title: Volume expansion potentiates cardiac sympathetic afferent reflex in dogs.
abstract: Our previous study (27) showed that the cardiac sympathetic afferent reflex (CSAR) was enhanced in dogs with congestive heart failure. The aim of this study was to test whether blood volume expansion, which is one characteristic of congestive heart failure, potentiates the CSAR in normal dogs. Ten dogs were studied with sino-aortic denervation and bilateral cervical vagotomy. Arterial pressure, left ventricular pressure, left ventricular epicardial diameter, heart rate, and renal sympathetic nerve activity were measured. Coronary blood flow was also measured and, depending on the experimental procedure, controlled. Blood volume expansion was carried out by infusion of isosmotic dextran into a femoral vein at 40 ml/kg at a rate of 50 ml/min. CSAR was elicited by application of bradykinin (5 and 50 microg) and capsaicin (10 and 100 microg) to the epicardial surface of the left ventricle. Volume expansion increased arterial pressure, left ventricular pressure, left ventricular diameter, and coronary blood flow. Volume expansion without controlled coronary blood flow only enhanced the RSNA response to the high dose (50 microg) of epicardial bradykinin (17. 3 +/- 1.9 vs. 10.6 +/- 4.8%, P < 0.05). However, volume expansion significantly enhanced the RSNA responses to all doses of bradykinin and capsaicin when coronary blood flow was held at the prevolume expansion level. The RSNA responses to bradykinin (16. 9 +/- 4.1 vs. 5.0 +/- 1.3% for 5 microg, P < 0.05, and 28.9 +/- 3.7 vs. 10.6 +/- 4.8% for 50 microg, P < 0.05) and capsaicin (29.8 +/- 6.0 vs. 9.3 +/- 3.1% for 10 microg, P < 0.05, and 34.2 +/- 2.7 vs. 15.1 +/- 2.7% for 100 microg, P < 0.05) were significantly augmented. These results indicate that acute volume expansion potentiated the CSAR. These data suggest that enhancement of the CSAR in congestive heart failure may be mediated by the concomitant cardiac dilation, which accompanies this disease state.
authors.affiliation: Department of Physiology and Biophysics, University of Nebraska College of Medicine, Omaha, Nebraska 68198-4575, USA. weiwang@unmc.edu
authors.forename: W
authors.initials: W
authors.lastname: Wang
authors.forename: H D
authors.initials: HD
authors.lastname: Schultz
authors.forename: R
authors.initials: R
authors.lastname: Ma
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001920:Bradykinin / Q000494:pharmacology; D002211:Capsaicin / Q000494:pharmacology; D002306:Cardiac Volume / Q000502:physiology*; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology; D004285:Dogs; D005260:Female; D006333:Heart Failure / Q000503:physiopathology; D007668:Kidney / Q000294:innervation; D008297:Male; D009475:Neurons, Afferent / Q000502:physiology*; D010101:Oxygen Consumption / Q000502:physiology; D010952:Plasma Substitutes / Q000494:pharmacology; D010953:Plasma Volume / Q000502:physiology; D012018:Reflex / Q000187:drug effects / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000166:cytology / Q000502:physiology*; D017725:Ventricular Pressure / Q000187:drug effects / Q000502:physiology
chemical_list: D010952:Plasma Substitutes; D002211:Capsaicin; D001920:Bradykinin