2004 41: 147–158.Ĭastillo-Hernandez JR., Torres-Tirado D., Barajas-Espinosa A., Chi-Ahumada E., Ramiro-Diaz J., Ceballos G., et al. Intracoronary Angiotensin II causes inotropic and vascular effects via different paracrine mechanisms. 2021 35: 2021.Ĭastillo-Hernandez JR., Rubio-Gayosso I., Sada-Ovalle I., Garcia- Vazquez A., Ceballos G., Rubio R. A limited vs a transient AT1R internalization indicates that distinct mechanisms of AT1R activation are possible. Blood Vessels 1975 12: 307–310.Ĭastillo-Hernández J., Rubio R., Maldonado-Cervantes MI. Evidence for alpha-adrenergic receptors on intimal endothelium. Evidence for a cell surface adenosine receptor on coronary myocytes and atrial muscle cells. Evidence for an adenosine receptor on the surface of dog coronary myocytes. Olsson RA., Davis CJ., Khouri EM., Paterson ER. The coronary endothelium: a highly active metabolic barrier for adenosine. Nees S., Herzog V., Becker BF., Bock M., Des Rosiers C., Gerlach E. Functional implications of sole and selective activation of intravascular coronary endothelial hormonal receptors. Intravascular adenosine: the endothelial mediators of its negative dromotropic effects. Endothelium‐mediated negative dromotropic effects of intravascular acetylcholine. Implications of the coronary vascular endothelium as a mediator of the vasodilatory and dromotropic actions of adenosine. The functional role of intravascular coronary endothelial adenosine receptors. Dextran-linked insulin: a soluble high molecular weight derivative with biological activity in vivo and in vitro. Göttingen: Vandenhoek und Ruprecht 1829.Īrmstrong KJ., Noall MW., Stouffer JE. Lehrbuch der Phsiologie des Menschen und der Thiere (1 ed.). The present challenges to achieving more rationale therapeutic effects are to design agonists or antagonists that exclusively gain access to a target compartment and have high specificity for the receptor of the cells in that compartment.īerthold AA. The quest of this review is to play down this misconception by pointing out key overlooked findings of the vascular endothelial wall: 1) The selective endothelial barrier physically separates two same-hormone-containing compartments the endocrine and the interstitial autocrine hormone compartments, 2) the hormone concentrations values in these compartments are independent of each other, 3) in each compartment the hormone acts solely on the receptors of that particular compartment, 4) multiple intravascular endocrine hormones act solely on their corresponding luminal endothelial membrane receptor (LEMR), without directly acting on the parenchymal cells, 5) Agonist-activation of LEMR triggers the release of specific paracrine endothelial agents that in conjunction with autocrine interstitial hormone modulate parenchymal function(s) and perhaps the turnover of the interstitial autocrine hormone, 6) these hormone compartments, functionally interact via paracrine exchange signaling, and the integrated intercourse of all these events result in the final hormonal organ effect. This misconception leads to inadequate interpretations of data, wrong diagnosis and therapeutic expectations, erroneous hypotheses, and misleads further research work. Such a simplistic view persists despite new knowledge of an endothelial wall barrier and implications for every parenchymal cell in the body. The circulatory hormone reaches the target organ, physically unimpeded acts directly on the parenchymal cells. In 1849, the first list of endocrine hormones was discovered and proposed that the synthesizing gland delivers it to the circulation.
0 kommentar(er)
