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前列腺素合成的抑制:应激性高血压的一种可能机制。

Inhibition of prostaglandin synthesis: a possible mechanism for stress-induced hypertension.

作者信息

Melby C L

出版信息

Med Hypotheses. 1983 Apr;10(4):445-9. doi: 10.1016/0306-9877(83)90010-5.

Abstract

Essential hypertension, while considered to be idiopathic, may be due to a variety of physiologic and/or psychologic factors, including stress. A possible mechanism for stress-induced hypertension is the inhibition of prostaglandin (PG) synthesis by the release of corticoids in the stereotypical stress response. PGI2 and PGE2, acting as vasodilators are important antagonists to the pressor effects of norepinephrine. However, a decreased synthesis of these PGs due to higher cortisol levels associated with stress, would negate their vasodilatory action, thus favoring vasoconstriction due to vascular suprasensitivity to norepinephrine. PGF2 alpha, a vasoconstrictor thought to be synthesized in the brain in response to a stressor, may also play a key role in the pathogenesis of hypertension.

摘要

原发性高血压虽被认为是特发性的,但可能由多种生理和/或心理因素引起,包括压力。压力诱导高血压的一种可能机制是在典型的应激反应中,皮质激素释放抑制前列腺素(PG)合成。作为血管舒张剂的前列环素(PGI2)和前列腺素E2(PGE2)是去甲肾上腺素升压作用的重要拮抗剂。然而,由于与压力相关的皮质醇水平升高导致这些前列腺素合成减少,会抵消它们的血管舒张作用,从而因血管对去甲肾上腺素超敏而有利于血管收缩。前列腺素F2α(PGF2α)是一种被认为在大脑中因应激源而合成的血管收缩剂,也可能在高血压发病机制中起关键作用。

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