Effects of neurochemical lesions restricted to spinal cord monoaminergic neurons on blood pressure and sympathetic activity of spontaneously hypertensive rats

1983 ◽  
Vol 39 (10) ◽  
pp. 1166-1168 ◽  
Author(s):  
M. O. Carruba ◽  
H. H. Keller ◽  
M. Da Prada
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Sympathetic Activity ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Monoaminergic Neurons

Neurokinin-1 receptors and spinal cord control of blood pressure in spontaneously hypertensive rats

1999 ◽  
Vol 815 (1) ◽  
pp. 116-120 ◽  
Author(s):  
Samuel G Solomon ◽  
Ida J Llewellyn-Smith ◽  
Jane B Minson ◽  
Leonard F Arnolda ◽  
John P Chalmers ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Neurokinin 1

Prevention of hypertension and maintenance of normotension in spontaneously hypertensive rats is dependent on continuous severe dietary sodium restriction

1987 ◽  
Vol 65 (4) ◽  
pp. 573-578 ◽  
Author(s):  
Esther A. Wilczynski ◽  
Frans H. H. Leenen
Keyword(s):  
Blood Pressure ◽  
Sympathetic Activity ◽  
Spontaneously Hypertensive Rats ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Ganglionic Blockade ◽  
Dietary Sodium Restriction

Spontaneously hypertensive rats were placed on a very low (9 μmol/g) or control (101 μmol/g) sodium diet at birth or 4 weeks of age. These diets were continued to 16 weeks of age, or at 10 weeks were increased from 9 to 26 or 101 μmol/g. Sodium restriction initiated up to 4 weeks of age and continued to 16 weeks of age severely retarded growth, prevented the development of hypertension, and reduced effective sympathetic activity as assessed by the response of blood pressure to ganglionic blockade. Only a small increase in sodium intake at 10 weeks of age (to 26 μmol/g or more) resulted in a marked increase in growth rate, an elevation of blood pressure, and a return of the response to ganglionic blockade towards normal. These data indicate that very severe sodium restriction must be continuous to maintain decreased sympathetic activity and normal blood pressure in spontaneously hypertensive rats. It appears that severe dietary sodium restriction suppresses one or more of the mechanisms involved in normal growth and development of hypertension in spontaneously hypertensive rats, but these mechanisms may still proceed once the sodium intake is increased.

Altered Neuropeptide Concentrations in Spontaneously Hypertensive Rats: Cause or Consequence?

1985 ◽  
Vol 68 (1) ◽  
pp. 35-43 ◽  
Author(s):  
W. Gaida ◽  
R. E. Lang ◽  
K. Kraft ◽  
Th. Unger ◽  
D. Ganten
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Brain Stem ◽  
Spontaneously Hypertensive Rats ◽  
Genetic Defect ◽  
Brain Regions ◽  
Intermediate Lobe ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

1. Changes in brain neuropeptide content in spontaneously hypertensive rats may be primarily related to the development of hypertension or may be secondary consequences of it. 2. We have measured brain concentrations of β-endorphin, Leu-enkephalin, arginine vasopressin (AVP) and oxytocin (OXT) in stroke-prone spontaneously hypertensive rats (SHRSP) and in age-matched normotensive Wistar Kyoto (WKY) controls, as well as in SHRSP with normalized blood pressure by chronic treatment with clonidine. Opioid peptide contents were measured in 12-, 18- and 24-week-old rats. β-Endorphin was measured in the neuro-intermediate and anterior lobes of the pituitary, the hypothalamus, midbrain and brain stem; Leu-enkephalin in the neuro-intermediate lobe of the pituitary, hypothalamus, mid-brain, brain stem, as well as in the spinal cord and adrenal glands. AVP and OXT were measured in the neuro-intermediate lobe of the pituitary, hypothalamus, brain stem and spinal cord. 3. β-Endorphin in the neuro-intermediate lobe of the pituitary was significantly higher in 12- and 18-week-old SHRSP. Adrenal gland Leu-enkephalin was lower in SHRSP as compared with the WKY. 4. OXT and AVP contents were markedly reduced in all brain regions of SHRSP except the neuro-intermediate lobe of the pituitary, where no significant changes were found. 5. In no case did long-term antihypertensive treatment with clonidine reverse the altered peptide content in the SHRSP. 6. We conclude that alterations in brain neuropeptide content in SHRSP are not secondary to hypertension. The blood pressure lowering activity of clonidine appears not to depend on major alterations of peptide concentrations. A genetic defect in the synthesis of adrenal enkephalins and hypothalamic OXT and AVP seems likely from these studies.

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