The cellular basis of contraction and relaxation in cardiac and vascular smooth muscle

Morgan, James P.; Perreault, C. L.; Morgan, Kathleen G.

doi:10.1016/0002-8703(91)90227-9

Cited by 56 publications

(25 citation statements)

References 27 publications

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“…The force generated by these muscles is also significantly greater than the average for muscles from the hearts of patients undergoing transplantation for end-stage cardiomyopathy, which we have found to be similar to that of controls at a 0.33-Hz stimulation frequency, 30°C, 2.5 or 16 mM [Ca"+]. (21,23). Digitalis (i.e., strophanthidin and acetylstrophanthidin) exacerbated systolic and diastolic dysfunction (Fig.…”

Section: Resultsmentioning

confidence: 55%

Diastolic dysfunction in hypertrophic cardiomyopathy. Effect on active force generation during systole.

Gwathmey¹,

Warren²,

Briggs³

et al. 1991

J. Clin. Invest.

167

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Section: Resultsmentioning

confidence: 55%

Diastolic dysfunction in hypertrophic cardiomyopathy. Effect on active force generation during systole.

Gwathmey¹,

Warren²,

Briggs³

et al. 1991

J. Clin. Invest.

167

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“…However, vasoconstriction modulation can be the result of Ca 2+ sensitization, the inhibition of myosin light chain phosphatase activity, and so independent of changes in Ca 2+ Fig. 1a and table 3 show a reduction in E within cells [26]. The inhibition of NO generation may be result in the impairment of endothelial-dependent dilation; [27] showed that NO synthase uncoupling and stimulation of reactive oxygen species (ROS) generation was associated with impaired pulmonary artery endothelial-dependent relaxation.…”

Section: Fig 2: Effect Of Apigenin Incubation (7 µM 20 Min) On the mentioning

confidence: 99%

Normal Vascular Reactivity Is Restored by Apigenin in Diabetic Rats

El-Bassossy

Desoky

Alahdal

et al. 2018

Int J Pharm Pharm Sci

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Objective: Diabetes is a disease whose complications have serious implications for the health of sufferers; one of the most serious such complications is the deterioration of vascular reactivity. Apigenin is a natural flavonoid with PKC inhibiting and antioxidant properties. In this study, the impact of apigenin on vascular reactivity deterioration was investigated.Methods: Insulin resistance (IR) and insulin deficiency (ID) were induced by fructose and streptozotocin respectively. The isolated aortae vasoconstriction response to phenylephrine (PE) and potassium chloride (KCl) in addition to the vasodilation response to acetylcholine (ACh) and sodium nitroprusside (SNP) were tested.Results: IR and ID were associated with significantly exaggerated vasoconstriction to KCl and PE while significantly impaired vasodilation to ACh. Response to SNP was not significantly affected by both IR and ID. In vitro incubation with apigenin (7 7µM) for 20 min restored normal responses to PE, KCl and ACh in aortae isolated from insulin-resistant or insulin-deficient rats. Incubation for one hour with the PKC stimulant, phorbol 12-myristate 13-acetate (PMA, 800 nM) resulted in aortic impairment similar to that seen in aortae isolated from IR and ID animals. Incubation with both apigenin prevented PMA-induced exaggerated vasoconstriction response to both PE and KCl.Conclusion: Apigenin alleviates vascular exaggerated vasoconstriction and impaired dilation associated with diabetes or PKC activated.

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“…Defective Ca 2+ homeostasis plays a critical role in human heart failure [30]. Ca 2+ plays an active role in the excitation-contraction coupling; when released into the cytosol, Ca 2+ mainly targets myofilaments and generates the contractile force of the heart, whereas the removal of Ca 2+ from the cytosol induces heart relaxation.…”

Section: Animal Models Of CCmentioning

confidence: 99%