Abstract
Acid-base homeostasis maintains systemic arterial pH within a narrow range. Whereas the normal range of pH for clinical laboratories is 7.35-7.45, in vivo pH is maintained within a much narrower range. In clinical and experimental settings, blood pH can vary in response to respiratory or renal impairment. This altered pH promotes changes in vascular smooth muscle tone with impact on circulation and blood pressure control. Changes in pH can be divided into those occurring in the extracellular space (pHo) and those occurring within the intracellular space (pHi), although, extracellular and intracellular compartments influence each other. Consistent with the multiple events involved in the changes in tone produced by altered pHo, including type of vascular bed, several factors and mechanisms, in addition to hydrogen ion concentration, have been suggested to be involved. The scientific literature has many reports concerning acid-base balance and endothelium function, but these concepts are not clear about acid-base disorders and their relations with the three known mechanisms of endothelium-dependent vascular reactivity: nitric oxide (NO/cGMP-dependent), prostacyclin (PGI2/cAMP-dependent) and hyperpolarization. During the last decades, many studies have been published and have given rise to confronting data on acid-base disorder and endothelial function. Therefore, the main proposal of this review is to provide a critical analysis of the state of art and incentivate researchers to develop more studies about these issues.
Highlights
Acid-base homeostasis maintains systemic arterial pH within a narrow range
In rat mesenteric resistance vessels the situation is different; changes in pHo cause large (70% pHo changes) and rapid (
The NO synthase (NOS) inhibitor, L-NAME (100 μM), failed to attenuate the increases in coronary flow during hypercapnia or metabolic acidosis, even though it significantly reduced basal flow. These results suggest that, nitric oxide (NO) contributes to the regulation of basal coronary vascular tone, it is not a mediator of the vasodilatory effects of hypercapnia and acidosis in this type of preparation [24]
Summary
Whereas the normal range of pH for clinical laboratories is 7.35-7.45, in vivo pH is maintained within a much narrower range This degree of tight regulation is accomplished by chemical buffering in extracellular and intracellular fluids and regulatory responses that are controlled by the respiratory and renal systems. In rat mesenteric resistance vessels the situation is different; changes in pHo cause large (70% pHo changes) and rapid (
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