Atrial natriuretic peptide concentrations in hypoxic secondary pulmonary hypertension: relation to haemodynamic and blood gas variables and response to supplemental oxygen.

Abstract

Plasma atrial natriuretic peptide concentrations, measured in samples drawn from the pulmonary artery, were raised in nine of 17 patients with hypoxic pulmonary hypertension but normal right atrial pressures at rest. No relationship was seen between atrial natriuretic peptide concentrations and mean pulmonary artery or right atrial pressure, or calculated pulmonary or systemic vascular resistance. Patients with the most severe hypoxaemia tended to have higher plasma atrial natriuretic peptide concentrations; three patients with no past history of oedema had concentrations more than twice the upper limit of normal. Treatment with supplementary oxygen for 30 minutes reduced pulmonary vascular resistance in all patients but had no significant effect on plasma atrial natriuretic peptide concentration. These findings suggest that atrial natriuretic peptide may be a factor in the control of sodium and water balance in hypoxic cor pulmonale, where the determinants of individual susceptibility to peripheral oedema are not well understood.

Fluid homeostasis in chronic obstructive lung disease

“…ANP also varies inversely with oxygen tension and seems to increase progressively with the severity of COPD [27,40,46]. The highest values are found in oedematous patients.…”

A Comparison of Pathophysiological Changes during Hypobaric and Normobaric Hypoxia in Rats

“…These changes are associ ated with the development of pulmonary hypertension [5], A depressed weight gain is also seen in rats kept at low oxygen concentrations [7], Hypoxic exposure is also associated with several bio chemical and humoral changes such as elevated plasma atrial natriuretic peptide (ANP) levels [13]. Increased lev els of ANP are also seen in human disease, such levels are thought to reflect the degree of pulmonary hypertension [14][15][16].…”

Neutral endopeptidase (NEP) inhibition in rats with established pulmonary hypertension secondary to chronic hypoxia

“…In support of this, plasma levels of ANP have been shown to be elevated in response to increased pulmonary artery pressure both in animal models (McKenzie et al, 1986;Jin et al, 1990) and in man (Winter et al, 1989;Morice et al, 1990). The vasodilatation caused by ANP is particularly potent in the pulmonary circulation (Jansen et al, 1987) with hypoxic vasoconstriction being preferentially inhibited (Rogers et al, 1992).…”

“…ANP is released in response to an increase in pulmonary artery pressure because of right atrial and ventricular distension. In disease states characterized by an increased pulmonary artery pressure, such as primary pulmonary hypertension (Morice et al, 1990), chronic obstructive airways disease (COAD) (Winter et al, 1989), acute respiratory distress syndrome (Eison et al, 1988), and chronic thromboembolism (Noll et al, 1990), ANP synthesis and secretion is increased and plasma levels are elevated.…”