Intact nitric oxide production is obligatory for the sustained flow response during hypercapnic acidosis in guinea pig heart

Abstract

The delayed steady state hypercapnic flow response in guinea pig heart requires intact NO production. The absence of a persisting decrease in coronary resistance under CF perfusion points to an important role of shear stress dependent NO production.

Cardiovascular and cerebrovascular responses to acute hypoxia following exposure to intermittent hypoxia in healthy humans

“…While the precise mechanisms for hypercapnic vasodilatation are not fully understood, it appears to be mediated by reduced extracellular and/or intracellular pH and by the presence of nitric oxide and prostacyclin (Hsu et al 1993; Wang et al 2003; Heintz et al 2005). Since only the presence of nitric oxide and prostacyclin are required and their graded release does not appear to be necessary for the hypercapnic vasodilatory response, this may be one explanation for which the cerebral blood flow response to hypercapnia was unaffected by IH (Hsu et al 1993; Heintz et al 2005). In addition, a normal cerebral blood flow response to hypercapnia was recently reported in severe OSA patients without coexisting cardiovascular disease (Foster et al 2009).…”

Prenatal hypoxia induces increased cardiac contractility on a background of decreased capillary density

“…More detailed analysis revealed preserved eNOS mRNA in coronary vessels, but decreased eNOS mRNA and protein in cardiomyocytes [ 16 ]. This may highlight important species differences in regulation of coronary flow, namely the importance of NO in the preservation of flow for the guinea pig [ 17 - 19 ] compared with the relative insensitivity of rat coronary flow to NOS inhibition [ 20 , 21 ]. Before investigating the impact of CHU on eNOS in the rat we must detail potential changes to cardiac work and factors that may influence coronary flow, including capillary density.…”

α1‐Adrenergic responsiveness in human skeletal muscle feed arteries: the impact of reducing extracellular pH

“…The vasodilatory effects of acidosis have been well described in animals both in vitro (Kontos et al 1977; Ishizaka & Kuo, 1996; Peng et al 1998; Ishizaka et al 1999; Lindauer et al 2003; Heintz et al 2005, 2008; Celotto et al 2011) and in vivo (Deal & Green, 1954; Daugherty et al 1967 a , b ; Kontos et al 1971), but it is not yet known whether these results translate into humans. Early work in humans indicated that hypercapnia or the infusion of hypercapnic saline elicited a profound hyperaemia (Kontos et al 1967, 1968 a , b ).…”

“…noradrenaline or phenylephrine (PE)]. Additional studies have determined that the disparate effect of pH upon vasocontraction may depend upon species (Medgett et al 1987), rodent strain (Rohra et al 2003 b ), vascular location and calibre (Ishizaka et al 1999; Lindauer et al 2003; Hyvelin et al 2004; Heintz et al 2005) and experimental model (Rohra et al 2003 a , 2005; Celotto et al 2011).…”