English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

The endothelium-derived relaxing factor (EDRF), probably nitric oxide (NO) or a closely related compound (EDRF/NO), is a potent vasodilator that appears to regulate vascular tone in several vascular beds. I have investigated whether EDRF/NO is also involved in the regulation of the cerebral circulation--in particular, whether EDRF/NO participates in the increases in cerebral blood flow elicited by hypercapnia. Rats were anesthetized with halothane, 1-2% (vol/vol), paralyzed, and artificially ventilated. Arterial pressure was monitored and blood gases were controlled. Cerebral blood flow was continuously monitored through a cranial window over the sensory cortex by a laser-Doppler probe. The window was superfused with Ringer's solution (pH 7.3-7.4 at 37 degrees C). During superfusion with Ringer's solution, hypercapnia (PCO2 = 55.8 +/- 0.8 mmHg) increased cerebral blood flow by 121 +/- 6% (n = 27; P less than 0.001; analysis of variance). Topical superfusion with the NO synthase inhibitors N omega-nitro-L-arginine (1 mM) attenuated the cerebrovasodilation by 93 +/- 6% (n = 8). In contrast, the vasodilation elicited by topical papaverine (1 mM) was not affected by N omega-nitro-L-arginine (n = 10). Application of N omega-nitro-D-arginine (1 mM) did not affect the cerebrovasodilation elicited by hypercapnia (P greater than 0.05; n = 8). N omega-Methyl-L-arginine (1 mM) attenuated the cerebrovasodilation elicited by hypercapnia by 44 +/- 4% (n = 8; P less than 0.001), an effect completely reversed by coapplication of L-arginine (10 mM; P greater than 0.05; n = 13). These findings indicate that the powerful effects of CO2 on the cerebral circulation are mediated by arginine-derived EDRF/NO. EDRF/NO is an important molecular signal whose actions may also include the regulation cerebral circulation.

Does nitric oxide mediate the increases in cerebral blood flow elicited by hypercapnia?