atrial-natriuretic-factor and Pain

Topics: Amino Acid Sequence; Angiotensin-Converting Enzyme Inhibitors; Animals; Atrial Natriuretic Factor; Behavior; Binding Sites; CD13 Antigens; Drug Design; Drug Tolerance; Enkephalins; Humans; Molecular Sequence Data; Neprilysin; Pain; Protease Inhibitors

It has been shown that atrial natriuretic peptide (ANP), an endogenous vasodilator, dilates coronary arteries and decreases coronary vascular resistance. The purpose of this study was to determine whether an intravenous administration of ANP attenuated exercise-induced myocardial ischemia in 14 patients with stable effort angina pectoris.. The first 12 patients (patients 1-12) who had exercise-induced ST segment depression underwent treadmill exercise testing and the last seven patients (patients 8-14) underwent the exercise 201Tl-single-photon emission computed tomography (SPECT) study while synthetic 28-amino acid alpha-human ANP (0.1 micrograms/kg per minute) or saline was intravenously infused in a double-blind, cross-over manner. The duration of exercise testing was the same during ANP and saline infusion, which was determined in preliminary exercise testings in each patient to cause a transient perfusion defect and/or ischemic ST segment depression. During saline infusion, all 12 patients developed exercise-induced ischemic ST segment depression, whereas no significant ST segment depression appeared during ANP infusion. Average ST segment depression during ANP infusion was significantly less (p < 0.01) than that during saline infusion (0.0 +/- 0.0 versus 0.2 +/- 0.1 mV, mean +/- SD). The averaged extent and severity scores assessed by 201Tl-SPECT were smaller (p < 0.05) during ANP infusion than during saline infusion (extent score: 0.22 +/- 0.20 versus 0.42 +/- 0.20; severity score: 18.77 +/- 23.45 versus 38.24 +/- 24.04, respectively). ANP decreased resting systolic blood pressure from 125 +/- 15 to 110 +/- 15 mm Hg (p < 0.01) but did not alter resting heart rate. At peak exercise, systolic blood pressure, heart rate, and the rate-pressure products did not differ during ANP and saline infusion. At peak exercise, plasma ANP increased from 98 +/- 45 to 4,383 +/- 2,782 pg/ml and cGMP increased from 3.6 +/- 1.7 to 34.5 +/- 16.1 pmol/ml during ANP infusion; values were significantly higher than those during saline infusion (from 96 +/- 42 to 133 +/- 66 pg/ml and from 3.4 +/- 1.8 to 4.6 +/- 1.8 pmol/ml, respectively).. An intravenous administration of ANP attenuated exercise-induced myocardial ischemia in patients with stable effort angina pectoris. Although the mechanism by which ANP attenuated myocardial ischemia was not defined, increased myocardial perfusion to the ischemic region might be an important factor.

Topics: Adult; Aged; Angina Pectoris; Atrial Natriuretic Factor; Coronary Circulation; Coronary Disease; Double-Blind Method; Electrocardiography; Exercise Test; Female; Hemodynamics; Humans; Infusions, Intravenous; Male; Middle Aged; Pain; Physical Exertion; Sodium Chloride; Tomography, Emission-Computed, Single-Photon

The neurotransmitter gamma-aminobuteric acid (GABA) is believed to have a controlling action on spinal locomotor networks. In spasticity, spinal locomotor networks are thought to play a role. A well known drug in the treatment of spasticity is the GABA(B) agonist Baclofen. We report an inhibitory effect of Baclofen on the ANP-mediated cGMP synthesis in the superficial dorsal horn (laminae I-III) of the rat cervical spinal cord. This inhibitory effect of Baclofen could not be detected after incubation with the NO donor SNP. The clinical effect of Baclofen on the reduction of spasticity might be explained by an enhancement of GABAergic inhibition of ANP mediated cGMP concentration in the spinal cord dorsal horn, thus reducing afferent input.

Topics: Aging; Animals; Atrial Natriuretic Factor; Baclofen; Cervical Vertebrae; Cyclic GMP; GABA Agonists; GABA-B Receptor Agonists; gamma-Aminobutyric Acid; Immunohistochemistry; Male; Muscle Spasticity; Nerve Net; Nitric Oxide Donors; Nociceptors; Pain; Posterior Horn Cells; Rats; Rats, Inbred Lew; Receptors, GABA-B

To investigate the relationship between plasma atrial natriuretic factor (ANF) levels, impaired myocardial contractility and pain intensity in acute myocardial infarction (AMI) we introduced a procedure estimating the pain component not influenced by the individual emotional reaction to stress, i.e., the original pain sensation. We deduced this pain component during AMI by correcting the personal report of AMI pain, quantified on a VAS, with the emotional reaction of each patient estimated by using a custom-built instrument which applies electrical stimuli of different intensities. Twenty-five patients with uncomplicated AMI were studied. According to plasma ANF levels and AMI pain values reported on the VAS, patients were categorized into 2 groups: pain and no-pain. Plasma ANF levels were significantly lower in pain (35.9 +/- 2.5 pg/ml) than in no-pain patients (70.8 +/- 3.3 pg/ml), whereas the ejection fraction (EF) was significantly higher in pain (49.6 +/- 1.7%) than in no-pain patients (29.3 +/- 1.9%). Within each group, a negative correlation was found between ANF and EF; the corresponding regression lines did not differ significantly in their slopes or intercepts, suggesting that AMI pain does not affect ANF release. The significant negative correlation between original pain sensation and EF found in pain patients indicates that this pain component may be useful to gauge the severity of impaired myocardial contractility during AMI. Moreover, the much higher plasma ANF levels observed in no-pain patients suggest that ANF may be involved in preventing AMI pain.

Topics: Aged; Atrial Natriuretic Factor; Cluster Analysis; Evaluation Studies as Topic; Female; Hemodynamics; Humans; Male; Middle Aged; Myocardial Contraction; Myocardial Infarction; Pain; Pain Measurement