scholarly journals The somato-sympathetic reflex in the spontaneous hypertensive rats

2003 ◽  
Vol 9 (3) ◽  
pp. 102-106
Author(s):  
Yu. I. Shcherbin ◽  
R. S. Khrustaleva ◽  
V. A. Cirlin
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Silent Period ◽  
Hypertensive Rats ◽  
Electrical Shock ◽  
Spontaneously Hypertensive ◽  
Shock Amplitude ◽  
Somatosympathetic Reflex ◽  
Cervical Sympathetic ◽  
Myelinated Fibres ◽  
Stimulation Of

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.

Diminished sympathetic silent period in spontaneously hypertensive rats

1979 ◽  
Vol 236 (3) ◽  
pp. R147-R152 ◽  
Author(s):  
L. P. Schramm ◽  
G. N. Barton
Keyword(s):  
Electrical Stimulation ◽  
Sympathetic Activity ◽  
Spontaneously Hypertensive Rats ◽  
Silent Period ◽  
Spontaneous Hypertension ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Splanchnic Nerves ◽  
Wistar Kyoto ◽  
Stimulation Of

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.

Stimulation of brain cannabinoid CB 1 receptors can ameliorate hypertension in spontaneously hypertensive rats

2020 ◽  
Vol 47 (7) ◽  
pp. 1254-1262
Author(s):  
Takahiro Shimizu ◽  
Masaki Yamamoto ◽  
Suo Zou ◽  
Shogo Shimizu ◽  
Youichirou Higashi ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Stimulation Of

Defective nitric oxide production impairs angiotensin II-induced Na-K-ATPase regulation in spontaneously hypertensive rats

2012 ◽  
Vol 302 (1) ◽  
pp. F47-F51 ◽  
Author(s):  
Apurva A. Javkhedkar ◽  
Mustafa F. Lokhandwala ◽  
Anees Ahmed Banday
Keyword(s):  
Nitric Oxide ◽  
Spontaneously Hypertensive Rats ◽  
Proximal Tubules ◽  
Ang Ii ◽  
Hypertensive Rats ◽  
High Concentration ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Proximal Tubular ◽  
Stimulation Of

Angiotensin (ANG) II via ANG II type 1 receptors (AT1R) activates renal sodium transporters including Na-K-ATPase and regulates sodium homeostasis and blood pressure. It is reported that at a high concentration, ANG II either inhibits or fails to stimulate Na-K-ATPase. However, the mechanisms for these phenomena are not clear. Here, we identified the signaling molecules involved in regulation of renal proximal tubular Na-K-ATPase at high ANG II concentrations. Proximal tubules from spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats were incubated with low concentrations of ANG II (pM), which activated Na-K-ATPase in both the groups; however, the stimulation was more robust in SHR. A high concentration of ANG II (μM) failed to stimulate Na-K-ATPase in WKY rats. However, in SHR ANG II (μM) continued to stimulate Na-K-ATPase, which was sensitive to the AT1R antagonist candesartan. In the presence of NG-nitro-l-arginine methyl ester (l-NAME), a nitric oxide (NO) synthase (NOS) inhibitor, ANG II (μM) caused stimulation of Na-K-ATPase in proximal tubules of WKY rats while having no further stimulatory effect in SHR. ANG II (μM), via AT1R, increased proximal tubular NO levels in WKY rats but not in SHR. In SHR, NOS was uncoupled as incubation of proximal tubules with ANG II and l-arginine, a NOS substrate, caused superoxide generation only in SHR and not in WKY rats. The superoxide production in SHR was sensitive to l-NAME. There was exaggerated proximal tubular AT1R-G protein coupling and NAD(P)H oxidase activation in response to ANG II (μM) in proximal tubules of SHR compared with WKY rats. In SHR, inhibition of NADPH oxidase restored NOS coupling and ANG II-induced NO accumulation. In conclusion, at a high concentration ANG II (μM) activates renal NO signaling, which prevents stimulation of Na-K-ATPase in WKY rats. However, in SHR ANG II (μM) overstimulates NADPH oxidase, which impairs the NO system and leads to continued Na-K-ATPase activation.

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