Publications by authors named "Ruhui Zeng"

Article Synopsis
  • - Prostaglandin I, produced by COX in endothelial cells, can cause vasodilation in some blood vessels while paradoxically leading to endothelium-dependent constriction (EDC) in others, particularly in diseases like hypertension, though the effects of PGIS deficiency on EDC and related cardiovascular issues are not well understood.
  • - The study utilized various mouse models, including wild-type and genetically modified knockouts, to measure the impact of PGIS deficiency and assess vasomotor responses, indicating alterations in nitric oxide production and signaling.
  • - Results showed that PGIS deficiency worsened EDC and led to increases in blood pressure and cardiac issues over time, but additional removal of the thromboxane receptor improved vascular function and reduced
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Prostaglandin (PG) D, a commonly considered vasodilator through D prostanoid receptor-1 (DP1), might also evoke vasoconstriction via acting on the thromboxane (Tx)-prostanoid receptor (the original receptor of TxA; TP) and/or E prostanoid receptor-3 (one of the vasoconstrictor receptors of PGE; EP3). This study aimed to test the above hypothesis in the mouse renal vascular bed (main renal arteries and perfused kidneys) and/or mesenteric resistance arteries and determine how the vasoconstrictor mechanism influences the overall PGD effect on systemic blood pressure under in vivo conditions. Experiments were performed on control wild-type (WT) mice and mice with deficiencies in TP (TP) and/or EP3 (EP3).

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The F prostanoid receptor (FP), which accounts for the therapeutic effect of PGF in uterine atony that leads to postpartum hemorrhage and maternal morbidity, could possibly mediate vasoconstrictor effect in small or resistance arteries to elevate blood pressure that limits the clinical use of the agent in patients with cardiovascular disorders. This study aimed to test the above hypothesis with genetically altered mice. Ex vivo and in vivo experiments were performed on control wild-type (WT) mice and mice with deficiencies in FP (FP ) or thromboxane (Tx)-prostanoid receptor (the original receptor of TxA ; TP ), and/or those with an additional deficiency in E prostanoid receptor-3 (one of the vasoconstrictor receptors of PGE ; EP3 ).

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This study was to determine how endothelium-dependent contractions (EDCs) change in iliac arteries of Wistar-Kyoto (WKYs) and spontaneously hypertensive rats (SHRs) during the transition from adolescence to adulthood and the underlying mechanism(s). We also aimed to elucidate effects of L-798106, an EP3 receptor antagonist, on EDCs and the blood pressure increase in adolescent SHRs. Blood vessels were isolated for functional and biochemical analyses.

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Vasomotor reactions of prostacyclin (prostaglandin I ; PGI ) can be collectively modulated by thromboxane prostanoid receptor (TP), E-prostanoid receptor-3 (EP3), and the vasodilator I prostanoid receptor (IP). This study aimed to determine the direct effect of PGI on renal arteries and/or the whole renal vasculature and how each of these receptors is involved. Experiments were performed on vessels or perfused kidneys of wild-type mice and/or mice with deficiency in TP (TP ) and/or EP3.

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Although recognized to have an in vivo vasodepressor effect blunted by the vasoconstrictor effect of E-prostanoid receptor-3 (EP3), prostaglandin E (PGE ) evokes contractions of many vascular beds that are sensitive to antagonizing the thromboxane prostanoid receptor (TP). This study aimed to determine the direct effect of PGE on renal arteries and/or the whole renal vasculature and how each of these two receptors is involved in the responses. Experiments were performed on isolated vessels and perfused kidneys of wild-type mice and/or mice with deficiency in TP (TP ), EP3 (EP3 ), or both TP and EP3 (TP /EP3 ).

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