c-fos antisense in rostral ventral medulla reduces arterial blood pressure

1994 ◽  
Vol 266 (4) ◽  
pp. R1418-R1422 ◽  
Author(s):  
S. Suzuki ◽  
P. Pilowsky ◽  
J. Minson ◽  
L. Arnolda ◽  
I. J. Llewellyn-Smith ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Antisense Oligonucleotide ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Arterial Blood ◽  
Ventral Medulla ◽  
Wistar Kyoto

The effect of blocking the expression of c-fos in the rostral ventral medulla (RVM) on the control of arterial blood pressure was determined. In six male Wistar-Kyoto rats (WKY), unilateral injection of an antisense oligonucleotide to c-fos mRNA suppressed the expression of Fos-like immunoreactivity in neurons in the RVM in response to inhibition of depressor neurons in the caudal ventrolateral medulla (CVLM). Under pentobarbital anesthesia the mean arterial pressure of rats injected with antisense oligonucleotide (n = 10) bilaterally into RVM was significantly reduced after 6 h compared with sense-treated controls (n = 9) (76.5 +/- 3.7 vs. 92.4 +/- 3.5 mmHg; P < 0.05). Furthermore, the pressor response to bilateral injection of muscimol into CVLM was significantly smaller in rats injected with antisense oligonucleotide 6 h earlier (n = 6) compared with sense-treated controls (n = 6) (changes in mean arterial pressure, +40.3 +/- 3.6 vs. +68.7 +/- 4.8 mmHg, P < 0.005). These studies demonstrate that expression of c-fos in the RVM can be blocked in vivo by treatment with an antisense oligonucleotide, and that basal and stimulated expression of the c-fos gene is important in the central control of arterial blood pressure.

scholarly journals Plasticity in breathing and arterial blood pressure following acute intermittent hypercapnic hypoxia in infant rat pups with a partial loss of 5-HT neurons

2015 ◽  
Vol 309 (10) ◽  
pp. R1273-R1284 ◽  
Author(s):  
Jennifer Magnusson ◽  
Kevin J. Cummings
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Partial Loss ◽  
Rat Pups ◽  
Arterial Blood ◽  
Hypercapnic Hypoxia ◽  
Long Term Facilitation

The role of serotonin (5-HT) neurons in cardiovascular responses to acute intermittent hypoxia (AIH) has not been studied in the neonatal period. We hypothesized that a partial loss of 5-HT neurons would reduce arterial blood pressure (BP) at rest, increase the fall in BP during hypoxia, and reduce the long-term facilitation of breathing (vLTF) and BP following AIH. We exposed 2-wk-old, 5,7-dihydroxytryptamine-treated and controls to AIH (10% O2; n = 13 control, 14 treated), acute intermittent hypercapnia (5% CO2; n = 12 and 11), or acute intermittent hypercapnic hypoxia (AIHH; 10% O2, 5% CO2; n = 15 and 17). We gave five 5-min challenges of AIH and acute intermittent hypercapnia, and twenty ∼20-s challenges of AIHH to mimic sleep apnea. Systolic BP (sBP), diastolic BP, mean arterial pressure, heart rate (HR), ventilation (V̇e), and metabolic rate (V̇o2) were continuously monitored. 5,7-Dihydroxytryptamine induced an ∼35% loss of 5-HT neurons from the medullary raphe. Compared with controls, pups deficient in 5-HT neurons had reduced resting sBP (∼6 mmHg), mean arterial pressure (∼5 mmHg), and HR (56 beats/min), and experienced a reduced drop in BP during hypoxia. AIHH induced vLTF in both groups, reflected in increased V̇e and V̇e/V̇o2, and decreased arterial Pco2. The sBP of pups deficient in 5-HT neurons, but not controls, was increased 1 h following AIHH. Our data suggest that a relatively small loss of 5-HT neurons compromises resting BP and HR, but has no influence on ventilatory plasticity induced by AIHH. AIHH may be useful for reversing cardiorespiratory defects related to partial 5-HT system dysfunction.

Increases in intramuscular pressure raise arterial blood pressure during dynamic exercise

2001 ◽  
Vol 91 (5) ◽  
pp. 2351-2358 ◽  
Author(s):  
K. M. Gallagher ◽  
P. J. Fadel ◽  
S. A. Smith ◽  
K. H. Norton ◽  
R. G. Querry ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Dynamic Exercise ◽  
Positive Pressure ◽  
Intramuscular Pressure ◽  
Arterial Blood ◽  
Exercise In Humans ◽  
Cuff Occlusion

This investigation was designed to determine the role of intramuscular pressure-sensitive mechanoreceptors and chemically sensitive metaboreceptors in affecting the blood pressure response to dynamic exercise in humans. Sixteen subjects performed incremental (20 W/min) cycle exercise to fatigue under four conditions: control, exercise with thigh cuff occlusion of 90 Torr (Cuff occlusion), exercise with lower body positive pressure (LBPP) of 45 Torr, and a combination of thigh cuff occlusion and LBPP (combination). Indexes of central command (heart rate, oxygen uptake, ratings of perceived exertion, and electromyographic activity), cardiac output, stroke volume, and total peripheral resistance were not significantly different between the four conditions. Mechanical stimulation during LBPP and combination conditions resulted in significant elevations in intramuscular pressure and mean arterial pressure from control at rest and throughout the incremental exercise protocol ( P < 0.05). Conversely, there existed no significant changes in mean arterial pressure when the metaboreflex was stimulated by cuff occlusion. These findings suggest that under normal conditions the mechanoreflex is tonically active and is the primary mediator of exercise pressor reflex-induced alterations in arterial blood pressure during submaximal dynamic exercise in humans.

Association between Intraoperative Hypotension and Myocardial Injury after Vascular Surgery

2016 ◽  
Vol 124 (1) ◽  
pp. 35-44 ◽  
Author(s):  
Judith A. R. van Waes ◽  
Wilton A. van Klei ◽  
Duminda N. Wijeysundera ◽  
Leo van Wolfswinkel ◽  
Thomas F. Lindsay ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Surgery ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Myocardial Injury ◽  
Arterial Blood ◽  
Intraoperative Hypotension ◽  
Cumulative Duration

Abstract Background Postoperative myocardial injury occurs frequently after noncardiac surgery and is strongly associated with mortality. Intraoperative hypotension (IOH) is hypothesized to be a possible cause. The aim of this study was to determine the association between IOH and postoperative myocardial injury. Methods This cohort study included 890 consecutive patients aged 60 yr or older undergoing vascular surgery from two university centers. The occurrence of myocardial injury was assessed by troponin measurements as part of a postoperative care protocol. IOH was defined by four different thresholds using either relative or absolute values of the mean arterial blood pressure based on previous studies. Either invasive or noninvasive blood pressure measurements were used. Poisson regression analysis was used to determine the association between IOH and postoperative myocardial injury, adjusted for potential clinical confounders and multiple comparisons. Results Depending on the definition used, IOH occurred in 12 to 81% of the patients. Postoperative myocardial injury occurred in 131 (29%) patients with IOH as defined by a mean arterial pressure less than 60 mmHg, compared with 87 (20%) patients without IOH (P = 0.001). After adjustment for potential confounding factors including mean heart rates, a 40% decrease from the preinduction mean arterial blood pressure with a cumulative duration of more than 30 min was associated with postoperative myocardial injury (relative risk, 1.8; 99% CI, 1.2 to 2.6, P &lt; 0.001). Shorter cumulative durations (less than 30 min) were not associated with myocardial injury. Postoperative myocardial infarction and death within 30 days occurred in 26 (6%) and 17 (4%) patients with IOH as defined by a mean arterial pressure less than 60 mmHg, compared with 12 (3%; P = 0.08) and 15 (3%; P = 0.77) patients without IOH, respectively. Conclusions In elderly vascular surgery patients, IOH defined as a 40% decrease from the preinduction mean arterial blood pressure with a cumulative duration of more than 30 min was associated with postoperative myocardial injury.

Transient changes in blood pressure during spontaneous deep breaths in rats with sinoaortic deafferentation

1992 ◽  
Vol 72 (3) ◽  
pp. 920-924 ◽  
Author(s):  
B. H. Machado ◽  
H. Mauad ◽  
M. L. Glass
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Context Effects ◽  
Pulmonary Ventilation ◽  
General Pattern ◽  
Arterial Blood ◽  
Moment Control ◽  
Arterial Pressure Lability

Sinoaortic deafferentation (SAD) in rats produces moderate increases in mean arterial pressure (MAP) along with a large augmentation of arterial pressure lability (APL). The mechanisms generating this APL are incompletely understood. To study the possible influence of breathing activity on APL in conscious SAD rats, we simultaneously recorded pulmonary ventilation and arterial blood pressure. The general pattern of pulmonary ventilation was the same in normal, sham-operated, and SAD rats. In all groups single large tidal volumes were regularly interposed in 1- to 2-min periods of shallower breathing. In SAD rats these single large inspirations were consistently accompanied by substantial and abrupt reductions of MAP, whereas this effect was markedly smaller or absent in normal and sham-operated rats. The data reflect the lack of fast moment-to-moment control of arterial pressure normally exerted by the aortic and carotid baroreceptors. In this context, effects of ventilatory changes must be considered along with humoral and neurogenic factors to explain APL after SAD.

scholarly journals Multi-Model Adaptive Predictive Control System for Automated Regulation of Mean Blood Pressure

2019 ◽  
Vol 15 (11) ◽  
pp. 69 ◽  
Author(s):  
Humberto Silva ◽  
Celina Leão ◽  
Eurico Seabra
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Infusion Rate ◽  
Weighting Factor ◽  
Control Procedure ◽  
Drug Infusion ◽  
Arterial Blood ◽  
Simulation Results

After cardiac surgery operation, severe complications may occur in patients due to hypertension. To decrease the chances of complication it is necessary to reduce elevated mean arterial pressure (MAP) as soon as possible. Continuous infusion of vasodilator drugs, such as sodium nitroprusside (Nipride), it is used to reduce MAP quickly in most patients. For maintaining the desired blood pressure, a constant monitoring of arterial blood pressure is required and a frequently adjust on drug infusion rate. The manual control of arterial blood pressure by clinical professionals it is very demanding and time consuming, usually leading to a poor control quality of the hypertension. The objective of the study is to develop an automated control procedure of mean arterial pressure (MAP), during acute hypotension, for any patient, without changing the controller. So, a multi-model adaptive predictive methodology was developed and, for each model, a Predictive Controller can be a priori designed (MMSPGPC). In this paper, a sensitivity analysis was performed and the simulation results showed the importance of weighting factor (φ), which controls the initial drug infusion rate, to prevent hypotension and thus preserve patient's health. Simulation results, for 51 different patients, showed that the MMSPGPC provides a fast control with mean settling time of 04:46 min, undershoots less than 10 mmHg and steady-state error less than ± 5 %  from the MAP setpoint.

Effects of the angiotensin II receptor antagonist Losartan (DuP 753/MK 954) on arterial blood pressure, heart rate, plasma concentrations of angiotensin II and renin and the pressor response to infused angiotensin II in the salt-deplete dog

1992 ◽  
Vol 83 (5) ◽  
pp. 549-556 ◽  
Author(s):  
R. J. MacFadyen ◽  
M. Tree ◽  
A. F. Lever ◽  
J. L. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Pressor Response ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Plasma Angiotensin

1. The blood pressure, heart rate, hormonal and pressor responses to constant rate infusion of various doses of the angiotensin (type 1) receptor antagonist Losartan (DuP 753/MK 954) were studied in the conscious salt-deplete dog. 2. Doses in the range 0.1–3 μmin−1 kg−1 caused no change in blood pressure, heart rate or pressor response to angiotensin II (54 ng min−1kg−1), and a dose of 10 μgmin−1 kg−1 had no effect on blood pressure, but caused a small fall in the pressor response to angiotensin II. Infusion of Losartan at 30 μmin−1 kg−1 for 3 h caused a fall in mean blood arterial pressure from baseline (110.9 ± 11.2 to 95.0 ± 12.8 mmHg) and a rise in heart rate (from 84.6 ± 15.1 to 103 ± 15.2 beats/min). Baseline plasma angiotensin II (42.5 ± 11.8 pg/ml) and renin (64.5 ± 92.7 μ-units/ml) concentrations were already elevated in response to salt depletion and rose significantly after Losartan infusion to reach a plateau by 70 min. The rise in mean arterial blood pressure after a test infusion of angiotensin II (35.3 ± 11.6 mmHg) was reduced at 15 min (11.8 ± 6.8 mmHg) by Losartan and fell progressively with continued infusion (3 h, 4.3 ± 3.3 mmHg). The peak plasma angiotensin II concentration during infusion of angiotensin II was unaffected by Losartan, but the rise in plasma angiotensin II concentration during infusion was reduced because of the elevated background concentration. Noradrenaline infusion caused a dose-related rise in mean blood arterial pressure (1000 ngmin−1kg−1, +19.9 ± 8 mmHg; 2000ngmin−1 kg−1, +52.8 ± 13.9 mmHg) with a fall in heart rate (1000 ng min−1 kg−1, −27.9 ± 11.5 beats/min; 2000 ng min−1 kg−1, −31.2 ± 17.3 beats/min). During Losartan infusion the 1000 but not the 2000 ng min−1 kg−1 noradrenaline infusion caused a greater rise in mean arterial blood pressure and a greater fall in heart rate. The fall in heart rate tended to decrease with continued infusion of Losartan. Plasma catecholamine concentrations were unaffected by Losartan. In a further study, higher doses of Losartan (100, 300 and 1000 μg min−1 kg−1; 30 min) produced greater falls in mean arterial blood pressure also with a rise in heart rate and complete blockade of the pressor effect of infused angiotensin II. Some animals became disturbed at the highest dose. 3. Losartan produces rapid dose-related falls in blood pressure and a rise in heart rate and renin release with elevation of plasma angiotensin II. Pressor responses to angiotensin II are reduced at intermediate doses and are eliminated at high doses. Losartan does not appear to inhibit angiotensin II clearance from the plasma and may in some way increase it.

Cardiovascular actions of dogfish urotensin II in the dogfish Scyliorhinus canicula

1993 ◽  
Vol 265 (3) ◽  
pp. R573-R576 ◽  
Author(s):  
N. Hazon ◽  
C. Bjenning ◽  
J. M. Conlon
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Pulse Pressure ◽  
Bolus Injection ◽  
Urotensin Ii ◽  
Scyliorhinus Canicula ◽  
Arterial Blood ◽  
Dose Dependent

Bolus injections of synthetic dogfish urotensin II (0.1-1.0 nmol) into the celiac artery of the conscious dogfish Scyliorhinus canicula (n = 8) resulted in sustained and dose-dependent increases in arterial blood pressure and pulse pressure. A maximum rise in mean arterial pressure of 10.5 +/- 1.2 mmHg (equivalent to 38.6 +/- 4.2% over mean basal values) and a maximum increase in pulse pressure of 3.9 +/- 0.8 mmHg was elicited by injection of 0.5 nmol of peptide. In comparison, a bolus injection of epinephrine (5 nmol) elicited a rise of 24.8 +/- 3.3% in mean arterial pressure. Bolus injection of 0.5 nmol synthetic goby (Gillichthys mirabilis) urotensin II under the same conditions did not elicit a significant hypertensive response. When dogfish urotensin II (0.5 nmol) was administered 3 min after an intra-arterial injection of phentolamine, the rise in arterial blood pressure was completely abolished. Dogfish urotensin II produced a dose-dependent contraction (pD2 = 6.58 +/- 0.07; n = 8) of isolated rings of vascular muscle prepared from the first afferent branchial artery of the dogfish. A maximum contractile force of 1.3 mN was produced by 10(-5) M peptide. The urotensin II-induced contraction of the vascular rings was unaffected by pretreatment with tetrodotoxin (1 microM) or indomethacin (14 microM). It is concluded that urotensin II has potent hypertensive activity in the dogfish that is mediated, at least in part, through release of catecholamines, but the sustained nature of the pressor response suggests that the peptide may have a direct action on the heart.

Physiological elevation in plasma angiotensinogen increases blood pressure

2001 ◽  
Vol 281 (5) ◽  
pp. R1437-R1441 ◽  
Author(s):  
Christoph P. R. Klett ◽  
Joey P. Granger
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Femoral Vein ◽  
Formation Rate ◽  
Plasma Concentrations ◽  
Sprague Dawley ◽  
Arterial Blood

Hepatic angiotensinogen secretion is controlled by a complex pattern of physiological or pathophysiological mediators. Because plasma concentrations of angiotensinogen are close to the Michaelis-Menten constant, it was hypothesized that changes in circulating angiotensinogen affect the formation rate of ANG I and ANG II and, therefore, blood pressure. To further test this hypothesis, we injected purified rat angiotensinogen intravenously in Sprague-Dawley rats via the femoral vein and measured mean arterial blood pressure after arterial catheterization. In controls, mean arterial pressure was 131 ± 2 mmHg before and after the injection of vehicle (sterile saline). The injection of 0.8, 1.2, and 2.9 mg/kg angiotensinogen caused a dose-dependent increase in mean arterial blood pressure of 8 ± 0.4, 19.3 ± 2.1, and 32 ± 2.4 mmHg, respectively. In contrast, the injection of a purified rabbit anti-rat angiotensinogen antibody (1.4 mg/kg) resulted in a significant decrease in mean arterial pressure (−33 ± 3.2 mmHg). Plasma angiotensinogen increased to 769 ± 32, 953 ± 42, and 1,289 ± 79 pmol/ml, respectively, after substrate and decreased by 361 ± 28 pmol/ml after antibody administration. Alterations in plasma angiotensinogen correlated well with changes in plasma renin activity. In summary, variations in circulating angiotensinogen can result in changes in blood pressure. In contrast to renin, which is known as a tonic regulator for the generation of ANG I, angiotensinogen may be a factor rather important for long-term control of the basal activity of the renin-angiotensin system.

Interaction of vasopressin and opioids during rapid hemorrhage in conscious rabbits

1991 ◽  
Vol 260 (2) ◽  
pp. R373-R381 ◽  
Author(s):  
J. C. Schadt ◽  
E. M. Hasser
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Endogenous Opioids ◽  
Adrenergic Blockade ◽  
Arterial Blood ◽  
Conscious Rabbits

We investigated possible interactions between arginine vasopressin (AVP) and endogenous opioid peptides during rapid hypotensive hemorrhage and subsequent opioid receptor blockade in conscious rabbits. Plasma AVP concentration did not change after normotensive hemorrhage but increased after hypotensive hemorrhage. Blockade of V1-AVP receptors (AVPX) did not affect prehemorrhage arterial pressure, heart rate, or hindquarter blood flow and vascular resistance. AVPX did not alter the hemodynamic response to hemorrhage or the blood loss required to reduce mean arterial pressure to less than 40 mmHg. However, hindquarter blood flow was higher and mean arterial pressure and hindquarter resistance lower after hypotensive hemorrhage in AVPX-treated animals. These differences were maintained after naloxone or saline injection. Naloxone increased mean arterial pressure and hindquarter resistance and decreased heart rate with or without AVPX. At 2 min postinjection, plasma AVP values were greater after saline than after naloxone. When naloxone's pressor response was reduced by alpha-adrenergic blockade, plasma AVP values were higher after naloxone than after saline. Thus AVP was not vital to maintenance of blood pressure during rapid normotensive hemorrhage or to the abrupt decrease in arterial blood pressure and resistance after rapid hypotensive hemorrhage. AVP release was important to spontaneous recovery from acute hypotensive hemorrhage but only of minor importance to naloxone's pressor response. Finally, AVP release appeared to be inhibited by endogenous opioids during acute hemorrhagic hypotension.

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