Vascular protein kinase C in Wistar-Kyoto and spontaneously hypertensive rats

Silver, Paul J.; Cumiskey, Wayne R.; Harris, Andrea

doi:10.1016/0014-2999(92)90322-u

Cited by 13 publications

(6 citation statements)

References 26 publications

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“…In this study, we demonstrated the increased responsiveness of SHR aortae to TPA in Ca2+-free condition, which is consistent with previous reports (Bruschi et al, 1988 ;MacKay and Cheung, 1987 ;Silver et al, 1988Silver et al, , 1992Soloviev and Bershtein, 1992 ;Turla and Webb, 1987). This finding supports our conclusion that the participation of PKC in 5-HT-, PE-, and…”

Section: Role Of Pkc In Agonist-induced Contractionssupporting

confidence: 93%

Relationship between Intracellular Ca2+ Store and Protein Kinase C in Agonist-Induced Contraction of Hypertensive Rat Aortae.

Shimamoto

Daniel

et al. 1999

J. Smooth Muscle Res.

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The roles of intracellular Ca2+ store and protein kinase C (PKC) in vascular contractile responses independent of Ca2+ influx were studied using aortic rings from spontaneously hypertensive rat (SHR) and Wistar-Kyoto rat (WKY). The functional sizes of agonistsensitive intracellular Ca2+ store were estimated as the peak response to agonist after PKC inhibition with calphostin C (Cal-C), a PKC inhibitor. The participation of PKC in 5hydroxytryptamine-, phenylephrine-, and endothelin-1 (ET-1)-induced contractions in aortae of SHR was equal to, or greater than that in WKY. In contrast, compared with WKY, SHR aortae possessed a greater size of endothelin-1-sensitive Ca2+ store, a similar size of 5-hydroxytryptamine-sensitive Ca2+ store, and a smaller size of phenylephrinesensitive Ca2+ store. Based on these data, both PKC activation and functional size of intracellular Ca2+ store differ between SHR and WKY and these differences are selective among agosists.

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Section: Role Of Pkc In Agonist-induced Contractionssupporting

confidence: 93%

Relationship between Intracellular Ca2+ Store and Protein Kinase C in Agonist-Induced Contraction of Hypertensive Rat Aortae.

Shimamoto

Daniel

et al. 1999

J. Smooth Muscle Res.

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“…PKC also plays a role in the regulation of the enhanced contraction in SHR [29,30]. However, the contribution of PKC to agonist-induced contractions in the aortas of SHR has been reported to be equal to the equivalent contribution in WKY [31].…”

Section: Discussionmentioning

confidence: 88%

Sevoflurane inhibits angiotensin II-induced Rho kinase-mediated contraction of vascular smooth muscle from spontaneously hypertensive rat

et al. 2011

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“…In the hypertensive situation, increased contractile responses to agonists have been correlated with an enhanced protein kinase C activity [7], augmented phosphoinositide metabolism [8], and increased Ca 2+ mobilization [9]. Whether these alterations are related to a specific · 1 -adrenoceptor subtype in the vasculature of SHR, different to the one present in WKY, is not exactly known [10].…”

Section: Introductionmentioning

confidence: 99%

Hypotensive Effects of Eugenosedin-A with Serotonin, Alpha- and Beta-Adrenoceptor Antagonistic Activities in Spontaneously Hypertensive and Normotensive Rats

Shen

Chiu²,

Chen³

et al. 2004

Pharmacology

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Eugenosedin-A is a newly synthesized compound with special serotonergic, α- and β₁-adrenergic blocking actions. Intravenous injection of eugenosedin-A significantly caused dose-dependent decreases in the mean arterial blood pressure and heart rate in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). The effects of eugenosedin-A-decreased blood pressure and heart rate in SHR were more potent than in WKY. In in vitro experiments, eugenosedin-A competitively antagonized the serotonin-, norepinephrine- and clonidine-induced vasocontraction in a concentration-dependent manner in isolated thoracic aorta of WKY and SHR. We also observed that eugenosedin-A competitively antagonized the isoproterenol-induced positive inotropic effects in a concentration-dependent manner in the isolated left atrium of WKY and SHR. These findings clearly suggested that eugenosedin-A possesses α₁/α₂, β₁ and 5-HT_2A receptor-blocking activities. The order of pA₂ values in isolated tissues of WKY was 5-HT_2A > α₁/α₂ > β₁. However, the order of pA₂ values in isolated tissues of SHR was α₁/α₂ >5-HT_2A > β₁. Similarly, we found that the in vitro functional activity of eugenosedin-A is quite different between WKY and SHR. On the other hand, in the isolated rabbit ear artery sensitized with 16 mmol/l K⁺, eugenosedin-A antagonized 5-nonyloxytryptamine- and serotonin-induced vasocontractions, indicating that it also blocked 5-HT_1B and 5-HT_2A receptors. In radioligand binding experiments, eugenosedin-A had significant binding affinities on α₁/α₂, β₁, 5-HT_1B and 5-HT_2A receptors. Finally, we suggest that the hypotensive effects of eugenosedin-A can be attributed to its multiple actions on the blockade of 5-HT_1B, 5-HT_2A, α and β₁ receptors in both WKY and SHR strains.

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Vascular protein kinase C in Wistar-Kyoto and spontaneously hypertensive rats

Cited by 13 publications

References 26 publications

Relationship between Intracellular Ca2+ Store and Protein Kinase C in Agonist-Induced Contraction of Hypertensive Rat Aortae.

Relationship between Intracellular Ca2+ Store and Protein Kinase C in Agonist-Induced Contraction of Hypertensive Rat Aortae.

Sevoflurane inhibits angiotensin II-induced Rho kinase-mediated contraction of vascular smooth muscle from spontaneously hypertensive rat

Hypotensive Effects of Eugenosedin-A with Serotonin, Alpha- and Beta-Adrenoceptor Antagonistic Activities in Spontaneously Hypertensive and Normotensive Rats

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