hypertension and renal, intestinal, and placental vasoconstriction. Placental vascular resistance rose from 0.14 +/- 0.01 to 0.18 +/- 0.01 mmHg.min.kg fetal wt.ml-1 during the ANG II infusion period (P less than 0.05). The addition of prostacyclin to the ANG II infusion resulted in a return to control values for fetal blood pressure and renal and intestinal resistance. However, placental vasoconstriction was not reversed by addition of prostacyclin as placental vascular resistance remained significantly elevated over the control value (0.17 +/- 0.01 mmHg.min.kg fetal wt.ml-1). Although unchanged by ANG II infusion, fetal pH decreased significantly during the ANG II plus prostacyclin infusion period. We conclude that ANG II causes fetal hypertension and renal and intestinal vasoconstriction, which are reversed by prostacyclin.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Novel mechanism within the paraventricular nucleus reduces both blood pressure and hypothalamic pituitary-adrenal axis responses to acute stress

2015 ◽  
Vol 309 (4) ◽  
pp. H634-H645 ◽  
Author(s):  
Benedek Erdos ◽  
Rebekah R. Clifton ◽  
Meng Liu ◽  
Hongwei Li ◽  
Michael L. McCowan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Water Stress ◽  
Paraventricular Nucleus ◽  
Viral Vector ◽  
Cardiovascular Responses ◽  
Hypothalamic Pituitary Adrenal Axis ◽  
Ang Ii ◽  
Hypothalamic Pituitary Adrenal ◽  
Adrenal Axis ◽  
Pituitary Adrenal Axis

Macrophage migration inhibitory factor (MIF) counteracts pressor effects of angiotensin II (ANG II) in the paraventricular nucleus of the hypothalamus (PVN) in normotensive rats, but this mechanism is absent in spontaneously hypertensive rats (SHRs) due to a lack of MIF in PVN neurons. Since endogenous ANG II in the PVN modulates stress reactivity, we tested the hypothesis that replacement of MIF in PVN neurons would reduce baseline blood pressure and inhibit stress-induced increases in blood pressure and plasma corticosterone in adult male SHRs. Radiotelemetry transmitters were implanted to measure blood pressure, and then an adeno-associated viral vector expressing either enhanced green fluorescent protein (GFP) or MIF was injected bilaterally into the PVN. Cardiovascular responses to a 15-min water stress (1-cm deep, 25°C) and a 60-min restraint stress were evaluated 3–4 wk later. MIF treatment in the PVN attenuated average restraint-induced increases in blood pressure (37.4 ± 2.0 and 27.6 ± 3.5 mmHg in GFP and MIF groups, respectively, P < 0.05) and corticosterone (42 ± 2 and 36 ± 3 μg/dl in GFP and MIF groups, respectively, P < 0.05). MIF treatment in the PVN also reduced stress-induced elevations in the number of c-Fos-positive cells in the rostral ventrolateral medulla (71 ± 5 in GFP and 47 ± 5 in MIF SHRs, P < 0.01) and corticotropin-releasing factor mRNA expression in the PVN. However, MIF had no significant effects on the cardiovascular responses to water stress in SHRs or to either stress in Sprague-Dawley rats. Therefore, viral vector-mediated restoration of MIF in PVN neurons of SHRs attenuates blood pressure and hypothalamic pituitary adrenal axis responses to stress.

scholarly journals Air pollution and cardiac remodeling: a role for RhoA/Rho-kinase

2009 ◽  
Vol 296 (5) ◽  
pp. H1540-H1550 ◽  
Author(s):  
Zhekang Ying ◽  
Peibin Yue ◽  
Xiaohua Xu ◽  
Mianhua Zhong ◽  
Qinghua Sun ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Air Pollution ◽  
Cardiac Remodeling ◽  
Rho Kinase ◽  
Cardiovascular Responses ◽  
Ambient Air ◽  
Ambient Air Pollution ◽  
Experimental Hypertension ◽  
Ang Ii ◽  
Rhoa Activation

Exposure to ambient air pollution has been associated with increases in blood pressure. We have previously demonstrated activation of the Rho/Rho kinase pathway in experimental hypertension in rats. In this investigation, we evaluated the effects of particulate matter of <2.5 μm (PM2.5) exposure on cardiovascular responses and remodeling and tested the effect of Rho kinase inhibition on these effects. C57BL/6 mice were exposed to concentrated ambient PM2.5 or filtered air for 12 wk followed by a 14-day ANG II infusion in conjunction with fasudil, a Rho kinase antagonist, or placebo treatment. Blood pressure was monitored, followed by analysis of vascular function and ventricular remodeling indexes. PM2.5 exposure potentiated ANG II-induced hypertension, and this effect was abolished by fasudil treatment. Cardiac and vascular RhoA activation was enhanced by PM2.5 exposure along with increased expression of the guanine exchange factors (GEFs) PDZ-RhoGEF and p115 RhoGEF in PM2.5-exposed mice. Parallel with increased RhoA activation, PM2.5 exposure increased ANG II-induced cardiac hypertrophy and collagen deposition, with these increases being normalized by fasudil treatment. In conclusion, PM2.5 potentiates cardiac remodeling in response to ANG II through RhoA/Rho kinase-dependent mechanisms. These findings have implications for the chronic cardiovascular health effects of air pollution.

scholarly journals Inhibition of BDNF signaling in the paraventricular nucleus of the hypothalamus lowers acute stress-induced pressor responses

2018 ◽  
Vol 120 (2) ◽  
pp. 633-643 ◽  
Author(s):  
Chris L. Schaich ◽  
Theresa L. Wellman ◽  
Zachary Einwag ◽  
Richard A. Dutko ◽  
Benedek Erdos
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Body Weight ◽  
Food Intake ◽  
Paraventricular Nucleus ◽  
Neurotrophic Factor ◽  
Restraint Stress ◽  
Acute Stress ◽  
Cardiovascular Responses ◽  
High Affinity

Brain-derived neurotrophic factor (BDNF) expression increases in the paraventricular nucleus of the hypothalamus (PVN) during stress, and our recent studies indicate that BDNF induces sympathoexcitatory and hypertensive responses when injected acutely or overexpressed chronically in the PVN. However, it remained to be investigated whether BDNF is involved in the mediation of stress-induced cardiovascular responses. Here we tested the hypothesis that inhibition of the high-affinity BDNF receptor TrkB in the PVN diminishes acute stress-induced cardiovascular responses. Male Sprague-Dawley rats were equipped with radiotelemetric transmitters for blood pressure measurement. BDNF-TrkB signaling was selectively inhibited by viral vector-mediated bilateral PVN overexpression of a dominant-negative truncated TrkB receptor (TrkB.T1, n = 7), while control animals ( n = 7) received green fluorescent protein (GFP)-expressing vector injections. Rats were subjected to acute water and restraint stress 3–4 wk after vector injections. We found that body weight, food intake, baseline mean arterial pressure (MAP), and heart rate were unaffected by TrkB.T1 overexpression. However, peak MAP increases were significantly reduced in the TrkB.T1 group compared with GFP both during water stress (GFP: 39 ± 2 mmHg, TrkB.T1: 27 ± 4 mmHg; P < 0.05) and restraint stress (GFP: 41 ± 3 mmHg, TrkB.T1: 34 ± 2 mmHg; P < 0.05). Average MAP elevations during the poststress period were also significantly reduced after both water and restraint stress in the TrkB.T1 group compared with GFP. In contrast, heart rate elevations to both stressors remained unaffected by TrkB.T1 overexpression. Our results demonstrate that activation of BDNF high-affinity TrkB receptors within the PVN is a major contributor to acute stress-induced blood pressure elevations. NEW & NOTEWORTHY We have shown that inhibition of the high-affinity brain-derived neurotrophic factor receptor TrkB in the paraventricular nucleus of the hypothalamus significantly reduces blood pressure elevations to acute stress without having a significant impact on resting blood pressure, body weight, and food intake.

Spinal angiotensin II influences reflex cardiovascular responses to muscle contraction

1995 ◽  
Vol 269 (4) ◽  
pp. R864-R868 ◽  
Author(s):  
C. L. Stebbins ◽  
S. Bonigut
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Angiotensin Ii ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Ang Ii ◽  
Exercise Pressor Reflex ◽  
Static Contraction ◽  
Pressor Reflex

We tested the hypothesis that inhibition of angiotensin II (ANG II) AT1 receptors in the thoracic spinal cord attenuates the reflex cardiovascular response to electrically induced hindlimb static contraction (exercise pressor reflex). Consequently, in alpha-chloralose-anesthetized cats, contraction-induced increases in mean arterial blood pressure, maximal rate of rise in left ventricular pressure (dP/dt), and heart rate were compared before and after intrathecal injection of the AT1 receptor antagonist losartan (100 or 1,000 micrograms; n = 7). Losartan significantly diminished increases in blood pressure and maximal dP/dt provoked by static contraction by 33 +/- 5 and 31 +/- 6%, respectively. Conversely, these contraction-induced responses were unaffected by similar injection of ANG II into the lumbosacral spinal cord (n = 5). Moreover, intravenous injection of 100 micrograms losartan did not affect the cardiovascular response to contraction. Our data suggest that ANG II has a excitatory effect on the efferent arm of the exercise pressor reflex, which may be due to a facilitatory action on sympathetic nerve activity.

mu-Opioid peptide modulation of cardiovascular and sympathoadrenal responses to stress

1989 ◽  
Vol 257 (4) ◽  
pp. R901-R908 ◽  
Author(s):  
L. Marson ◽  
J. A. Kiritsy-Roy ◽  
G. R. Van Loon
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Restraint Stress ◽  
Plasma Catecholamines ◽  
Cardiovascular Responses ◽  
Opioid Peptide ◽  
Receptor Activation ◽  
Plasma Catecholamine ◽  
Arterial Blood ◽  
Selective Agonist

The effects of mu- and delta-opioid receptor activation on sympathoadrenal and cardiovascular responses to stress were examined in conscious rats. The mu-selective agonist [D-Ala2,N-Me-Phe4,Gly5-ol]enkephalin (DAGO) or the delta-selective agonist [D-Pen2,D-Pen5]enkephalin (DPDPE) was injected into a lateral cerebral ventricle, then rats were stressed by restraint. Plasma catecholamines were measured, and arterial blood pressure and heart rate were recorded continuously. Restraint stress evoked increases in plasma catecholamines and heart rate in saline-pretreated rats. Both DAGO and DPDPE increased basal plasma levels of catecholamines and blood pressure, and DAGO, 5 nmol, produced bradycardia. DAGO, 5 nmol, but not DPDPE, potentiated the plasma catecholamine responses to restraint. However, the presence of DAGO or DPDPE during restraint resulted in decreases in heart rate and blood pressure. The effects of DAGO and DPDPE on plasma catecholamines, heart rate, and blood pressure were blocked by a mu-selective dose of naloxone but were not reversed by the delta-selective antagonist ICI 174864. These results indicate that mu-receptor stimulation during restraint stress facilitates sympathoadrenal and parasympathetic outflow and results in vasodilatation of some peripheral vascular beds.

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