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Ex vivo platelet aggregation

depending upon the target cell, a chloride (outward movement), K+ (outward movement), or Na+ (outward movement) channel is opened. Thus, a wide variety of the pleiotropic biological effects of endothelins can be explained by these many signal transduction events. However, even though endothelins are highly potent vasoconstrictors, much additional detail is required to achieve an in-depth understanding of the contributions of these hormones to their minute-by-minute contribution to the regulation of blood pressure.

There are emerging reports of a separate sphere of actions of endothelins associated with the reproductive system. Plasma levels of ET-1 increase during pregnancy, and estradiol increases the ET receptor present in the endometrium. ET-1 is also present in ovarian follicular fluid. In addition, in the hypothalamus-hypophyseal system, ET is a local modulator of the secretion of gonadotropins, prolactin, growth hormone, and TSH. The basis for these diverse actions of ET is not yet known.

FIGURE 15-13 Paracrine and autocrine actions of endothelins in the vascular wall. ET, formed from big ET outside the endothelial cell, can act in an autocrine fashion by stimulating the production of endothelium-derived relaxing factors (EDRF) and PGI^ activating the angiotensin-converting enzyme (ACE), and promoting gene expression and mitogenesis (Mito). In a paracrine fashion, ET binds to the underlying vascular smooth muscle (VSM) cell, triggers vasoconstriction, and may facilitate mitogenesis. The release of prostacyclin (PGI2) and EDRF by ET from endothelial cells can mediate vasodilation. Facilitated production of angiotensin II (All), on the other hand, acts synergistically with ET. The biosynthesis of ET is inhibited by EDRF and by unknown factors (X) released from VSM cells. Proteolytic enzymes at or near the VSM cell surface can degrade ET-1, reducing its bioactivity. Continuous lines and arrows with plus (+) signs indicate facilitation; interrupted lines with minus (—) signs indicate inhibition. Modified from Rubanyi, G. M., and Parker-Botelho, L. H. (1991). Endothelins. FASEB J. 5, 2713-2720.

FIGURE 15-13 Paracrine and autocrine actions of endothelins in the vascular wall. ET, formed from big ET outside the endothelial cell, can act in an autocrine fashion by stimulating the production of endothelium-derived relaxing factors (EDRF) and PGI^ activating the angiotensin-converting enzyme (ACE), and promoting gene expression and mitogenesis (Mito). In a paracrine fashion, ET binds to the underlying vascular smooth muscle (VSM) cell, triggers vasoconstriction, and may facilitate mitogenesis. The release of prostacyclin (PGI2) and EDRF by ET from endothelial cells can mediate vasodilation. Facilitated production of angiotensin II (All), on the other hand, acts synergistically with ET. The biosynthesis of ET is inhibited by EDRF and by unknown factors (X) released from VSM cells. Proteolytic enzymes at or near the VSM cell surface can degrade ET-1, reducing its bioactivity. Continuous lines and arrows with plus (+) signs indicate facilitation; interrupted lines with minus (—) signs indicate inhibition. Modified from Rubanyi, G. M., and Parker-Botelho, L. H. (1991). Endothelins. FASEB J. 5, 2713-2720.

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Cure Tennis Elbow Without Surgery

Cure Tennis Elbow Without Surgery

Everything you wanted to know about. How To Cure Tennis Elbow. Are you an athlete who suffers from tennis elbow? Contrary to popular opinion, most people who suffer from tennis elbow do not even play tennis. They get this condition, which is a torn tendon in the elbow, from the strain of using the same motions with the arm, repeatedly. If you have tennis elbow, you understand how the pain can disrupt your day.

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