Reduced baroreceptor sensitivity during hypotension in ANP-knockout mice

2001 ◽  
Vol 79 (3) ◽  
pp. 201-205 ◽  
Author(s):  
Uwe Ackermann ◽  
Robin Donna Deliva
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Nervous Activity ◽  
Heart Rate Change ◽  
The Other ◽  
Sympathetic Nervous Activity ◽  
Baroreceptor Sensitivity ◽  
Arterial Blood ◽  
Change In Mean ◽  
Atrial Natriuretic

We studied baroreflex gain in inactin-anesthetized mice that had been genetically modified to be depleted of atrial natriuretic peptide (ANP -/-). Wild-type mice (ANP +/+) served as controls. ANP -/- mice had a significantly higher basal arterial blood pressure (ABP) than ANP +/+ mice [112 ± 7 vs. 80 ± 5 mmHg (mean ± SEM)]. Their basal heart rates were not different (491 ± 13 vs. 446 ± 19 bpm). A third group, composed of ANP +/+ mice only, was rendered acutely hypertensive by an intravenous infusion of arginine vasopressin acetate (0.3 pg bolus followed by 0.3 pg/h) so as to serve as a control for the elevated ABP in the ANP -/- mice. Transient changes in ABP were caused by bolus injections of oxymetazoline hydrochloride (1.5-3 ng) or sodium nitroprusside (20-100 ng). Baroreflex gain was calculated as the ratio of the peak heart rate change that followed the peak change in mean ABP resulting from injection of oxymetazoline or nitroprusside. There were no significant differences among the groups in their responses to transient hypertension. On the other hand, the ANP -/- mice showed a significantly depressed tachycardic response to transient hypotension when compared with the other two groups. We conclude that the ANP -/- mice are unable to increase efferent sympathetic nervous activity adequately above the high basal activity that is a feature of this animal model.Key words: atrial natriuretic peptides, knockouts, arterial blood pressure.

Sympathetic nervous activity and arterial blood pressure control in conscious rat during rest and behavioral stress

1994 ◽  
Vol 267 (5) ◽  
pp. R1241-R1249 ◽  
Author(s):  
D. C. Randall ◽  
D. R. Brown ◽  
L. V. Brown ◽  
J. M. Kilgore
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Neural Control ◽  
Nervous Activity ◽  
Sympathetic Nervous Activity ◽  
Initial Increase ◽  
Conditional Response ◽  
Arterial Blood ◽  
Behavioral Stress ◽  
Sympathetic Nervous

The object of this experiment is to analyze the neural control of arterial blood pressure (BP) during rest and a sudden behavioral stress. Sprague-Dawley rats were classically conditioned by following a 15-s tone (CS+) with a 0.5-s tail shock. Bipolar renal nerve electrodes and a caudal artery catheter were implanted. Two days later BP and sympathetic nervous activity (SNA) were recorded in the behaviorally trained animals. The CS+ evoked a large initial increase in BP (peak, 14 +/- 5 mmHg, mean +/- SD; n = 12) that lasted 3.9 +/- 0.8 s. An abrupt (latency = 0.16 +/- 0.03 s), short (duration = 0.58 +/- 0.12 s), and intense (4.09 +/- 1.02 times average control) burst in sympathetic activity preceded this first component (C1) of the BP conditional response. The size of C1 was related to the magnitude of the SNA burst. SNA then fell below control; this quiet period preceded a fall in BP after the C1 peak. Pressure rose again (C2; peak = 6 +/- 3 mmHg, average increase = 3 +/- 3 mmHg) for the remainder of the CS+. SNA increased to 1.24 +/- 0.14 of control during this second component of the BP conditional response. Ganglionic blockade eliminated the BP and SNA conditional response (n = 3). The C1 pressure increase appears to result from an “open-loop” process in which a brief barrage of nerve activity governs BP changes lasting several seconds. The quite period probably results from a negative feedback (i.e., baroreflex) relationship between SNA and BP.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypoxemia raises muscle sympathetic activity but not norepinephrine in resting humans

1989 ◽  
Vol 66 (4) ◽  
pp. 1736-1743 ◽  
Author(s):  
L. B. Rowell ◽  
D. G. Johnson ◽  
P. B. Chase ◽  
K. A. Comess ◽  
D. R. Seals
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous Activity ◽  
Plasma Concentrations ◽  
Random Order ◽  
Sympathetic Nervous Activity ◽  
Severe Hypoxemia ◽  
Arterial Blood ◽  
End Tidal ◽  
Venous Plasma

The experimental objective was to determine whether moderate to severe hypoxemia increases skeletal muscle sympathetic nervous activity (MSNA) in resting humans without increasing venous plasma concentrations of norepinephrine (NE) and epinephrine (E). In nine healthy subjects (20–34 yr), we measured MSNA (peroneal nerve), venous plasma levels of NE and E, arterial blood pressure, heart rate, and end-tidal O2 and CO2 before (control) and during breathing of 1) 12% O2 for 20 min, 2) 10% O2 for 20 min, and 3) 8% O2 for 10 min--in random order. MSNA increased above control in five, six, and all nine subjects during 12, 10, and 8% O2, respectively (P less than 0.01), but only after delays of 12 (12% O2) and 4 min (8 and 10% O2). MSNA (total activity) rose 83 +/- 20, 260 +/- 146, and 298 +/- 109% (SE) above control by the final minute of breathing 12, 10, and 8% O2, respectively. NE did not rise above control at any level of hypoxemia; E rose slightly (P less than 0.05) at one time only with both 10 and 8% O2. Individual changes in MSNA during hypoxemia were unrelated to elevations in heart rate or decrements in blood pressure and end-tidal CO2--neither of which always fell. We conclude that in contrast to some other sympathoexcitatory stimuli such as exercise or cold stress, moderate to severe hypoxemia increases leg MSNA without raising plasma NE in resting humans.

scholarly journals Chronic Endothelium-Dependent Regulation of Arterial Blood Pressure by Atrial Natriuretic Peptide: Role of Nitric Oxide and Endothelin-1

Endocrinology ◽  
2009 ◽  
Vol 150 (5) ◽  
pp. 2382-2387 ◽  
Author(s):  
Karim Sabrane ◽  
Markus-N. Kruse ◽  
Alexandra Gazinski ◽  
Michaela Kuhn
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Methyl Ester ◽  
Atrial Natriuretic Peptide ◽  
Arterial Blood Pressure ◽  
Natriuretic Peptide ◽  
Endothelin 1 ◽  
Arterial Blood ◽  
Atrial Natriuretic

Atrial natriuretic peptide (ANP), via its guanylyl cyclase (GC)-A receptor, plays a key role in the regulation of arterial blood pressure (ABP) and volume. Endothelial-restricted deletion of GC-A in mice [endothelial cell (EC) GC-A knockout (KO)] resulted in hypervolemic hypertension, demonstrating that the endothelium participates in the hypotensive and hypovolemic actions of ANP. Published studies showed that ANP modulates the release of the vasoactive factors nitric oxide (NO) and endothelin-1 (ET-1) from cultured endothelia. Based on these observations, we examined the role of these endothelial factors in ANP-dependent vasodilatation (studied in isolated arteries) and chronic regulation of ABP (measured in awake mice by tail-cuff plethysmography). ANP induced concentration-dependent vasorelaxations of aortic, carotid, and pulmonary arteries. These responses were not different between control and EC GC-A KO mice, and were significantly enhanced after inhibition of NO synthase [by N(G)-nitro-l-arginine-methyl ester]. Intravenous administration of N(G)-nitro-l-arginine-methyl ester to conscious mice significantly increased ABP. The extent of these hypertensive reactions was similar in EC GC-A KO mice and control littermates (increases in systolic blood pressure by ∼25 mm Hg). Conversely, antagonism of ET-1/endothelin-A receptors with BQ-123 reduced ABP significantly and comparably in both genotypes (by ∼11 mm Hg). Finally, the vascular and tissue expression levels of components of the NO system and of immunoreactive ET-1 were not different in control and EC GC-A KO mice. We conclude that the endothelium, but not modulation of endothelial NO or ET-1, participates in the chronic regulation of ABP by ANP.

Regulation of Cardiac Output during 2,4-Dinitrophenol-Induced Tissue Hypermetabolism in the Dog

1977 ◽  
Vol 53 (1) ◽  
pp. 17-25
Author(s):  
C. Liang ◽  
W. B. Hood
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Venous Blood ◽  
The Other ◽  
Pulmonary Artery Wedge Pressure ◽  
Systemic Arterial Blood Pressure ◽  
Arterial Blood ◽  
Wedge Pressure

1. Cardiac output increased in proportion to oxygen consumption in intact chloralose-anaesthetized dogs after four successive intravenous infusions of 2,4-dinitrophenol (11 μmol/kg; 2 mg/kg). 2. Splenectomy abolished the increase in cardiac output after the first three doses of 2,4-dinitrophenol. β-Adrenoreceptor blockade by practolol, on the other hand, did not prevent the cardiac output rise after the first 2,4-dinitrophenol infusion, but further increases by 2,4-dinitrophenol infusion were abolished. When splenectomy and β-adrenoreceptor blockade were combined, cardiac output did not increase significantly after all four doses of 2,4-dinitrophenol. 3. Cardiac output and mean systemic arterial blood pressure increased when the splenic venous blood collected after 2,4-dinitrophenol infusion was infused intraportally. 4. In a vascularly isolated, but normally innervated, lower half-body cross-perfusion preparation, cardiac output and mean systemic arterial blood pressure increased in the upper half-body when tissue hypermetabolism was produced in the cross-perfused area by 2,4-dinitrophenol. Neither pulmonary artery wedge pressure nor heart rate changed significantly. 5. This circulatory stimulation, after regional 2,4-dinitrophenol infusion, was abolished or was prevented from occurring by splenectomy. 6. It appears that the normal cardiac output response to tissue hypermetabolism requires both an intact spleen and normally functioning β-adrenoreceptors.

scholarly journals Erythropoietin-induced hypertension in rat is not mediated by alterations of plasma endothelin, vasopressin, or atrial natriuretic peptide levels.

1997 ◽  
Vol 8 (6) ◽  
pp. 901-905
Author(s):  
X J Zhou ◽  
D Pandian ◽  
X Q Wang ◽  
N D Vaziri
Keyword(s):  
Blood Pressure ◽  
Atrial Natriuretic Peptide ◽  
Arterial Blood Pressure ◽  
Natriuretic Peptide ◽  
Clinical Studies ◽  
Controlled Study ◽  
Recombinant Erythropoietin ◽  
Arterial Blood ◽  
Induced Hypertension ◽  
Atrial Natriuretic

Regular administration of recombinant erythropoietin (EPO) in patients with chronic renal failure (CRF) is frequently complicated by a rise in arterial blood pressure. Clinical studies intended to discern the possible role of endothelin (ET) in the pathogenesis of EPO-induced hypertension have produced contradictory results. Given the limitations of the clinical studies, this placebo-controlled study was carried out in CRF (5/6 nephrectomized) rats treated with either EPO, 150 U/kg intraperitoneally, or the vehicle alone twice weekly for 6 wk. Plasma ET was measured at baseline, and weeks 2, 4, and 6. In addition, plasma arginine vasopressin (AVP) and atrial natriuretic peptide (ANP) were determined at the conclusion of the study period. As expected, blood pressure rose markedly after 1 wk of EPO therapy as compared with the placebo therapy. However, there was no significant difference in plasma ET levels between the EPO- and placebo-treated groups during the study period. Likewise, EPO therapy had no effect on plasma ANP level but depressed plasma AVP concentration. Thus, this placebo-controlled animal study revealed that EPO therapy markedly raised arterial blood pressure but had no effect on plasma ET in the CRF rats. This observation suggests that EPO-induced hypertension in this model is not mediated by an increased circulating ET level. However, the possible effect, if any, of EPO on local vascular tissue ET level is uncertain and awaits further investigation.

Fluid balance and arterial blood pressure during intracarotid infusions of atrial natriuretic peptide (ANP) in water-deprived goats

1989 ◽  
Vol 137 (2) ◽  
pp. 249-257 ◽  
Author(s):  
K. OLSSON ◽  
K. DAHLBORN ◽  
K. NYGREN ◽  
R. E. KARLBERG ◽  
N.-E. ANDÉN ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Atrial Natriuretic Peptide ◽  
Arterial Blood Pressure ◽  
Natriuretic Peptide ◽  
Fluid Balance ◽  
Arterial Blood ◽  
Atrial Natriuretic

Atrial natriuretic peptide in the locus coeruleus and its possible role in the regulation of arterial blood pressure, fluid and electrolyte homeostasis

Life Sciences ◽  
1991 ◽  
Vol 49 (12) ◽  
pp. 869-879 ◽  
Author(s):  
Helmut Geiger ◽  
Udo Bahner ◽  
Miklos Palkovits ◽  
August Heidland ◽  
R.Bernd Sterzel
Keyword(s):  
Blood Pressure ◽  
Atrial Natriuretic Peptide ◽  
Locus Coeruleus ◽  
Arterial Blood Pressure ◽  
Natriuretic Peptide ◽  
Arterial Blood ◽  
Electrolyte Homeostasis ◽  
Atrial Natriuretic

Cardiovascular changes during spontaneous micturition in conscious cats

1979 ◽  
Vol 237 (2) ◽  
pp. H213-H217
Author(s):  
G. Baccelli ◽  
G. Mancia ◽  
A. Del Bo ◽  
R. Albertini ◽  
A. Zanchetti
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Marked Decrease ◽  
Blood Pressure Level ◽  
Systemic Circulation ◽  
Hemodynamic Changes ◽  
Blood Flows ◽  
Arterial Blood ◽  
Change In Mean

The hemodynamic changes occurring during spontaneous micturition were recorded in conscious cats. Arterial blood pressure was continuously measured by chronically implanted arterial catheter, heart rate (HR) by a cardiotachometer, and cardiac output (CO), superior mesenteric (MF), renal (RF), and external iliac blood flows (IF) by chronically implanted electromagnetic flow probes. Spontaneous micturition was accompanied by little change in mean arterial pressure (-9.7 +/- 0.7%), but by a marked decrease in HR (-49.0 +/- 1.2%) and CO (-28.6 +/- 2.5%), and therefore by a marked decrease in total peripheral conductance (-21.0 +/- 3.5%). Visceral and hindlimb blood flows were markedly reduced during micturition (MF, -34.7 +/- 2.1%; RF, -22.6 +/- 1.5%; and IF, -48.7 +/- 1.5%, respectively) due to a marked reduction in regional conductances in both these areas. The vasomotor changes in the regional circulations were prevented by local sympathectomy. Thus spontaneous micturition is associated with marked changes in cardiac function and systemic circulation. Cardiac output is decreased, but diffuse nervous systemic vasoconstriction compensates for this and provides maintenance of arterial blood pressure level.

Baroreceptor activity in muskrats (Ondatra zibethica) during nasal stimulation

1988 ◽  
Vol 66 (11) ◽  
pp. 2520-2527
Author(s):  
M. A. Douse ◽  
David R. Jones
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Neural Activity ◽  
The Other ◽  
Similar Increase ◽  
Receptor Level ◽  
Efferent Activity ◽  
Arterial Blood ◽  
Diastolic Interval

Nasal stimulation with water (simulated dive) in anesthetized muskrats (Ondatra zibethica) caused a significant increase in cardiac interval (209 ± 8 to 1370 ± 280 ms; mean ± SE) and decrease in mean arterial blood pressure (86 ± 8.6 mmHg to 75.7 ± 7.9 mmHg; 1 mmHg = 133.32 Pa). Baroreceptor activity, recorded from the peripheral end of a cut sinus nerve, stopped during the prolonged initial diastolic interval and in 3 of 10 fibres was absent for the first three heartbeats. Chemoreceptor activity did not change at the start of the nasal stimulation. As nasal stimulation continued, mean arterial blood pressure significantly increased (to 118.1 ± 9.5 mmHg), while cardiac interval decreased (to 740 ± 102 ms). This resulted in an increase in baroreceptor activity comparable with that seen during a similar increase in blood pressure in a pressor test. An increase in chemoreceptor activity also occurred during the latter part of nasal stimulation. Two types of efferent activity were recorded from the central end of a cut sinus nerve. One efferent responded to nasal stimulation with an immediate increase in neural activity, while activity of the other efferent halted. These responses would be expected to inhibit rather than foster baroreceptor activity in the intact nerve. The results suggest that there is no facilitation of the baroreflex engendered by changes at the receptor level that might contribute to the initiation of the dive bradycardia.

Effect of natural and synthetic atrial natriuretic factor on arterial blood pressure, natriuresis and cyclic GMP excretion in spontaneously hypertensive rats

1985 ◽  
Vol 69 (6) ◽  
pp. 721-726 ◽  
Author(s):  
Stephen C. Pang ◽  
Minh-Chau Hoang ◽  
Johanne Tremblay ◽  
Marc Cantin ◽  
Raul Garcia ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Cyclic Gmp ◽  
Atrial Natriuretic Factor ◽  
Blood Pressure Lowering Effect ◽  
Spontaneously Hypertensive ◽  
Arterial Blood ◽  
Natriuretic Factor ◽  
Pressure Natriuresis ◽  
Atrial Natriuretic

1. The differential effects of extracted and synthetic atrial natriuretic factor (ANF) on arterial blood pressure, natriuresis, and cyclic GMP excretion were studied in normotensive (WKY) and spontaneously hypertensive (SHR and SHRSP) rats. 2. Atrial extracts or synthetic (101–126)-ANF decreased arterial blood pressure in all tested animals, but the blood pressure-lowering effect was more pronounced in hypertensive than in normotensive rats. ANF-induced diuresis and natriuresis were two- to three-fold higher in the hypertensive groups. However, a several-fold increase in total urinary cyclic GMP level after the infusion of ANF was essentially equal in the three groups. 3. Our data suggest that acute infusion of ANF reveals a defect of sodium and water handling in SHR. It is possible that this defect is located at the distal nephron, and is made apparent by the action of ANF on glomeruli via a cyclic GMP-induced vascular effect.

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