Mineralocorticoid antagonist inhibits stress-induced blood pressure response after repeated daily warming

1994 ◽  
Vol 267 (6) ◽  
pp. E921-E926 ◽  
Author(s):  
D. T. Van den Berg ◽  
W. de Jong ◽  
E. R. de Kloet
Keyword(s):  
Blood Pressure ◽  
Restraint Stress ◽  
Blood Pressure Response ◽  
Direct Method ◽  
Pressor Response ◽  
Blood Pressure Measurement ◽  
Training Procedure ◽  
Intracerebroventricular Infusion ◽  
Mineralocorticoid Antagonist ◽  
Corticosterone Response

We report here that with a direct method for measurement of cardiovascular parameters in conscious rats, intracerebroventricular administration of the mineralocorticoid receptor (MR) antagonist RU-28318 (100 ng) reduces the blood pressure, heart rate, and the corticosterone response to a brief restraint stress, provided the rats were previously subjected to a daily 30-min exposure to 32 degrees C for 2 wk. The daily exposure to warming and restraint stress are applied identically to the training procedure required for indirect blood pressure measurement using the tail-cuff method. The basal arterial pressure is not affected by the MR antagonist. The effect of the MR antagonist on the stress-induced pressor response develops with a delay of several hours in the normotensive rats. The corticosterone response to daily warming and stress is also attenuated by the intracerebroventricular infusion of MR antagonist but with shorter onset and shorter duration. The findings suggest that conditioning to daily warming and stress imposes mineralocorticoid dependency of the pressor response, which involves MR functioning in brain.

GRANGER CAUSALITY ANALYSIS BETWEEN INTRA-OSSEOUS PRESSURE AND ARTERIAL BLOOD PRESSURE IN AFRICAN GREY PARROTS (PSITTACUS ERITHACUS)

2021 ◽  
pp. 1-8
Author(s):  
Yi-Tse Hsiao ◽  
Yun-Wen Peng ◽  
Pin Huan Yu
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Granger Causality ◽  
Arterial Blood Pressure ◽  
Pressure Measurement ◽  
Direct Method ◽  
Blood Pressure Measurement ◽  
Rational Approach ◽  
Arterial Blood ◽  
The Relationship

Monitoring blood pressure helps a clinical veterinarian assess various conditions in birds. Blood pressure is not only a bio-indicator of renal or cardiovascular disease but is also a vital indicator for anesthesia. Anesthetic- and sedation-related mortality is higher in birds than dogs or cats. The traditional method of blood pressure measurement in mammals mainly relies on indirect methods. However, indirect blood pressure measurement is not reliable in birds, making the direct method the only gold standard. Although an arterial catheter can provide continuous real-time arterial pressure in birds, the method requires technical skill and is limited by bird size, and is thus not practical in birds with circulatory collapse. Intra-osseous (IO) blood pressure is potentially related to arterial pressure and may be a much easier and safer technique that is less limited by animal size. However, the relationship between IO pressure and arterial blood pressure has not been established. This study used mathematical methods to determine the relationship between IO pressure and arterial blood pressure. The Granger causality (G.C.) theory was applied in the study and used to analyze which pressure signal was leading the other. Our findings suggest that IO pressure is G.C. by arterial blood pressure; thus, the use of IO pressure measurements as an alternative to arterial blood pressure measurement is a rational approach.

scholarly journals Overexpression of Central ACE2 (Angiotensin-Converting Enzyme 2) Attenuates the Pressor Response to Chronic Central Infusion of Ang II (Angiotensin II)

Hypertension ◽  
2020 ◽  
Vol 76 (5) ◽  
pp. 1514-1525
Author(s):  
Anyun Ma ◽  
Lie Gao ◽  
Ahmed M. Wafi ◽  
Li Yu ◽  
Tara Rudebush ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Angiotensin Converting Enzyme ◽  
Pressor Response ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Intracerebroventricular Infusion

We investigated the mechanism by which ACE2 (angiotensin-converting enzyme 2) overexpression alters neurohumoral outflow and central oxidative stress. Nrf2 (nuclear factor [erythroid-derived 2]-like 2) is a master antioxidant transcription factor that regulates cytoprotective and antioxidant genes. We hypothesized that upregulation of central ACE2 inhibits the pressor response to Ang II (angiotensin II) by reducing reactive oxygen species through a Nrf2/antioxidant enzyme–mediated mechanism in the rostral ventrolateral medulla. Synapsin human Angiotensin Converting Enzyme 2 positive (SynhACE2 +/+ ) mice and their littermate controls synhACE2 −/− were used to evaluate the consequence of intracerebroventricular infusion of Ang II. In control mice, Ang II infusion evoked a significant increase in blood pressure and norepinephrine excretion, along with polydipsia and polyuria. The pressor effect of central Ang II was completely blocked in synhACE2 +/+ mice. Polydipsia, norepinephrine excretion, and markers of oxidative stress in response to central Ang II were also reduced in synhACE2 +/+ mice. The MasR (Mas receptor) agonist Ang 1–7 and blocker A779 had no effects on blood pressure. synhACE2 +/+ mice showed enhanced expression of Nrf2 in the rostral ventrolateral medulla which was blunted following Ang II infusion. Ang II evoked nuclear translocation of Nrf2 in cultured Neuro 2A (N2A) cells. In synhACE2 −/− mice, the central Ang II pressor response was attenuated by simultaneous intracerebroventricular infusion of the Nrf2 activator sulforaphane; blood pressure was enhanced by knockdown of Nrf2 in the rostral ventrolateral medulla in Nrf2 floxed (Nrf2 f/f ) mice. These data suggest that the hypertensive effects of intracerebroventricular Ang II are attenuated by selective overexpression of brain synhACE2 and may be mediated by Nrf2-upregulated antioxidant enzymes in the rostral ventrolateral medulla.

Intracerebroventricular infusion of RU28318 blocks aldosterone-salt hypertension

1990 ◽  
Vol 258 (3) ◽  
pp. E482-E484 ◽  
Author(s):  
E. P. Gomez-Sanchez ◽  
C. M. Fort ◽  
C. E. Gomez-Sanchez
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Systolic Blood Pressure ◽  
Urine Volume ◽  
Intracerebroventricular Infusion ◽  
Mineralocorticoid Antagonist ◽  
Salt Hypertension ◽  
The Central Nervous System ◽  
Dose Dependent

The chronic intracerebroventricular (icv) infusion of aldosterone in rats and dogs elevates the blood pressure within 10-14 days at doses far below those that produce hypertension systemically. The effect in rats is dose dependent and blocked by the concomitant icv infusion of the antimineralocorticoid, prorenone. The effect of the icv infusion of RU28318, another specific spironolactone mineralocorticoid antagonist, on the hypertension produced by chronic subcutaneous (sc) administration of aldosterone in sensitized rats was reported. Miniosmotic pumps were used to deliver 1 micrograms/h aldosterone sc and 1.1 micrograms/h RU8318 icv. Over a 24-day period the indirect systolic blood pressure of the control, RU28318 icv, and aldosterone sc plus RU28318 icv groups increased from 105 to 123 mmHg and were not significantly different from each other, whereas the aldosterone sc group increased to 156 mmHg. RU28318, icv or sc, did not alter the increase in urine volume produced by aldosterone sc, and there was no significant differences in weight between the groups. This study provides evidence of the importance of the central nervous system in the pathogenesis of hypertension produced by systemic mineralocorticoid excess.

Muscle chemoreflex alters vascular conductance in nonischemic exercising skeletal muscle

1994 ◽  
Vol 77 (6) ◽  
pp. 2761-2766 ◽  
Author(s):  
S. W. Mittelstadt ◽  
L. B. Bell ◽  
K. P. O'Hagan ◽  
P. S. Clifford
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Response To Exercise ◽  
Muscle Chemoreflex

Previous studies have shown that the muscle chemoreflex causes an augmented blood pressure response to exercise and partially restores blood flow to ischemic muscle. The purpose of this study was to investigate the effects of the muscle chemoreflex on blood flow to nonischemic exercising skeletal muscle. During each experiment, dogs ran at 10 kph for 8–16 min and the muscle chemoreflex was evoked by reducing hindlimb blood flow at 4-min intervals (0–80%). Arterial blood pressure, hindlimb blood flow, forelimb blood flow, and forelimb vascular conductance were averaged over the last minute at each level of occlusion. Stimulation of the muscle chemoreflex caused increases in arterial blood pressure and forelimb blood flow and decreases in forelimb vascular conductance. The decrease in forelimb vascular conductance demonstrates that the muscle chemoreflex causes vasoconstriction in the nonischemic exercising forelimb. Despite the decrease in vascular conductance, the increased driving pressure caused by the pressor response was large enough to produce an increased forelimb blood flow.

Attenuation of Electroconvulsive Therapy Induced Hypertension with Sublingual Nifedipine

1989 ◽  
Vol 17 (1) ◽  
pp. 31-33 ◽  
Author(s):  
D. G. Wells ◽  
G. G. Davies ◽  
F. Rosewarne
Keyword(s):  
Blood Pressure ◽  
Electroconvulsive Therapy ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Systolic Pressure ◽  
Response To Therapy ◽  
Induced Hypertension ◽  
Sublingual Nifedipine ◽  
History Of ◽  
Significant Attenuation

Five patients known to be previously hypertensive but not currently receiving anti-hypertensive medications were studied for a total of twenty-six administrations of electroconvulsive therapy Patients randomly received sublingual nifedipine 10 mg, 20 minutes prior to half of their treatments, and for the remaining treatments acted as their own controls. The use of nifedipine resulted in significant attenuation of the blood pressure response to therapy. Systolic pressure increase was 24 mmHg (SD 14) versus 62 mmHg (SD 24) (P< 0.01). There was no difference in heart rate between the two groups. It is concluded that nifedipine reduces the pressor response to electroconvulsive therapy in individuals with a history of hypertension.

PRESSOR RESPONSIVENESS FOLLOWING ACUTE ELEVATION OF SODIUM IN THE RAT

1957 ◽  
Vol 35 (1) ◽  
pp. 327-331 ◽  
Author(s):  
Sydney M. Friedman ◽  
W. A. Webber ◽  
J. D. Jamieson ◽  
Constance L. Friedman
Keyword(s):  
Blood Pressure ◽  
Sodium Acetate ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
High Plasma ◽  
Potassium Citrate ◽  
Plasma Sodium ◽  
Adult Rats ◽  
Sodium Potassium ◽  
Acute Elevation

In order to test the effects of various ions on pressor responsiveness, groups of adult rats were infused with solutions containing sufficient sodium, potassium, calcium, or magnesium to elevate the plasma concentration of these ions. The infusions were completed within 5 minutes and in no case was more than 0.5 ml. injected. The test solutions used were sodium acetate, potassium citrate, calcium chloride, and magnesium sulphate. Control solutions of ammonium acetate, ammonium sulphate, sodium chloride, and sucrose were also infused. In no case was the amount of salt infused sufficient to affect the blood pressure during the infusion. The blood pressure response to 1 γ of norepinephrine or to 20 mU. of pitressin was recorded before infusion and again at the end of the infusion. A significant effect was observed only with sodium acetate. This consisted of a profound suppression of the ordinary pressor response to both norepinephrine and pitressin. The effect was not due to the acetate ion and hence may be specifically referable to the high plasma sodium. These results support our previous conclusions that pressor responsiveness and sodium mobility are causally connected.

scholarly journals Hemodynamic effects of pressures applied to the upper airway during sleep

2000 ◽  
Vol 89 (2) ◽  
pp. 537-548 ◽  
Author(s):  
P. R. Eastwood ◽  
A. K. Curran ◽  
C. A. Smith ◽  
J. A. Dempsey
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Upper Airway ◽  
Intrathoracic Pressure ◽  
Nrem Sleep ◽  
Pressure Response ◽  
Central Apnea ◽  
Tracheal Occlusion ◽  
Negative Pressures

The increase in systemic blood pressure after an obstructive apnea is due, in part, to sympathetically mediated vasoconstriction. We questioned whether upper airway (UA) receptors could contribute reflexly to this vasoconstriction. Four unanesthetized dogs were studied during wakefulness and non-rapid-eye-movement (NREM) sleep. The dogs breathed via a fenestrated tracheostomy tube sealed around the tracheal stoma. The snout was sealed with an airtight mask, thereby isolating the UA when the fenestration was closed and exposing the UA to negative inspiratory intrathoracic pressure when it was open. The blood pressure response to three UA perturbations was studied: 1) square-wave negative pressures sufficient to cause UA collapse with the fenestration closed during a mechanical hyperventilation-induced central apnea; 2) tracheal occlusion with the fenestration open vs. closed; and 3) high-frequency pressure oscillations (HFPO) with the fenestration closed. During NREM sleep, 1) blood pressure response to tracheal occlusion was similar with the fenestration open or closed; 2) collapsing the UA with negative pressures failed to alter blood pressure during a central apnea; and 3) application of HFPO to the UA during eupnea and resistive-loaded breaths increased heart rate and blood pressure. However, these changes were likely to be secondary to the effects of HFPO-induced reflex changes on prolonging expiratory time. These findings suggest that activation of UA pressure-sensitive receptors does not contribute directly to the pressor response associated with sleep-disordered breathing events.

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