Role of endothelial nitric oxide in pulmonary and systemic arteries during hypoxia

cIMP synthesized by sGC as a mediator of hypoxic contraction of coronary arteries

“…These results provide further support for a critical role of sGC in the hypoxia-induced further increases in tension. It should be noted that, although the hypoxic conditions in the present study were obtained with 95% N 2 -5% CO 2 , evidence suggests that endothelium-dependent and sGC-dependent augmentation of vasoconstriction occurs when arteries are exposed to hypoxia obtained with a gas mixture containing either 0%, 5%, or 10% O 2 (5,15,23,26). cGMP is considered the sole second messenger mediating the actions of sGC (11,12).…”

“…Previous work has shown that hypoxia causes endotheliumdependent augmentation of contractions of isolated coronary arteries that require endogenous NO, the primary activator of sGC (5,15,23,25). Such augmentation is inhibited by ODQ, which inhibits sGC via oxidation of the prosthetic heme group of sGC (10), but also by other inhibitors of the enzyme (5,15).…”

“…soluble guanylyl cyclase; inosine 3=,5=-cyclic monophosphate; hypoxic vasoconstriction; endothelium A PREVIOUS STUDY reported that acute hypoxia caused a rapid further increase in tension of contracted canine saphenous veins (31). Subsequent findings demonstrated that such a phenomenon, termed hypoxic augmentation of vasoconstriction (5, 15), occurs in a number of blood vessel types (5,7,8,15,21,23,25,26) contracted with norepinephrine (7, 8), phenylephrine (23), PGF 2␣ (15,25), and the TP receptor agonist U-46619 (21), indicating that it is not unique for a specific vasoconstrictor. It occurs in isolated coronary arteries with but not without endothelium (5,15,25,26).…”

Role of gap junctions in the contractile response to agonists in the mesenteric resistance artery of rats with acute hypoxia

“…Hypoxia vascular model. An acute hypoxia model of MRA segments in vitro was established according to previous studies (4,19,20). The rats were euthanized and the descending third-order branch of the MRA (~10 mg) was removed.…”

Activation of α1A‐adrenoceptors desensitizes the rat aorta response to phenylephrine through a neuronal NOS pathway, a mechanism lost with ageing

“…Endothelial NO exerts an opposing modulatory effect on the vasoconstriction induced by α 1 ‐adrenoceptor agonists, since removal of the endothelium or inhibition of NO synthesis increases the α 1 ‐adrenoceptor‐mediated vasoconstriction (Looft‐Wilson et al, ; Nuñez et al , ). NO also plays an important role in the decreased ability of a vessel to respond to subsequent stimulation by the same agonist, a process called ‘NO‐mediated desensitization’, which had been previously observed on activation of α 1 ‐ adrenoceptors (Hiremath et al , ; Kaneko and Sunano; ; Hu et al , ; Kamata and Makino, ; Gürdal et al , ).…”