Adrenergic nerves mediate the venoconstrictor response to PVN stimulation

• Published in: Brain research Vol. 1076; no. 1; pp. 93 - 100
• Main Authors: Martin, D.S., Egland, M.C., Barnes, L.U., Vogel, E.M.
• Format: Journal Article
• Language: English
• Published: London Elsevier B.V 03-03-2006; Amsterdam Elsevier; New York, NY
• Subjects: Adrenal Medulla - physiology; Adrenal medullectomy; Adrenergic Agents - pharmacology; Adrenergic beta-Agonists - pharmacology; Adrenergic beta-Antagonists - pharmacology; Adrenergic nerve; Albuterol - pharmacology; Animals; Bicuculline - analogs & derivatives; Bicuculline - pharmacology; Biological and medical sciences; Blood Circulation - drug effects; Blood pressure; Blood Pressure - drug effects; Blood Pressure - physiology; Epinephrine - metabolism; Fundamental and applied biological sciences. Psychology; GABA Antagonists - pharmacology; Ganglionic Blockers - pharmacology; Guanethidine - pharmacology; Heart rate; Heart Rate - drug effects; Male; Mean circulatory filling pressure; Motor control and motor pathways. Reflexes. Control centers of vegetative functions. Vestibular system and equilibration; Paraventricular Hypothalamic Nucleus - blood supply; Paraventricular Hypothalamic Nucleus - physiology; Propanolamines - pharmacology; Rats; Rats, Sprague-Dawley; Sympathetic Nervous System - drug effects; Sympathetic Nervous System - physiology; Vasoconstriction - drug effects; Vasoconstriction - physiology; Veins - drug effects; Veins - physiology; Venous Pressure; Venous tone; Vertebrates: nervous system and sense organs; Heart rate; Adrenal medullectomy; Blood pressure; Venous tone; Adrenergic nerve; Mean circulatory filling pressure; Cardiovascular control; Rat; Rodentia; Central nervous system; Adrenergic transmission; Hypothalamus; Paraventricular nucleus; Encephalon; Vertebrata; Mammalia; Animal; Hemodynamics; Mean circulatory filling pressure Blood pressure Heart rate Venous tone Adrenal medullectomy Adrenergic nerve; Venous pressure
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/j.brainres.2005.12.116

Veins play an important role in the control of venous return, cardiac output and cardiovascular homeostasis. However, the central nervous system sites and effector systems involved in modulating venous function remain to be fully elucidated. The hypothalamic paraventricular nucleus (PVN) is an important site modulating autonomic outflow to the cardiovascular system. Venous tone can be modulated by sympathetic nerves or by adrenal catecholamines. The present study assessed the relative contribution of these autonomic effector systems to the venoconstrictor response elicited by stimulation of the hypothalamic paraventricular nucleus. Male Sprague–Dawley rats were subjected to sham operation or bilateral adrenal demedullation fitted with PVN guide cannulae and fitted with catheters for recording arterial pressure (AP) and intrathoracic vena caval pressure (VP). A latex balloon was advanced into the right atrium. MCFP was calculated from the AP and VP recorded after 4 s of right atrial occlusion. MCFP = VP + (AP − VP)/60. Mean arterial pressure (MAP), heart rate (HR), VP and MCFP responses to injections of BMI (25 ng/side) into the PVN were recorded from conscious rats to avoid the complicating effects of anesthesia. In sham-operated rats, injection of BMI into the PVN increased MAP by 13 ± 3 mm Hg and HR by 56 ± 6 bpm. MCFP was also increased significantly by 0.98 ± 0.15 mm Hg indicating an increase in venomotor tone. Adrenal medullectomy did not affect the pressor (ΔMAP = 12 ± 2 mm Hg), tachycardic (ΔHR = 48 ± 7 bpm) or venoconstrictor (ΔMCFP = 0.73 ± 0.11 mm Hg) responses. Ganglionic blockade abolished the PVN-induced responses in both groups of rats. In a separate group, pretreatment with the adrenergic neuron blocker, guanethidine (20 mg/kg), also abolished the PVN-mediated venoconstrictor responses. Conversely, selective β2 adrenergic receptor blockade did not affect MCFP responses to BMI. These data indicate that adrenomedullary catecholamines are not necessary for full expression of the venoconstrictor response to PVN stimulation.