Possible involvement of sodium pump in the relaxation of rat aorta induced by .ALPHA.-human atrial natriuretic polypeptide.

Sato, Koichi; Murakami, Kazuyasu; Nishimura, Kanami; Ito, Katsuaki; Kangawa, Kenji; Matsuo, Hisayuki

doi:10.2170/jjphysiol.38.187

Cited by 3 publications

(2 citation statements)

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“…Activation of the type A natriuretic peptide receptor (NPR-A) leads to an increase in intracellular cGMP [22] which in turn appears to reduce intracellular calcium by a number of mechanisms [23]. Alternatively, a direct effect on ion channels has been proposed for ANP [24] where either intracellular cation concentration changes may affect other voltage sensitive channels or prevent closure of the potassium channel directly.…”

Section: Discussionmentioning

confidence: 99%

Acute effects of ANP and BNP on hypoxic pulmonary vasoconstriction in humans.

Cargill

Lipworth

1995

Brit J Clinical Pharma

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1 Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) have pulmonary vasorelaxant activity with plasma concentrations being elevated in patients with hypoxaemic pulmonary hypertension. However, their effects on acute hypoxic pulmonary vasoconstriction (HPV), the initiating stimulus for pulmonary hypertension have not to date been investigated. We have therefore studied the effects of ANP and BNP on acute HPV in humans. 2 Eight healthy volunteers were studied on three separate occasions. After reaching a resting haemodynamic state (to), an infusion of either ANP (10 pmol kg-1 min-'), BNP (10 pmol kg-1 min-1) or placebo (5% dextrose) was commenced. This was given alone for 30 min (t30) before subjects were rendered hypoxaemic (SaO2 75-80%) for a further 30 min (t60), with the initial infusion continuing to t60. Pulsed-wave Doppler analysis of pulmonary artery flow was used to measure mean pulmonary arterial pressure (MPAP) and hence total pulmonary vascular resistance (PVR) was calculated. Keywords natriuretic peptides hypoxaemia pulmonary circulation Introduction remains unknown but the beneficial effects of lung blood flow redistribution are more clear. Vasoconstriction in The vasoconstriction of the mammalian pulmonary areas of alveolar hypoxia leads to diversion of blood vasculature in response to hypoxia has intrigued physiol-flow away from hypoxic regions hence improving overall ogists since the phenomenon was first described by Von ventilation/perfusion matching [2]. This response can, Euler & Liljestrand [ 1]. The exact mechanism under-however, be detrimental if hypoxia is chronic and affects lying acute hypoxic pulmonary vasoconstriction (HPV) the whole lung, as is seen in hypoxaemic chronic

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Section: Discussionmentioning

confidence: 99%

Acute effects of ANP and BNP on hypoxic pulmonary vasoconstriction in humans.

Cargill

Lipworth

1995

Brit J Clinical Pharma

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Section: Discussionmentioning

confidence: 99%

Acute Effects of Anp and Bnp on Hypoxic Pulmonary Vasoconstriction in Humans

Cargill

Lipworth

1995

Clinical Science

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1 Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) have pulmonary vasorelaxant activity with plasma concentrations being elevated in patients with hypoxaemic pulmonary hypertension. However, their effects on acute hypoxic pulmonary vasoconstriction (HPV), the initiating stimulus for pulmonary hypertension have not to date been investigated. We have therefore studied the effects of ANP and BNP on acute HPV in humans. 2 Eight healthy volunteers were studied on three separate occasions. After reaching a resting haemodynamic state (to), an infusion of either ANP (10 pmol kg-1 min-'), BNP (10 pmol kg-1 min-1) or placebo (5% dextrose) was commenced. This was given alone for 30 min (t30) before subjects were rendered hypoxaemic (SaO2 75-80%) for a further 30 min (t60), with the initial infusion continuing to t60. Pulsed-wave Doppler analysis of pulmonary artery flow was used to measure mean pulmonary arterial pressure (MPAP) and hence total pulmonary vascular resistance (PVR) was calculated. 3 MPAP and PVR both tended to decrease in response to ANP and BNP infusion, although compared with placebo, the difference at t30 was only statistically significant for PVR. Hypoxaemia increased MPAP and PVR, although values at t60 were significantly lower following both ANP and BNP compared with placebo. 4 In terms of the actual change in PVR (APVR) induced by hypoxaemia (from t30 to t60), BNP (146(16) dynscm-5), but not ANP (183(21) dynscm-5) significantly attenuated APVR compared with placebo (194(26) dyns s cm-'):mean difference BNP versus placebo 48 dyn s cm-5, 95% Cl 3-93. An identical pattern was observed for AMPAP where BNP (15.9(1.1) mmHg), but not ANP (18.0(1.2) mmHg) significantly attenuated AMPAP compared with placebo (19.0(1.7) mmHg): mean difference BNP versus placebo 3.1 mmHg, 95% Cl 0.7-5.5. 5 Thus, although both ANP and BNP exhibit pulmonary vasorelaxant activity, only BNP significantly attenuated the MPAP and PVR responses to acute hypoxaemia. This suggests that the natriuretic peptides may have a role in attenuating pulmonary hypertension secondary to hypoxaemia.

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EFFECTS OF ATRIAL NATRIURETIC FACTOR ON CYCLIC GMP CONTENT IN THE RAT AORTIC SMOOTH MUSCLE: STUDIES ON THE ROLE OF MEMBRANE Na⁺,K⁺‐ATPase

Hegde

Defeo

Jandhyala

1989

Clin Exp Pharma Physio

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1. These studies were conducted to determine whether preservation of the functional integrity of the membrane, Na+,K+-stimulated ATPase is essential for the atrial natriuretic factor (r-ANF-8-33) to enhance guanosine 3',5'-monophosphate (cGMP) content in the rat aortic smooth muscle. In freshly dissected rat aortic tissues, levels of cGMP were estimated using radioimmunoassay. 2. ANF (0.1 mumol/L in Krebs-Henseleit media) produced significant elevation in cGMP levels in the aortic smooth muscle when compared with that incubated in the control media, whereas suppression of Na+-pump with ouabain (1.0 mmol/L) and/or K+-free media did not produce any significant changes in the basal cGMP level; these two experimental manoeuvres did not prevent enhancement of cGMP by ANF. 3. Incubation of the tissues in the media containing ouabain plus vasoconstrictor concentrations of norepinephrine (0.3 mumol/L) also did not alter basal cGMP levels and did not prevent the ability of ANF to elevate cGMP. 4. These studies demonstrate that the antagonism by ouabain, of vasorelaxant effects of ANF (as reported in the literature) are not due to the prevention of the ability of ANF to enhance cGMP levels in the arterial smooth muscle. It is proposed that such an antagonism may be related to the actions of ouabain and ANF on diverse, and perhaps independent, mechanisms which affect Ca2+-fluxes across the cell membrane.

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Possible involvement of sodium pump in the relaxation of rat aorta induced by .ALPHA.-human atrial natriuretic polypeptide.

Cited by 3 publications

References 27 publications

Acute effects of ANP and BNP on hypoxic pulmonary vasoconstriction in humans.

Acute effects of ANP and BNP on hypoxic pulmonary vasoconstriction in humans.

Acute Effects of Anp and Bnp on Hypoxic Pulmonary Vasoconstriction in Humans

EFFECTS OF ATRIAL NATRIURETIC FACTOR ON CYCLIC GMP CONTENT IN THE RAT AORTIC SMOOTH MUSCLE: STUDIES ON THE ROLE OF MEMBRANE Na⁺,K⁺‐ATPase

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Possible involvement of sodium pump in the relaxation of rat aorta induced by .ALPHA.-human atrial natriuretic polypeptide.

Cited by 3 publications

References 27 publications

Acute effects of ANP and BNP on hypoxic pulmonary vasoconstriction in humans.

Acute effects of ANP and BNP on hypoxic pulmonary vasoconstriction in humans.

Acute Effects of Anp and Bnp on Hypoxic Pulmonary Vasoconstriction in Humans

EFFECTS OF ATRIAL NATRIURETIC FACTOR ON CYCLIC GMP CONTENT IN THE RAT AORTIC SMOOTH MUSCLE: STUDIES ON THE ROLE OF MEMBRANE Na+,K+‐ATPase

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EFFECTS OF ATRIAL NATRIURETIC FACTOR ON CYCLIC GMP CONTENT IN THE RAT AORTIC SMOOTH MUSCLE: STUDIES ON THE ROLE OF MEMBRANE Na⁺,K⁺‐ATPase