Norepinephrine Release in Arteries of Spontaneously Hypertensive Rats

Zsoter, T; Wolchinsky, C.; Lawrin, M.; Sirko, S.

doi:10.3109/10641968209060753

Cited by 18 publications

(9 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Sybertz, personal communication In the young (46-day-old) SHR, vasoconstrictor responses and transmitter release in the perfused renal vascular bed were greater (approximately 2-fold at 6 Hz) than in normotensive controls (Collis et al, 1980). Also, in 7-to 9-week-old SHR, tail arteries transmural stimulation released approximately twice as much 3 H-labeled adrenergic transmitter as in WKY control rats (Zsoter et al, 1982). Older (6month-old) SHR exhibited a decrease in norepinephrine overflow in the perfused kidney preparation during nerve stimulation, compared with WKY controls (Vanhoutte et al, 1982), yet, in this and other studies, the vasoconstrictor responses to stimulation were similar (Lais et al, 1974;.…”

Section: Facilitation Of Adrenergic Transmitter Releasesupporting

confidence: 50%

Peripheral neurogenic factors in acute and chronic alterations of arterial pressure.

Zimmerman¹

1983

Circulation Research

View full text Add to dashboard Cite

ReferencesAdJer-Graschinsky E, Langer SZ (1975) Possible role of a 0adrenoceptor in the regulation of noradrenaline release by nerve stimulation through a positive feed-back mechanism. Br J Pharmacol 53: 43-50 Angus JA, West MJ, Korner PI (1975) Estimation of magnitude of autonomic and non-autonomic components of rundlimb vascular resistance in renal hypertension. Clin Exp Pharmacol Physiol (suppl 2): 149-152 Antonaccio MJ, Kerwin L (1980) Evidence for prejunctional inhibition of norepinephrine release by captopril in spontaneously hypertensive rats.

show abstract

Section: Facilitation Of Adrenergic Transmitter Releasesupporting

confidence: 50%

Peripheral neurogenic factors in acute and chronic alterations of arterial pressure.

Zimmerman¹

1983

Circulation Research

View full text Add to dashboard Cite

show abstract

“…Zsoter et al 19 also found significantly more fHJnorepinephrine overflow upon electrical stimulation in tail artery from 7-9-week-old SHR than the WKY control rats. Recently, one of us 20 examined the Ca 2+ dependency of norepinephrine release and vascular responsiveness in the perfused mesenteric preparations of SHR and deoxycorticosterone acetate (DOCA)-salt hypertensive rats and found that norepinephrine overflow was enhanced only in young SHR (7-8-week-old) and in the chronic phase of DOCA-salt hypertension.…”

Section: Week-old) Shr As An Indicationmentioning

confidence: 87%

“…By use of tissue in vitro labeled with [ 3 H]norepinephrine, Vanhoutte et al 16 -18 also found significantly more tritium overflow from the kidney of young SHR but not in the kidney of adult rats (4-6 months of age) when compared with the normotensive controls whereas Zsoter et al 19 observed more tritium over- 'Significant difference between 7-week-old WKY and SHR by one-way analysis of variance.…”

Section: Discussionmentioning

confidence: 99%

Norepinephrine overflow in perfused mesenteric arteries of spontaneously hypertensive rats.

Hano

Rho

1989

Hypertension

View full text Add to dashboard Cite

We examined the overflow of endogenous norepinephrine with electrical stimulation, the associated pressor response, and rate of initial neuronal uptake of [ 3 H] norepinephrine in perfused mesenteric arteries of 7-and 13-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. The tissues of two rats, a spontaneously hypertensive and a WKY control rat, were simultaneously processed and subjected to the same electrical stimulation. Both absolute and fractional overflow of endogenous norepinephrine during periarterial nerve stimulation (5 and 10 Hz for 1 minute) in the tissue of 7-week-old SHR was significantly greater whereas overflow of 13-week-old SHR was equivalent as compared with that of the age-matched WKY rats. The tissue content of norepinephrine was 20-25% higher in SHR of both ages. There was significantly enhanced [ 3 H] norepinephrine uptake in the tissues of young SHR, but no difference was observed in the older SHR. The pressor response to periarterial nerve stimulation was significantly enhanced in 7-week-old SHR and much more so at the older age as compared with the WKY control rats. Exogenous norepinephrine dose-response curves in the tissues of 7-week-old SHR exhibited a parallel leftward shift, characteristic of a change in sensitivity, whereas that of 13-week-old SHR showed a much steeper slope as compared with the respective WKY control rats. This finding suggests that in addition to smooth muscle supersensitivity, structural alterations had occurred in vasculature of 13-week-old SHR. These data indicate that in SHR both the exocytotic release of norepinephrine and the responsiveness of the vascular smooth muscle cells are enhanced in the developmental stage of hypertension whereas smooth muscle supersensitivity to norepinephrine and nonspecific structural alterations primarily contribute to the maintenance of hypertension at 13 weeks of age. {Hyperten-sion 1989;14:44-53)

show abstract

“…An established model in which an activated sympathetic tone plays a major role is the SHR strain, which develops hypertensive blood pressure levels at 5 to 6 weeks of age, followed by cardiac and vascular hypertrophy and ultimately end-organ failure later in life, if the hypertension remains untreated [24]. In SHR, an increased NE overflow from postganglionic nerve terminals has already been shown before [14], [15]. Thus, we chose SHR to study the effects of the novel adenosine-A 1 agonist on the regulation of the sympathetic tone, and compared them to the effects in Wistar rats.…”

Section: Discussionmentioning

confidence: 99%

“…To test this hypothesis, the effects of the adenosine-A 1 agonist capadenoson on the NE release in vitro as well as on heart rate in vivo was evaluated in two rat strains with genetically different levels of sympathetic activity, Wistar and Spontaneously Hypertensive rats (SHR). The latter strain has an increased sympathetic tone already at rest and exhibits a much stronger increase in sympathetic tone upon restraint stress than Wistar rats [14], [15].…”

Section: Introductionmentioning

confidence: 89%

Selective Attenuation of Norepinephrine Release and Stress-Induced Heart Rate Increase by Partial Adenosine A1 Agonism

et al. 2011

View full text Add to dashboard Cite

The release of the neurotransmitter norepinephrine (NE) is modulated by presynaptic adenosine receptors. In the present study we investigated the effect of a partial activation of this feedback mechanism. We hypothesized that partial agonism would have differential effects on NE release in isolated hearts as well as on heart rate in vivo depending on the genetic background and baseline sympathetic activity. In isolated perfused hearts of Wistar and Spontaneously Hypertensive Rats (SHR), NE release was induced by electrical stimulation under control conditions (S1), and with capadenoson 6 · 10−8 M (30 µg/l), 6 · 10−7 M (300 µg/l) or 2-chloro-N6-cyclopentyladenosine (CCPA) 10−6 M (S2). Under control conditions (S1), NE release was significantly higher in SHR hearts compared to Wistar (766+/−87 pmol/g vs. 173+/−18 pmol/g, p<0.01). Capadenoson led to a concentration-dependent decrease of the stimulation–induced NE release in SHR (S2/S1 = 0.90±0.08 with capadenoson 6 · 10−8 M, 0.54±0.02 with 6 · 10−7 M), but not in Wistar hearts (S2/S1 = 1.05±0.12 with 6 · 10−8 M, 1.03±0.09 with 6 · 10−7 M). CCPA reduced NE release to a similar degree in hearts from both strains. In vivo capadenoson did not alter resting heart rate in Wistar rats or SHR. Restraint stress induced a significantly greater increase of heart rate in SHR than in Wistar rats. Capadenoson blunted this stress-induced tachycardia by 45% in SHR, but not in Wistar rats. Using a [35S]GTPγS assay we demonstrated that capadenoson is a partial agonist compared to the full agonist CCPA (74+/−2% A1-receptor stimulation). These results suggest that partial adenosine A1-agonism dampens stress-induced tachycardia selectively in rats susceptible to strong increases in sympathetic activity, most likely due to a presynaptic attenuation of NE release.

show abstract

Norepinephrine Release in Arteries of Spontaneously Hypertensive Rats

Cited by 18 publications

References 18 publications

Peripheral neurogenic factors in acute and chronic alterations of arterial pressure.

Peripheral neurogenic factors in acute and chronic alterations of arterial pressure.

Norepinephrine overflow in perfused mesenteric arteries of spontaneously hypertensive rats.

Selective Attenuation of Norepinephrine Release and Stress-Induced Heart Rate Increase by Partial Adenosine A1 Agonism

Contact Info

Product

Resources

About