For the past nine years, the objectives of my research have been to identify the CNS sites, the central neurochemical systems, and the peripheral physiological mechanisms which regulate the cardiovascular system. Previous studies from my laboratory and others have demonstrated that electrical stimulation of specific regions in the hypothalamus controls vasomotor tone and regional vascular resistance in individual peripheral vascular beds. These results led to the hypothesis that there is a discrete arrangement of neural structures in this brain region that controls vasomotor tone in peripheral organ systems. Interpretation of these previous studies is limited since: 1) only electrical stimulation was tested 2) only regional blood flow was measured; and 3) there was no direct evaluation of effector mechanisms. To extend previous findings and address these concerns, the proposed Specific Aims will determine: 1) CNS sites; 2) CNS neurotransmitter systems; 3) CNS nerve pathways; and 4) the peripheral effector mechanisms which control specific regional and microvascular responses.
These aims will be achieved by using: CNS microstimulation, microinjection, and knife cuts; autoradiography; horseradish peroxidase techniques; central and peripheral administration of pharmacological agents; pulsed Doppler analysis of regional blood flow; and intravital microscopy. Regional blood flow in the mesenteric, renal, and hindquarter circulations, and microvascular responses in skin, intestine and skeletal muscle will be compared during electrical and chemical stimulation of discrete neural sites in the hypothalamus previously implicated in the regulation of regional vascular resistance. Additional experiments will be determine neurotransmitters and other CNS sites involved. Finally, peripheral effector mechanisms will be tested by evaluating microvascular responses in tissue suffused with pharmacological blocking agents during CNS stimulation. This project relates directly to defining the role of the brain in cardiovascular homeostasis, and will add to our understanding of the interaction between the CNS and peripheral effector mechanisms which regulate regional and total peripheral resistance.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
5R01HL025877-09
Application #
3338348
Study Section
Cardiovascular and Renal Study Section (CVB)
Project Start
1988-08-01
Project End
1993-07-31
Budget Start
1990-08-01
Budget End
1991-07-31
Support Year
9
Fiscal Year
1990
Total Cost
Indirect Cost
Name
University of Tennessee Health Science Center
Department
Type
Schools of Medicine
DUNS #
941884009
City
Memphis
State
TN
Country
United States
Zip Code
38163
Bealer, Steven L (2002) Systemic angiotensin II alters intrinsic heart rate through central mechanisms. Brain Res Bull 58:61-5
Bealer, S L (2000) Systemic angiotensin II and volume expansion release norepinephrine in the preoptic recess. Brain Res 864:291-7
Bealer, S L (2000) Central control of cardiac baroreflex responses during peripheral hyperosmolality. Am J Physiol Regul Integr Comp Physiol 278:R1157-63
Bealer, S L (1999) Preoptic recess noradrenergic receptors control modification of baroreflex sensitivity by hypertonicity. Am J Physiol 276:R44-51
Mayne, R G; Armstrong, W E; Crowley, W R et al. (1998) Cytoarchitectonic analysis of Fos-immunoreactivity in brainstem neurones following visceral stimuli in conscious rats. J Neuroendocrinol 10:839-47
Bealer, S L (1997) Acute hypertension increases norepinephrine release in the diagonal band of Broca. Brain Res 745:313-6
Bealer, S L (1997) Preoptic recess alpha-adrenoceptors control cardiovascular responses to hyperosmolality. Am J Physiol 272:R1283-9
Wang, Y X; Crofton, J T; Bealer, S L et al. (1997) Sexual dimorphism in regional blood flow responses to vasopressin in conscious rats. Am J Physiol 273:R1126-31
Cabrera, C L; Bealer, S L; Bohr, D F (1996) Central depressor action of nitric oxide is deficient in genetic hypertension. Am J Hypertens 9:237-41
Bealer, S L (1996) Preoptic recess lesions reduce right atrial pressure responses to volume expansion. J Auton Nerv Syst 60:175-81

Showing the most recent 10 out of 36 publications