PRESSOR RESPONSIVENESS FOLLOWING ACUTE ELEVATION OF SODIUM IN THE RAT

1957 ◽  
Vol 35 (6) ◽  
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.

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.

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.

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.

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.

Muscle fiber recruitment and blood pressure response to isometric exercise

1981 ◽  
Vol 50 (1) ◽  
pp. 32-37 ◽  
Author(s):  
J. S. Petrofsky ◽  
C. A. Phillips ◽  
M. N. Sawka ◽  
D. Hanpeter ◽  
A. R. Lind ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Venous Blood ◽  
Isometric Exercise ◽  
Motor Units ◽  
Medial Gastrocnemius ◽  
Isometric Contractions ◽  
Slow Twitch ◽  
K Concentration

Blood pressure was recorded during fatiguing and nonfatiguing isometric contractions of a slow-twitch muscle (the soleus) and a mixed muscle (the medial gastrocnemius) of the cat. Four tensions were examined in each muscle; 10, 25, 40, and 70% of the muscle's initial strength (tetanic tension of the unfatigued muscle). All experiments were also repeated at two muscle temperatures, 28 and 38 degrees C. For the soleus muscle, there was no change in the blood pressure during isometric contractions. For the medial gastrocnemius muscle, both the systolic and diastolic blood pressure increased markedly when either all or just the fast-twitch motor units were stimulated; however, when only the slow-twitch motor units were stimulated, a lower pressor response was observed. Venous blood samples were drawn before, during, and after fatiguing and nonfatiguing contractions of both muscles to determine the K+ concentration in the venous blood. The mean increase in the K+ concentration during contractions was 0.6 meq/l for the slow-twitch motor units of the soleus and 5.1 meq/l for the motor units in the medial gastrocnemius.

scholarly journals Hypertension from chronic central sodium chloride in mice is mediated by the ouabain-binding site on the Na,K-ATPase α2-isoform

2011 ◽  
Vol 301 (5) ◽  
pp. H2147-H2153 ◽  
Author(s):  
James W. Van Huysse ◽  
Iva Dostanic ◽  
Jerry B. Lingrel ◽  
Xiaohong Hou ◽  
Hengwei Wu
Keyword(s):  
Blood Pressure ◽  
Sodium Chloride ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Dietary Sodium ◽  
Wild Type ◽  
Similar Extent ◽  
Ouabain Binding ◽  
Endogenous Ouabain ◽  
The Brain

A chronic increase in the concentration of sodium chloride in the cerebrospinal fluid (CSF) (↑CSF [NaCl]) appears to be critically important for the development of salt-dependent hypertension. In agreement with this concept, increasing CSF [NaCl] chronically by intracerebroventricular (icv) infusion of NaCl-rich artificial CSF (aCSF-HiNaCl) in rats produces hypertension by the same mechanisms (i.e., aldosterone-ouabain pathway in the brain) as that produced by dietary sodium in salt-sensitive strains. We first demonstrate here that icv aCSF-HiNaCl for 10 days also causes hypertension in wild-type (WT) mice. We then used both WT and gene-targeted mice to explore the mechanisms. In WT mice with a ouabain-sensitive Na,K-ATPase α2-isoform (α2S/S), mean arterial pressure rose by ∼25 mmHg within 2 days of starting aCSF-HiNaCl (0.6 nmol Na/min) and remained elevated throughout the study. Ouabain (171 pmol/day icv) increased blood pressure to a similar extent. aCSF-HiNaCl or ouabain given at the same rates subcutaneously instead of intracerebroventricularly had no effect on blood pressure. The pressor response to icv aCSF-HiNaCl was abolished by an anti-ouabain antibody given intracerebroventricularly but not subcutaneously, indicating that it is mediated by an endogenous ouabain-like substance in the brain. We compared the effects of icv aCSF-HiNaCl or icv ouabain on blood pressure in α2S/S versus knockout/knockin mice with a ouabain-resistant endogenous α2-subunit (α2R/R). In α2R/R, there was no pressor response to icv aCSF-HiNaCl in contrast to WT mice. The α2R/R genotype also lacked a pressor response to icv ouabain. These data demonstrate that chronic ↑CSF [NaCl] causes hypertension in mice and that the blood pressure response is mediated by the ouabain-like substance in the brain, specifically by its binding to the α2-isoform of the Na,K-ATPase.

Augmentation of the exercise pressor reflex in prehypertension: roles of the muscle metaboreflex and mechanoreflex

2013 ◽  
Vol 38 (2) ◽  
pp. 209-215 ◽  
Author(s):  
Hyun-Min Choi ◽  
Charles L. Stebbins ◽  
Og-Taeg Lee ◽  
Hosung Nho ◽  
Joon-Hee Lee ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Percentage Increase ◽  
Muscle Metaboreflex ◽  
Exercise Pressor Reflex ◽  
Arterial Blood ◽  
Static Contraction ◽  
Pressor Reflex

This study investigated the hemodynamic mechanisms underlying the exaggerated blood pressure response to muscle contraction in prehypertensive humans and the potential role of skeletal muscle metabo- and mechanoreceptors in this response. To accomplish this, changes in peak mean arterial blood pressure (ΔMAP), cardiac output, and total peripheral resistance (ΔTPR) were compared between prehypertensive (n = 23) and normotensive (n = 19) male subjects during 2 min of static contraction (at 50% of maximal tension), 2 min of postexercise muscle ischemia (metaboreflex), and 1 min of passive dorsiflexion of the foot (tendon stretch, mechanoreceptor reflex). These variables were assessed before and during the interventions. Percentage increases from baseline in MAP and TPR in response to the exercise pressor reflex were augmented in the prehypertensives, compared with the normotensives (44% ± 5% vs. 33% ± 4% and 34% ± 15% vs. 2% ± 8%, respectively) (p < 0.05). Metaboreflex-induced increases in MAP and TPR were also augmented in the prehypertensives (28% ± 5% vs. 14% ± 4% and 36% ± 12% vs. 14% ± 9%, respectively) (p < 0.05). In response to the mechanoreflex, no differences in the percentage increase in MAP or TPR were seen between groups. The results indicate that the reflex pressor response to static contraction is augmented in prehypertension and suggest that this phenomenon is due, at least in part, to enhanced activation of metaboreceptors.

scholarly journals Modulation of cardiac contractility by muscle metaboreflex following efforts of different intensities in humans

2006 ◽  
Vol 291 (6) ◽  
pp. H3035-H3042 ◽  
Author(s):  
Antonio Crisafulli ◽  
Enrico Salis ◽  
Gianluigi Pittau ◽  
Luigi Lorrai ◽  
Filippo Tocco ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Myocardial Contractility ◽  
Cardiovascular Response ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Cardiac Contractility ◽  
Preliminary Test ◽  
Knee Extension ◽  
Pressure Response ◽  
Sensory Nerves

Accumulation of metabolic end products within skeletal muscle stimulates sensory nerves, thus evoking a pressor response termed “metaboreflex.” The aim of this study was to evaluate changes in hemodynamics occurring during metaboreflex activation obtained by postexercise muscle ischemia (PEMI) after two different exercise intensities. In twelve healthy subjects, the metaboreflex was studied with the PEMI method at the start of recovery from one leg-dynamic knee extension performed at intensities of 30% (PEMI 30%) and 70% (PEMI 70%) of the maximum workload achieved in a preliminary test. Control exercise recovery tests at the same intensities were also conducted. Central hemodynamics were evaluated by means of impedance cardiography. The main findings were that 1) during metaboreflex, exercise conducted against the higher workload caused a more pronounced blood pressure increase than the strain conducted against the lower workload; and 2) during PEMI 70%, this blood pressure response was mainly achieved through enhancement of myocardial contractility that increased stroke volume and, in turn, cardiac output, whereas during PEMI 30%, the blood pressure response was reached predominantly by means of vasoconstriction. Thus a substantial enhancement of myocardial contractility was reached only in the PEMI 70% test. These results suggest that hemodynamic regulation during metaboreflex engagement caused by PEMI in humans is dependent on the intensity of the previous effort. Moreover, the cardiovascular response during metaboreflex is not merely achieved by vasoconstriction alone, but it appears that there is a complex interplay between peripheral vasoconstriction and heart contractility recruitment.

Abstract P195: Hypertension is Associated With an Abnormal Pressor Response to Voluntary Apnea

Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
Noah Jouett ◽  
Ryan Mason ◽  
Dorene Niv ◽  
Donald E Watenpaugh ◽  
Michael L Smith
Keyword(s):  
Blood Pressure ◽  
Effective Treatment ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Breath Hold ◽  
Primary Care Center ◽  
Hypertensive Patients ◽  
Control Subjects ◽  
Healthy Control ◽  
Voluntary Apnea

Background: Cardiovascular diseases are commonly associated with elevated sympathetic nerve activity (SNA). Previously, we have shown that the blood pressure response to a voluntary apnea is closely correlated with the SNA response in patients with sleep disordered breathing (SDB) and thus may serve as an index of SNA responsiveness. In the current study, we hypothesized that the pressor response to apnea is 1) reduced with effective treatment of SDB in SDB patients, and 2) that it is exaggerated in hypertensive patients (HTN) when compared to healthy control subjects. Methods: 22 OSA patients (14 treated and 8 untreated), 19 treated hypertensive patients and 23 healthy normotensive control subjects were recruited from the UNTHSC Primary Care Center and Sleep Consultants of Texas. Subjects completed a medical history questionnaire and Epworth Sleepiness survey. Blood pressure was measured by standard auscultatory assessment in the seated position. Baseline blood pressure was obtained in triplicate during quiet rest. Then after practicing a voluntary breath hold, subjects repeated three voluntary 20-second breath holds each beginning at end-expiration. Comparisons were made 1) between treated and untreated SDB patients, and 2) between HTN patients and healthy control subjects using a Student t test. Results: Importantly, as in prior studies the pressor response to apnea was not different from zero in the healthy control subjects (-1.0 ± 4.2 mmHg, p>0.05). In the SDB patients, the pressor response was significantly greater than zero in both treated (11.4 ± 3.9 mm Hg) and untreated (24.5 ± 9.8 mm Hg) SDB patients (p<0.001), and was significantly reduced in the treated SDB patients (p<0.001). In addition, the pressor response was significantly greater in the HTN patients (10.5 ± 5.3 mmHg, p<0.001) compared to the healthy control subjects. Conclusions: These data support our hypotheses that the pressor response to voluntary apnea is exaggerated in both untreated SDB and treated HTN patients and that effective treatment of SDB reduces this response, but does not normalize the response. These data suggest that the pressor response to apnea may be a simple physiologic index of exaggerated sympathetic responsiveness.

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