title: Cardiac sympathetic afferent stimulation augments the arterial chemoreceptor reflex in anesthetized rats.
abstract: Chronic heart failure (CHF) is well known to be associated with both an enhanced chemoreceptor reflex and an augmented cardiac "sympathetic afferent reflex" (CSAR). The augmentation of the CSAR may play an important role in the enhanced chemoreceptor reflex in the CHF state because the same central areas are involved in the sympathetic outputs of both reflexes. We determined whether chemical and electrical stimulation of the CSAR augments chemoreceptor reflex function in normal rats. Under anesthesia, renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) were recorded. The chemoreceptor reflex was tested by unilateral intra-carotid artery bolus injection of potassium cyanide (KCN) and nicotine. We found that 1) left ventricular epicardial application of capsaicin increased the pressor responses and the RSNA responses to chemoreflex activation induced by both KCN and nicotine; 2) when the central end of the left cardiac sympathetic nerve was electrically stimulated, both the pressor and the RSNA responses to chemoreflex activation induced by KCN were increased; 3) pretreatment with intracerebroventricular injection of losartan (500 nmol) completely prevented the enhanced chemoreceptor reflex induced by electrical stimulation of the cardiac sympathetic nerve; and 4) bilateral microinjection of losartan (250 pmol) into the nucleus tractus solitarii (NTS) completely abolished the enhanced chemoreceptor reflex by epicardial application of capsaicin. These results suggest that both the chemical and electrical stimulation of the CSAR augments chemoreceptor reflex and that central ANG II, specially located in the NTS, plays a major role in these reflex interactions.
authors.affiliation: Department of Cellular and Integrative Physiology, Univ. of Nebraska Medical Center, 985850 Nebraska Medical Center, Omaha, NE 68198-5850, USA.
authors.forename: Lie
authors.initials: L
authors.lastname: Gao
authors.forename: Yan-Xia
authors.initials: YX
authors.lastname: Pan
authors.forename: Wei-Zhong
authors.initials: WZ
authors.lastname: Wang
authors.forename: Yu-Long
authors.initials: YL
authors.lastname: Li
authors.forename: Harold D
authors.initials: HD
authors.lastname: Schultz
authors.forename: Irving H
authors.initials: IH
authors.lastname: Zucker
authors.forename: Wei
authors.initials: W
authors.lastname: Wang
mesh_terms: D018712:Analgesics, Non-Narcotic / Q000494:pharmacology; D000804:Angiotensin II / Q000502:physiology; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D000818:Animals; D001158:Arteries / Q000294:innervation / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002211:Capsaicin / Q000494:pharmacology; D002320:Cardiovascular Physiological Phenomena; D002319:Cardiovascular System / Q000294:innervation* / Q000503:physiopathology; D002628:Chemoreceptor Cells / Q000187:drug effects / Q000502:physiology*; D004558:Electric Stimulation; D019808:Losartan / Q000494:pharmacology; D008297:Male; D009475:Neurons, Afferent / Q000502:physiology*; D009538:Nicotine / Q000494:pharmacology; D011190:Potassium Cyanide / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1 / Q000187:drug effects / Q000502:physiology; D017552:Solitary Nucleus / Q000187:drug effects / Q000502:physiology; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology; D014474:Unconsciousness / Q000503:physiopathology*
chemical_list: D018712:Analgesics, Non-Narcotic; D047228:Angiotensin II Type 1 Receptor Blockers; D044140:Receptor, Angiotensin, Type 1; D000804:Angiotensin II; D009538:Nicotine; D019808:Losartan; D011190:Potassium Cyanide; D002211:Capsaicin