Exploring the mechanism of endothelial involvement in acidosis-induced vasodilatation of aortic tissues from normal and diabetic rats

Arteriolar and capillary responses to CO2 and H+ in hamster skeletal muscle microvasculature: Implications for active hyperemia

“…As H + is a relatively impermeable ion, decreasing the pH of the interstitial space for short periods of time is assumed to have little affect on the intracellular compartment, therefore, signal transduction mechanisms for H + are assumed to be due to extracellular stimulation. The signal transduction pathway for H + ‐induced vasodilation has been investigated in large arteries and cerebral, mesenteric, coronary, and retinal arterioles and appear to share many common signaling elements including NO modulation, ATP‐dependent potassium channels, calcium‐activated potassium channels, and subsequent hyperpolarization . Hyperpolarization of the skeletal muscle arteriolar endothelial cells should induce a conducted response (for review see), but we did not observe conducted responses initiated by H + at the level of the arteriole or the capillary.…”

“…Further strengthening a potential role for CO 2 and H + in the matching of blood flow and metabolic demand is their vasodilatory ability. CO 2 and H + have been shown to cause vasodilation independently or in combination in a variety of vascular beds and vascular models including large arteries (for example) and arterioles in the mesentery, heart, and the brain (for example). Despite the extensive literature supporting the vasodilatory role for CO 2 and H + in multiple tissues, there is little evidence to indicate whether the skeletal muscle microvasculature can be stimulated by these two metabolic by‐products.…”

Protective Role of Acidic pH-Activated Chloride Channel in Severe Acidosis-Induced Contraction from the Aorta of Spontaneously Hypertensive Rats

“…Because I Cl,acid is activated by very acidic extracellular pH (pH <5.5) [6]–[9], I Cl,acid may protect the normal artery against excess vasoconstriction under extremely acidic conditions. This mechanism is important for maintaining normal vascular function under some pathological conditions such as ischemia [19], hypoxia [20], and metabolic disorders [21] causing local or systemic extracellular acidification.…”