PMID- 7141603
OWN - NLM
STAT- MEDLINE
DCOM- 19830107
LR  - 20190722
IS  - 0194-911X (Print)
IS  - 0194-911X (Linking)
VI  - 4
IP  - 6
DP  - 1982 Nov-Dec
TI  - Contribution of the sympathetic nervous system to the hypertensive effect of a 
      high sodium diet in stroke-prone spontaneously hypertensive rats.
PG  - 773-81
AB  - In stroke-prone spontaneously hypertensive rats (SHRSP) plasma norepinephrine 
      levels and vascular reactivity to norepinephrine are increased and intravascular 
      volume is reduced during the developmental phase of hypertension. Since the 
      accelerated rise in blood pressure following sodium-loading in SHRSP cannot be 
      attributed to the volume-retaining properties of sodium, the effects of an 
      increased dietary intake of sodium on biochemical parameters of sympathetic 
      vascular tone were investigated. The following results were obtained. First, the 
      increased reactivity of vascular smooth muscle was further augmented in 
      sodium-treated SHRSP; the degree of supersensitivity was positively correlated to 
      the plasma sodium concentration. After blockade of the neuronal uptake by 30 
      microM cocaine, no difference in vascular reactivity to norepinephrine was 
      detected between SHRSP on a normal and SHRSP on a high-sodium diet. Second, the 
      inactivation of norepinephrine by the neuronal uptake was impaired in rats on a 
      high-sodium diet, the impairment being more pronounced in SHRSP than in 
      Wistar-Kyoto (WKY) rats. This decreased inactivation could be expected to cause 
      higher concentrations of the neurotransmitter at the receptor site if the 
      transmitter release from the nerve ending remains constant. Third, the release of 
      norepinephrine and epinephrine into the plasma was increased in sodium-loaded 
      SHRSP but not in sodium-loaded WKY. Cold exposure exaggerates these differences 
      between normotensive and hypertensive rats. These findings suggest that a 
      high-sodium intake modifies the transmission of sympathetic impulses at the level 
      of the nerve terminal in both WKY and SHRSP. In the normotensive rats, moderate 
      impairment of norepinephrine inactivation, however, was balanced by an 
      appropriate reduction in central sympathetic discharge following sodium-loading. 
      In the hypertensive rats, the peripheral disturbance in norepinephrine 
      inactivation due to sodium-loading was obviously not balanced by an adequate 
      withdrawal of central sympathetic discharge. The resultant hemodynamic change was 
      a further increase in the sympathetically mediated vasoconstriction, which is 
      regarded as at least one of the main mechanisms of the sodium-dependent 
      acceleration of hypertension in SHRSP.
FAU - Dietz, R
AU  - Dietz R
FAU - Schomig, A
AU  - Schomig A
FAU - Rascher, W
AU  - Rascher W
FAU - Strasser, R
AU  - Strasser R
FAU - Luth, J B
AU  - Luth JB
FAU - Ganten, U
AU  - Ganten U
FAU - Kubler, W
AU  - Kubler W
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Hypertension
JT  - Hypertension (Dallas, Tex. : 1979)
JID - 7906255
RN  - 451W47IQ8X (Sodium Chloride)
RN  - X4W3ENH1CV (Norepinephrine)
SB  - IM
MH  - Animals
MH  - Cerebrovascular Disorders/physiopathology
MH  - Disease Susceptibility
MH  - Female
MH  - Hindlimb/blood supply
MH  - Hypertension/chemically induced/*genetics
MH  - Muscle, Smooth, Vascular/drug effects
MH  - Norepinephrine/pharmacology
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Sodium Chloride/*adverse effects
MH  - Sympathetic Nervous System/*physiology
EDAT- 1982/11/01 00:00
MHDA- 1982/11/01 00:01
CRDT- 1982/11/01 00:00
PHST- 1982/11/01 00:00 [pubmed]
PHST- 1982/11/01 00:01 [medline]
PHST- 1982/11/01 00:00 [entrez]
AID - 10.1161/01.hyp.4.6.773 [doi]
PST - ppublish
SO  - Hypertension. 1982 Nov-Dec;4(6):773-81. doi: 10.1161/01.hyp.4.6.773.