Adrenergic nerves mediate the venoconstrictor response to PVN stimulation.
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 (DeltaMAP = 12 +/- 2 mm Hg), tachycardic (DeltaHR = 48 +/- 7 bpm) or venoconstrictor (DeltaMCFP = 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 beta2 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.
Basic Biomedical Sciences, University of South Dakota, 414 East Clark Street, Vermillion, SD 57069, USA. dsmartin@usd.edu
D S
DS
Martin
M C
MC
Egland
L U
LU
Barnes
E M
EM
Vogel
D000313:Adrenal Medulla / Q000502:physiology; D018663:Adrenergic Agents / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000420:Albuterol / Q000494:pharmacology; D000818:Animals; D001640:Bicuculline / Q000031:analogs & derivatives / Q000494:pharmacology; D001775:Blood Circulation / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D004837:Epinephrine / Q000378:metabolism*; D018756:GABA Antagonists / Q000494:pharmacology; D005730:Ganglionic Blockers / Q000494:pharmacology; D006145:Guanethidine / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects; D008297:Male; D010286:Paraventricular Hypothalamic Nucleus / Q000098:blood supply / Q000502:physiology*; D011412:Propanolamines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology*; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*; D014680:Veins / Q000187:drug effects / Q000502:physiology; D014690:Venous Pressure
D018663:Adrenergic Agents; D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D018756:GABA Antagonists; D005730:Ganglionic Blockers; D011412:Propanolamines; C026777:ICI 118551; C006749:bicuculline methochloride; D000420:Albuterol; D001640:Bicuculline; D004837:Epinephrine; D006145:Guanethidine