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Hunter C. Champion

Researcher at Johns Hopkins University

Publications -  275
Citations -  23191

Hunter C. Champion is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Pulmonary hypertension & Adrenomedullin. The author has an hindex of 74, co-authored 275 publications receiving 21959 citations. Previous affiliations of Hunter C. Champion include Johns Hopkins University School of Medicine & National Institutes of Health.

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Tissue Factor Pathway Inhibitor Overexpression Inhibits Hypoxia-Induced Pulmonary Hypertension

TL;DR: It is demonstrated that overexpression of TFPI results in improved hemodynamic performance and reduced pulmonary vascular remodeling in a murine model of hypoxia-induced PH, which is in part due to the autocrine and paracrine effects of T FPI overexpressive.
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Proadrenomedullin N-Terminal 20 Peptide (PAMP), Acting Through PAMP(12–20)-Sensitive Receptors, Inhibits Ca2+-Dependent, Agonist-Stimulated Secretion of Human Adrenal Glands

TL;DR: It is suggested that both C- and N-terminal sequences of the PAMP molecule are required for this peptide to exert its antisecretagogue action on the human adrenal gland, and that PAMP(12-20) acts as a weak antagonist of PAMP receptors.
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Adrenomedullin induces penile erection in the cat

TL;DR: It is demonstrated that intracavernous injection of adrenomedullin induces a short-lived erection in cats that is not due to the release of nitric oxide.
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Tone-dependent vasodilator responses to proadrenomedullin NH2-terminal 20 peptide in the hindquarters vascular bed of the rat.

TL;DR: Vasodilator responses to PAMP and ADM were correlated with the basal level of tone, suggesting that responses to both peptides are dependent on the baseline level of vasoconstrictor tone in the hindquarters vascular bed of the rat.
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Vasodilator responses to acetylcholine, bradykinin, and substance P are mediated by a TEA-sensitive mechanism.

TL;DR: TEA attenuates vasodilator responses to acetylcholine, bradykinin, and substance P by inhibiting the release of endothelium-derived relaxing factor, suggesting that a TEA-sensitive mechanism is not involved in the maintenance of baseline tone in this vascular bed.