Diminished sympathetic silent period in spontaneously hypertensive rats

1979 ◽  
Vol 236 (3) ◽  
pp. R147-R152 ◽  
Author(s):  
L. P. Schramm ◽  
G. N. Barton

To determine if elevated sympathetic activity occurs in spontaneously hypertension, the silent period induced in splanchnic nerves following electrical stimulation of dorsal medullary sympathoexcitatory sites was compared in anesthetized normotensive Wistar Kyoto rats (WKYs) and Okamoto spontaneously hypertensive rats (SHRs). The strength of silent periods was defined as the degree of inhibition of responses to testing stimuli delivered at various latencies following conditioning trains, and it was assumed to be inversely related to the level of sympathetic activity. Weanling SHRs exhibited weaker silent periods than weanling WKYs although, at that age, the arterial pressures of the strains were not significantly different. Silent periods were also weaker in adult SHRs than in adult WKYs. This difference persisted after arterial pressures, which fell under anesthesia, were raised by phenylephrine infusions to the respective "normal" levels in each strain. These results support the hypothesis that elevated sympathetic activity exists during both the development and maintenance of spontaneous hypertension in rats.

1980 ◽  
Vol 59 (s6) ◽  
pp. 171s-173s ◽  
Author(s):  
R. Dietz ◽  
A. Schoumig ◽  
W. Rascher ◽  
R. Strasser ◽  
W. Kubler

1. Salt loading accelerates and increases the rise in blood pressure (spSH) in stroke-prone spontaneously hypertensive rats, but not in Wistar-Kyoto (WK) rats. 2. In both strains a slight increase in plasma volume was obtained during salt loading. 3. Salt loading caused a distinct increase in plasma noradrenaline concentration in spSH rats, but a slight decrease in WK rats. Plasma adrenaline and dopamine concentrations remained unaffected. 4. Exposure to cold resulted in a more marked stimulation of sympathoadrenal and sympathoneuronal activity in salt-loaded spSH rats than in spSH rats on a normal sodium diet. 5. It is concluded that salt loading results in a further increase of the already elevated sympathetic activity in spSH rats.


2003 ◽  
Vol 284 (3) ◽  
pp. R682-R688 ◽  
Author(s):  
Delphine Behr-Roussel ◽  
Philippe Chamiot-Clerc ◽  
Jacques Bernabe ◽  
Katell Mevel ◽  
Laurent Alexandre ◽  
...  

Hypertensive men have a higher prevalence of erectile dysfunction (ED) than the general population. Experimental evidence of ED in hypertensive animals is scarce. This study evaluates the erectile function of spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar-Kyoto rats (WKY) in vivo by the increase in intracavernosal pressure after electrical stimulation of the cavernous nerve (CN) and by isometric tension studies on corporal strips. Frequency-dependent erectile responses to CN stimulations were reduced in SHR. Phenylephrine induced lower corporal contractions in SHR although pD2 values were similar to WKY. Endothelium-dependent relaxations to ACh were impaired significantly in SHR, and indomethacin improved these relaxations in both WKY and SHR, the latter thus reaching values similar to WKY. Corporal relaxations to sodium nitroprusside were enhanced in SHR. Thus a dysfunctional α-adrenergic contraction of the corporal smooth muscle, an increased cyclooxygenase-dependent constrictor tone, and/or a defect in endothelium-dependent reactivity are associated with the altered erectile mechanisms in SHR. Drugs targeting endothelial dysfunction may delay the occurrence of ED as a complication of hypertension.


1999 ◽  
Vol 277 (4) ◽  
pp. R1057-R1062 ◽  
Author(s):  
Takahiro Nagayama ◽  
Takayuki Matsumoto ◽  
Makoto Yoshida ◽  
Mizue Suzuki-Kusaba ◽  
Hiroaki Hisa ◽  
...  

We investigated the role of nicotinic and muscarinic receptors in secretion of catecholamines induced by transmural electrical stimulation (ES) from isolated perfused adrenal glands of spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto (WKY) rats. ES (1–10 Hz) produced frequency-dependent increases in epinephrine (Epi) and norepinephrine (NE) output as measured in perfusate. The ES-induced increases in NE output, but not Epi output, were significantly greater in adrenal glands of SHRs than in those of WKY rats. Hexamethonium (10–100 μM) markedly inhibited the ES-induced increases in Epi and NE output from adrenal glands of SHRs and WKY rats. Atropine (0.3–3 μM) inhibited the ES-induced increases in Epi and NE output from adrenal glands of SHRs, but not from those of WKY rats. These results suggest that endogenous acetylcholine-induced secretion of adrenal catecholamines is predominantly mediated by nicotinic receptors in SHRs and WKY rats and that the contribution of muscarinic receptors may be different between these two strains.


2003 ◽  
Vol 9 (3) ◽  
pp. 102-106
Author(s):  
Yu. I. Shcherbin ◽  
R. S. Khrustaleva ◽  
V. A. Cirlin

In chloralose anesthetized and paralyzed spontaneously hypertensive rats (SHR) a somatosympathetic reflex in the cervical sympathetic trunk elicited by a single electrical shock to forelimb afferent fibres in the median nerve was recorded. It has been shown that the somatosympathetic reflex consists of two responses and following silent period. The А-response evoked by the somatic myelinated afferent fibres stimulation, and C-respon.se elicited by the both stimulation of myelinated and unmyelinated afferent fibres. The silent period occurred with the myelinated fibres stimulation. Its duration was proportional to the electrical shock amplitude. The А-response consisted of four waves, the three of them formed early and late responses.


1993 ◽  
Vol 264 (6) ◽  
pp. H2051-H2055 ◽  
Author(s):  
F. H. Leenen ◽  
E. Harmsen ◽  
H. Yu ◽  
C. Ou

High dietary Na+ intake enhances pressor and sympathoexcitatory responses in spontaneously hypertensive rats (SHR) but not Wistar-Kyoto (WKY) rats. To evaluate the possible contribution of central ouabain-like activity (OLA), brain and peripheral OLA was assessed in SHR vs. WKY rats at 4 wk of age and after 2 and 4 wk of high vs. control Na+ intake started at 4 wk of age. In SHR, hypertension developed with maturation and was exacerbated by high Na+ intake. With control Na+ intake, SHR showed higher OLA at 4, 6, and 8 wk of age in the pituitary and hypothalamus and also by 8 wk in the adrenals and left ventricle but not in plasma. High Na+ intake increased OLA in all tissues examined in both WKY rats and SHR. After 2 wk on high Na+, only OLA in hypothalamus and pituitary was higher in SHR vs. WKY rats; after 4 wk on high Na+, peripheral (i.e., adrenals, left ventricle, and plasma) OLA was also higher. These results indicate that in SHR the development of hypertension is associated early on with increases in central OLA and in a later phase with increases in peripheral OLA as well. High Na+ intake increases OLA in both SHR and WKY rats, but the higher OLA may affect sympathetic activity and blood pressure only in SHR.


1982 ◽  
Vol 243 (5) ◽  
pp. R506-R511 ◽  
Author(s):  
L. P. Schramm ◽  
E. S. Chornoboy

To test the hypothesis that sympathetic hyperactivity and hyperexcitability in spontaneously hypertensive rats (SHR) is generated at spinal and/or ganglionic levels, we measured integrated renal nerve activity (before ganglionic blockade) and adrenal nerve activity (after ganglionic blockade) in 12- to 14-wk-old SHR and normotensive Wistar-Kyoto rats (WKY). Rats were anesthetized with alpha-chloralose, artificially respired, and paralyzed. Spinal cords were transected at C1 to eliminate normal supraspinal control of sympathetic activity. The effectiveness of descending sympathoexcitatory and sympathoinhibitory pathways was tested by measuring changes in nerve activity elicited by graded spinal stimulation. Spontaneous renal nerve activity was elevated in SHR, but stimulation of descending excitatory pathways caused similar responses in SHR and WKY. Spontaneous adrenal preganglionic nerve activity was similar in SHR and WKY, but excitatory stimulation elicited larger adrenal nerve responses in SHR. We conclude that spinal and/or ganglionic mechanisms may generate a component of the sympathetic hyperactivity exhibited by SHR. The larger adrenal preganglionic nerve responses to excitatory stimulation in SHR suggest that spinal systems may be partially responsible for adrenomedullary hyperexcitability in spontaneous hypertension.


1987 ◽  
Vol 65 (12) ◽  
pp. 2386-2389 ◽  
Author(s):  
P. K. T. Pang ◽  
S. Harvey ◽  
P. A. Doris

Plasma parathyroid hormone levels (pPTH) have been measured by radioimmunoassay (RIA) in young spontaneously hypertensive rats (SHR) and normotensive Wistar–Kyoto controls (WKY) aged from 6 to 16 weeks to assess the possible role of PTH during the development of hypertension. Three antisera were used in the RIAs. One antiserum was directed toward the inactive C-terminal fragment of PTH, another toward the bioactive N-terrninal fragment (PTH 1–34), and a third was obtained by immunization against intact PTH 1–84. Blood pressures were measured by tail-cuff plethysmography with prewarming. Blood ionized calcium and sodium concentrations (b[Ca2+] and b[Na+]) were determined by ion-selective electrolyte analysis. No significant differences were observed between pPTH in the SHR compared with WKY during the development of hypertension. Neither were significant differences in b[Ca2+] or b[Na+] present at any age. The expected progression of hypertension in SHRs was observed and blood pressure was significantly greater in SHR than in WKY at all times. The results suggest that differences in pPTH and b[Ca2+] in SHR reported in other studies may be secondary phenomena to the establishment of hypertension. Our data suggest that PTH is not involved in the pathogenetic processes occurring during the development of spontaneous hypertension in rats.


2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Gean Domingos ◽  
Fernanda Santos‐Almeida ◽  
Luiz Eduardo Silva ◽  
Daniel Dias ◽  
Carlos Alberto Silva ◽  
...  

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