Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “atrial function”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 847 records · Page 47Linked to original sources

Effects of endogenous atrial natriuretic peptide released by rapid atrial pacing in dogs.

The relationships between the hemodynamic, renal, and endocrine changes induced by rapid atrial pacing were studied in seven chloralose-anesthetized greyhounds paced from the right atrial appendage for 60 min at 250 beats/min. Pacing increased mean pulmonary wedge pressure, decreased cardiac output, and decreased mean arterial pressure. Systemic vascular resistance did not change significantly. Coronary sinus atrial natriuretic peptide (ANP) concentrations rose maximally within 5 min of commencing pacing. The corresponding increase in arterial ANP concentrations during this time was only 44% of its maximum value after 30 min of pacing. Plasma concentrations of arginine vasopressin were unchanged. Plasma renin activity decreased during pacing and showed a marked rebound increase at 60 min postpacing. Plasma norepinephrine levels did not change significantly during pacing. Urine flow increased during the latter 30 min of pacing. There was no significant change in sodium clearance despite high sustained concentrations of ANP. The lack of significant natriuretic and systemic vasodilator effects in association with high arterial plasma concentrations of endogenous ANP, in the absence of antagonistic mechanisms, suggests that the natriuretic and vascular effects of ANP may not be its major physiological actions.

Animals↗

Stretch-induced reduction in atrial content of natriuretic factor is locally mediated.

Two groups of male Wistar rats were chronically implanted with small inflatable balloons at the right superior vena caval (SVC)-atrial junction. The balloons were inflated for 60 min in one-third of the rats in each group; the remainder served as noninflated controls. Extract was prepared from the right atria of the first and from the left atria of the second group and bioassayed in male Wistars to determine the content of atrial natriuretic factor (ANF). The bioassay rats received either two injections of sham extract (control) or an initial injection (I1) of sham extract followed by an injection (I2) of balloon-inflated extract (experimental). For right atrial extract, the incremental response to the experimental injection (I2/I1) was significantly less than the response to the control injection (experimental, 1.15 +/- 0.09 mueq/min, n = 14; control, 1.59 +/- 0.15 mueq/min, n = 13; P less than 0.01). However, in the case of left atrial extract, there was no such difference between the control group (1.35 +/- 0.13 mueq/min, n = 19) and the experimental group (1.25 +/- 0.11 mueq/min, n = 11; Student's t test). We conclude that right atrial distension causes release of ANF from the right atrium, but not the left, and that this release is probably locally mediated.

Animals↗

Role of atrial pressure and rate in release of atrial natriuretic peptide.

To investigate whether atrial natriuretic peptide (ANP) release during paroxysmal tachycardia is due to increased atrial rate or increased atrial pressure, plasma ANP concentrations were measured during atrial pacing at increasing rates in six alpha-chloralose-anesthetized dogs whose atrial pressures were maintained artificially low by balloon occlusion of the inferior vena cava (IVC). These ANP concentrations were compared with those seen during identical increasing atrial rates in the same dogs without IVC occlusion. During incremental pacing without IVC occlusion, pulmonary wedge pressure (PWP; mean +/- SE) rose progressively from 5.3 +/- 1.6 at 200 to 20.2 +/- 2.3 mmHg at 350 beats/min (P less than 0.01), and right atrial pressure (RAP) rose progressively from 2.5 +/- 0.9 at 200 to 6.7 +/- 2.1 mmHg at 350 beats/min (P less than 0.05). At the same time, arterial and coronary sinus ANP concentrations rose from 116 +/- 55 and 339 +/- 91 to 1,126 +/- 226 and 1,960 +/- 456 pmol/l, respectively (P less than 0.01). In contrast, incremental pacing with IVC occlusion produced no significant increase in PWP and RAP. Arterial and coronary sinus ANP concentrations during IVC occlusion were, respectively, 208 +/- 126 and 388 +/- 159 at 200 and 261 +/- 83 and 345 +/- 80 pmol/l at 350 beats/min (NS). This study demonstrates that the release of ANP during tachycardia is primarily dependent on increased atrial pressure and not atrial rate.

Animals↗

Chronic atrial appendectomy alters sodium excretion in conscious monkeys.

The purpose of this study is to determine whether chronic removal of atrial appendages alters renal response to volume expansion in the conscious monkey. Chronic bilateral atrial appendectomy (ATX) was performed in six animals. Six additional animals served as sham-operated controls. Monkeys were studied 1-2 wk after chronic surgery. The protocol consisted of three consecutive 10-min urine collections followed by 20% ischemic blood volume expansion (VE) and 120 min of post-VE measurements. In sham animals, VE caused an increase in plasma atrial natriuretic peptide (ANP) levels (48 +/- 7 pg/ml to a peak of 108 +/- 34 pg/ml). Urine flow increased from 0.43 +/- 0.07 to 1.07 +/- 0.24 ml/min, sodium excretion increased from 17.9 +/- 2.6 to 74.9 +/- 12.0 mu eq/min, and fractional sodium excretion increased from 0.67 +/- 0.10 to 2.43 +/- 0.28%. ATX attenuated the increase in ANP (34 +/- 8 pg/ml to a peak of 38 +/- 9 pg/ml) in four of six animals. In these animals, renal response to VE was significantly attenuated. Urine flow increased from 0.21 +/- 0.05 to 0.30 +/- 0.01 ml/min, sodium excretion increased from 19.3 +/- 6.02 to 37.8 +/- 5.05 mu eq/min, and fractional sodium excretion increased from 0.79 +/- 0.08 to 1.43 +/- 0.17%. Renal response of two ATX animals with normal increases in atrial natriuretic factor was similar to the sham group. Effect of volume expansion on mean arterial pressure, central venous pressure, and renal hemodynamics was not altered by ATX. These findings demonstrate that bilateral atrial appendectomy in the monkey attenuates the increase in ANP and reduces renal response to VE.

Animals↗

Atrial distension of isolated rabbit hearts and release of atrial natriuretic factor.

Interventions that increase atrial pressures in humans or laboratory animals release atrial natriuretic factor (ANF) into the circulation. We studied the relation between distension of the right or left atrium and release of ANF in retrograde-perfused isolated rabbit hearts. A fluid-filled balloon within the right or left atrium was inflated to a mean pressure of 5, 10, 15, or 20 mmHg, and ANF in the cardiac effluent was measured by radioimmunoassay. The slope of the regression line relating ANF release to atrial distending pressure was steeper for the left than right atrium (P less than 0.001), indicating that, at comparable increases in mean pressures, the left atrium releases more ANF than does the right atrium. Left atrial tissue concentration of ANF was greater than right atrial (1.58 +/- 0.15 vs. 1.05 +/- 0.09 micrograms ANF/mg protein, P less than 0.01). In contrast to previous studies showing right atrial dominance in rats, the left atria of isolated, perfused rabbit hearts contain more ANF and release more in response to atrial distension.

Animals↗

Atrial pressure, distension, and pacing frequency in ANP secretion in isolated perfused rabbit atria.

It has been suggested in this laboratory that the principal stimulus for the secretion of atrial natriuretic peptide (ANP) is the reduction of atrial distension and that the secretion of ANP is dependent on both atrial reduction volume and reduction frequency. To investigate the relationship among the changes in atrial pressure, distension, pacing frequency, and ANP secretion, we performed a series of experiments in the isolated perfused rabbit atria. Increase in atrial pressure without changes in transmural pressure and thus without volume changes did not raise immunoreactive ANP (irANP) secretion. Atrial distension without changes in intracavitary atrial pressure increased irANP secretion with the reduction. Electrical stimulation with atrial distension resulted in an increase in irANP secretion in proportion to pacing frequency. Incremental response of irANP secretion to electrical stimulation was accentuated by increasing atrial distension. Neither atrial pacing without distension nor distension without pacing raised irANP secretion. These results suggest that the direct and principal stimulus for irANP secretion in response to atrial pacing and distension is the length shortening of atrial myocytes and that the incremental response of irANP secretion to increasing pacing frequency is the result of an increase in frequency of the length shortening of atrial myocytes.

Animals↗

Endothelin acts as a paracrine regulator of stretch-induced atrial natriuretic peptide release.

Several lines of evidence suggest a paracrine regulatory role for endothelin (ET) in the release of atrial natriuretic peptide (ANP). To investigate this possibility, we used the ET A-type receptor (ETA-R) competitive inhibitor cyclo(D-Asp-Pro-D-Val-Leu-D-Trp) (BQ-123) in isolated perfused atria to determine the effect of endogenously produced ET on the release of ANP. Initially, we found that high pressure (8-10 mmHg) increased the mean ANP secretion rate by 117.3 +/- 21.2% (P < 0.05). Next, we found that at high pressure 50 nM of exogenously applied ET significantly augmented the stretch-induced release of ANP (P < 0.05) and that this response could be significantly attenuated in a dose-dependent manner by 1 and 3 microM BQ-123 (P < 0.05). These experiments proved the efficacy of the inhibitor in our model. Subsequently, we found that the stretch-induced release of ANP was significantly reduced to 51.5 +/- 13.0 and 22.3 +/- 11.8% by 1 and 3 microM BQ-123, respectively (P < 0.05). Because the perfused atria model eliminates systemic cardiovascular effects, allows control and direct recording of the intra-atrial pressure, and preserves the potential endothelium-myocyte control system, we conclude that the stretch-induced release of ANP is partially regulated by ET and that the ET is locally produced and constitutes a paracrine control system.

Animals↗

Atrial, B-type, and C-type natriuretic peptides cause mesenteric vasoconstriction in conscious dogs.

Cardiovascular responses were compared with equimolar infusions of B-type (BNP) and C-type (CNP) with atrial natriuretic peptide (ANP) in conscious, instrumented dogs. On separate days, each natriuretic peptide or vehicle was infused (intravenously) at step-up doses of 2, 5, 10, and 20 pmol. kg-1. min-1 (20 min each dose) to increase circulating levels of the infused peptide from approximately 2- to 20-fold. Like ANP, infusions of BNP caused dose-related increases (P < 0.05) in mesenteric vascular resistance, urine flow, natriuresis, and hematocrit (changes at highest doses were 60 +/- 9, 334 +/- 113, 313 +/- 173, and 12 +/- 2%, respectively). BNP also lowered (P < 0. 05) plasma renin activity (-43 +/- 11%) and arterial pressure (-10 +/- 3%). Effects of BNP were independent of reflex sympathetic activation, since autonomic ganglion blockade did not attenuate the responses. CNP infusions had little effect except to increase (P < 0. 05) mesenteric vascular resistance (27 +/- 10%) and plasma ANP (41 +/- 7%). Cardiovascular actions of BNP, like those of ANP, counteract the renin-ANG system and may protect the heart by lowering cardiac preload (venous return) and afterload (arterial pressure) while maintaining blood flow to extrasplanchnic regions.

Animals↗

Renal response to atrial peptides is reduced in experimental nephrosis.

The aim of this study was to evaluate the renal response to atrial extracts (AE) and synthetic atrial natriuretic factor (ANF) in control rats and in rats with experimental nephrotic syndrome (NS). NS was obtained by a single intravenous injection of adriamycin (7.5 mg/kg). Bolus injection of AE from normal or NS rats resulted in marked increase of diuresis and natriuresis in bioassay control rats (AE from normal rats, urine flow rate, 14.87 +/- 2.94 to 186.18 +/- 55.86 microliters/min; Na excretion, 0.68 +/- 0.26 to 21.80 +/- 5.45 mu eq/min; AE from NS, urine flow rate, 13.49 +/- 4.30 to 167.14 +/- 51.44 microliters/min; Na excretion, 0.98 +/- 0.57 to 20.71 +/- 9.76 mu eq/min). In contrast, blunted diuretic (from 11.26 +/- 3.05 to 65.20 +/- 27.30 microliters/min) and natriuretic (from 0.58 +/- 0.15 to 4.52 +/- 1.59 mu eq/min) effect was observed when AE were injected in rats with NS. Injection of the vehicle in which AE were dissolved or ventricular extracts did not increase urinary flow rate or Na excretion in both control and NS animals. Bolus injection of synthetic ANF (Arg-101-Tyr-126) induced marked diuretic and natriuretic response in control but not in NS rats. Similar results were obtained when AE were infused by constant infusion in control or in NS bioassay rats. AE given by constant infusion induced comparable increase in glomerular filtration rate (GFR) over basal values both in control and NS animals (controls, 39%; NS rats, 40%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Role of cardiac atria in the human renal response to changing plasma volume.

We examined the role of cardiac atria in the renal response to sequential volume expansion and contraction, during and directly following water immersion. In immersed healthy volunteers (group 1, n = 9) atrial diameter, plasma levels of atrial natriuretic peptide (ANP), and natriuresis increased, whereas renal vascular resistance (RVR) and filtration fraction declined. Each parameter changed in an opposite direction postimmersion. An analysis of transglomerular dextran transport suggests that transglomerular hydraulic pressure difference (delta P) changed in parallel with filtration fraction. Baseline atrial diameter, plasma ANP, RVR, and filtration fraction were significantly elevated in nine recipients of denervated cardiac allografts (group 2). Atrial diameter and plasma ANP changed in parallel with group 1 during and after immersion. However, corresponding reciprocal changes in RVR were smaller and filtration fraction remained constant throughout. From transglomerular dextran transport, we compute that delta P increased progressively during and after immersion, suggesting predominant efferent arteriolar tone. The postimmersed state was associated also with enhanced sodium retention despite sixfold higher plasma ANP than in group 1. These findings are consistent with an effect of cardiac denervation to leave unopposed efferent sympathetic nervous traffic to the kidney. They suggest that the latter is an important modulator of the renal response to changing plasma volume in humans.

Atrial Function↗

Glomerular atrial natriuretic factor receptors during rehydration: plasma NH2- and COOH-terminal levels.

Atrial natriuretic factor (ANF) concentration in atria and plasma was investigated in relation to the density and affinity of renal glomerular ANF receptors during water deprivation and rehydration in the rat. Immunoreactive (IR) ANF-(99-126) was lower during water deprivation (4.2 +/- 0.5 fmol/ml) than in normally hydrated animals (10 +/- 1.5 fmol/ml); NH2-terminal IR ANF-(1-98) was also lower in water-deprived rats (75 +/- 2.4 fmol/ml) than in the controls (708 +/- 105 fmol/ml). These decreased plasma COOH- and NH2-terminal ANF concentrations were accompanied by significantly higher hematocrit, serum osmolality, and Na+ values. The renal glomerular ANF receptor population was greater in water-deprived animals than a control animals. After rehydration, IR ANF was elevated within 1 h and reached control values after 6 h. Hematocrit, serum osmolality, and Na+ did not normalize until 48, 6, and 24 h, respectively. The renal glomerular ANF receptor population, which was markedly higher in water-deprived rats, gradually declined after rehydration, so that no difference was observed with the control group 24 h later.

Animals↗

Right atrial pressure and ANP release during prolonged exercise in a hot environment.

To investigate the relationship between right atrial pressure (RAP) and atrial natriuretic peptide (ANP) release during prolonged exercise in a hot environment (30 degrees C, 20% relative humidity), we studied with a Swan-Ganz catheter five male volunteers exercising on a cycle ergometer at 60% of peak aerobic power for 50 min. The ANP level increased from 14 +/- 3 (SE) to 69 +/- 10 pg/ml (P < 0.001) during the first 10 min of exercise as RAP rose from 4.3 +/- 0.8 to 6.9 +/- 1.1 mmHg (P < 0.001). The 10-min ANP level was significantly correlated with RAP (r = 0.88, P < 0.05) but not with heart rate, pulmonary arterial blood temperature, plasma norepinephrine, or plasma epinephrine. The 10-min RAP value was inversely correlated with blood volume (r = -0.98, P < 0.01) and also with stroke volume (r = -0.96, P < 0.01). In the next 20 min of exercise, ANP continued to increase to 101 +/- 12 pg/ml (P < 0.02 vs. 10 min) and remained at this level until 50 min of exercise, whereas RAP decreased and reached a level not significantly different from baseline at 50 min (5.7 +/- 1.0 mmHg; P < 0.01 vs. 10 min). This dissociation of ANP and RAP may have been related to the significant increases from the 10-min values of heart rate, blood temperature, norepinephrine (all P < 0.01), and epinephrine (P < 0.02) during the same period. These results suggest that ANP release is primarily controlled by atrial distension at the onset of exercise but that other stimulators may be involved thereafter.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Does gender influence human cardiovascular and renal responses to water immersion?

We hypothesized that women and men exhibit similar cardiovascular and renal responses to thermoneutral water immersion (WI) to the neck. Ten women and nine men underwent two sessions in random order: 1) seated nonimmersed for 5.5 h (control) and 2) WI for 3 h, with subjects seated nonimmersed for 1.5 h pre- and 1 h postimmersion. We measured left atrial diameter, heart rate, arterial pressure, urine volume and osmolality, and urinary endothelin, urodilatin, sodium, and potassium excretion. No significant difference existed between groups in cardiovascular responses. The groups also exhibited mostly similar renal responses to immersion after adjustment for body mass. However, female urodilatin excretion per kilogram during immersion was over twofold that of men, and the female kaliuretic response to immersion was delayed and less pronounced relative to that in men. Men may excrete more potassium than women during immersion because men possess greater lean body mass (potassium per kilogram). Results obtained in men during WI may be cautiously extrapolated to women, yet urodilatin and potassium responses exhibit gender differences.

Adult↗

Effect of upper gastrointestinal endoscopy on circulation in the elderly.

BACKGROUND: Upper gastrointestinal endoscopy in the elderly is increasingly becoming more common, despite the possibility that a minimal load on the circulation can cause serious complications such as shock and cardiac arrest. OBJECTIVE: The effects of endoscopy on the heart and the possibility of predicting circulatory accidents were studied using natriuretic peptide levels. METHODS: The patients were randomly chosen according to their age and divided into an elderly group (over 60 years of age, 64 patients) and a young group (under 30 years of age, 20 patients). The patients in the elderly group were further subdivided into two groups based on the presence or absence of circulatory complications (46 patients with circulatory complications and 18 without complications). The load on the heart was evaluated by measuring human atrial natriuretic peptide (hANP) and human brain natriuretic peptide (hBNP) which are secreted by the myocardial cells in response to cardiac load. Specimens were obtained before and after endoscopy. RESULTS: The hANP level was significantly higher after endoscopy in the elderly group, regardless of the presence or absence of circulatory complications. No significant difference was observed in the hBNP level. No significant increase in hANP or hBNP levels was observed after endoscopy in the young group. CONCLUSIONS: These observations suggest an increased atrial load during endoscopy in the elderly. The increase in pulse rate during endoscopy is one possible cause of atrial load. Therefore, the risk of circulatory system damage must be recognized when endoscopy is performed in the elderly. The measurement of plasma hANP and hBNP levels may provide effective indices for evaluating cardiac load during endoscopy.

Adult↗

Is there a pericardial restriction to the cardiac secretion of atrial natriuretic factor?

Atrial natriuretic factor (ANF) is secreted from atrial myocytes in response to increased atrial wall stress caused by increased transmural pressure. This study investigates whether the presence of an intact pericardium restricts the ANF secretory response to an increment in left atrial pressure caused by acute aortic constriction in anaesthetized open-chest pigs. The rise in ANF plasma concentration secondary to constriction was higher when the pericardium had been surgically opened than when it was left intact. Furthermore, an opened pericardium led to a larger increase during constriction in left atrial diameter as measured by sonomicrometry. The results suggest that the intact pericardium restricts the cardiac release of ANF secondary to aortic constriction, probably by restricting left atrial dilatation.

Animals↗

Plasma atrial natriuretic peptide levels in children with cardiac diseases: correlation with cGMP levels and haemodynamic parameters.

In children with various forms of cardiac diseases (aged 2 months to 16 years) significantly higher plasma atrial natriuretic peptide (ANP; range 36-680, median 247 pg/ml) and cyclic 3'5'-guanosine monophosphate (cGMP; range 0.2-46, median 8.2 pmol/ml) levels were found than in control children (p less than 0.0001). In control children (aged 4 months to 17 years) plasma ANP and cGMP levels were measured in the range of 2.4-98 pg/ml and of 0.2-2.8 pmol/ml, respectively. There was a linear correlation between the two parameters in children with cardiac diseases (r = 0.62, p less than 0.01). Children with elevated mean right atrial pressure (i.e., greater than 6 mm Hg) showed significantly higher plasma ANP levels than children with normal atrial pressure (p less than 0.01). However, there was only a weak linear correlation between mean right atrial pressure and plasma ANP levels (r = 0.48, p less than 0.01). Plasma ANP levels from right atrium, pulmonary artery, left atrium and left ventricle were significantly higher than those from vena cava (p less than 0.05). Analysis of ANP-like immunoreactive material by high performance liquid chromatography suggested that alpha-ANP is the major form of circulating ANP in blood of children with cardiac diseases.

Adolescent↗

Increased release of atrial natriuretic peptide by the atria of rats with experimental renal failure.

Indirect evidence suggests that atrial natriuretic peptide (ANP) secretion is augmented in chronic renal disease. The object of our present study is to examine the release of ANP from isolated atria obtained from chronic renal failure rats to directly determine whether ANP secretions are increased under these conditions. Experiments were conducted on male Wistar rats (200-225 g) who were subjected to 5/6 nephrectomy of sham operation. Plasma blood urea nitrogen was significantly elevated in 5/6 nephrectomized rats (65 +/- 7 vs. 16 +/- 1 mg%). Overall glomerular filtration rate was 2.36 +/- 0.06 ml/min in sham-operated animals, as opposed to 0.55 +/- 0.11 ml/min in 5/6 nephrectomized rats. Fractional excretion of sodium was significantly higher in 5/6 nephrectomized rats (0.52 +/- 0.01 vs. 1.68 +/- 0.21%). Plasma ANP was 102 +/- 4 pg/ml in normal rats and 161 +/- 14 pg/ml in 5/6 nephrectomized ones. We have also measured immunoreactive ANP in the atria of normal and 5/6 nephrectomized rats. ANP content and concentration in the atria were lower in 5/6 nephrectomized rats. (652 +/- 34 vs. 515 +/- 46 ng/mg of tissue). Right atria from normal and nephrectomized animals was superfused with a modified Langendorff preparation. Spontaneous release of ANP was significantly higher from the nephrectomized rats (17.5 +/- 0.6 pg/min/mg) than from the normal rats (9.8 +/- 0.3 pg/min/mg). These results suggest that ANP may play a role in sodium homeostasis in rats with reduced renal mass.

Animals↗

Hormonal responses to cardiac tamponade: inhibition of release of atrial natriuretic factor despite elevation of atrial pressures.

Atrial distension, rather than change in intra-atrial pressure, has been suggested as a principal mediator of release of atrial natriuretic factor (ANF). During cardiac tamponade, atrial pressures rise whereas transmural pressures and atrial stretch may not be affected. The roles of atrial pressure and atrial distension were investigated in six open-chest dogs subjected to cardiac tamponade and rapid volume expansion as disparate means of affecting intra-atrial pressures and atrial stretch. Hemodynamic measurements, immunoreactive ANF (ir-ANF), plasma renin activity, antidiuretic hormone, epinephrine, and norepinephrine were monitored before, during, and after three interventions: (1) tamponade, (2) rapid volume loading followed by tamponade, and (3) volume loading during tamponade. Volume expansion increased right atrial pressure and caused a significant rise in ir-ANF. Elevations of right atrial pressure caused by tamponade were comparable to those induced by volume infusion, but an increase in ir-ANF was not elicited during tamponade, and the ir-ANF response to volume loading was abolished when performed during tamponade. The relation between the change in ANF concentration and change in right atrial pressure were highly significant in the absence of tamponade, when atrial stretch was freely responsive to volume expansion (r = .73, p less than .0001), but not when stretch was inhibited (r = -.16, p = NS). These observations underscore the importance of considering the modulating effects of atrial compliance, transmural pressure, and atrial stretch on the relation between atrial pressures and ANF release.

Animals↗