title: Influence of dopamine receptor and adrenoceptor blockade on the hemoconcentrating and hypotensive actions of atrial natriuretic peptide.
abstract: Atrial natriuretic peptide (ANP) lowers mean arterial pressure (MAP) and increases hematocrit through reduction in plasma volume caused by a transcapillary shift of plasma fluid and protein toward the interstitium. We examined the consequences of blockade of the dopaminergic and adrenergic systems on the hypotensive and hemoconcentrating responses to ANP. Changes in MAP, hematocrit, and plasma protein concentration (PPC) were measured in anesthetized acutely binephrectomized rats, during infusion of ANP alone (1 microgram.kg-1.min-1 for 45 min) or in the presence of haloperidol (20 micrograms.kg-1.min-1), phentolamine (15 micrograms.kg-1.min-1), or propranolol (10 micrograms.kg-1.min-1). Infusion of ANP reduced MAP by 8.6 +/- 1.3% and increased hematocrit by 9.0 +/- 0.6% (both p < 0.005 vs. vehicle). PPC increased (4.4 +/- 0.6%; p < 0.005 vs. vehicle) significantly less than hematocrit, indicating extravasation of proteins. The ANP-evoked reduction in MAP was not affected in haloperidol- or phentolamine-treated rats (-8.8 +/- 2.3 and -10.5 +/- 2.4%, respectively; both p < 0.005 vs. vehicle) but was abolished in propranolol-treated rats (+3.2 +/- 1.3%; p = ns vs. vehicle). The ANP-induced increase in hematocrit was slightly attenuated in haloperidol-, phentolamine-, and propranolol-treated rats (7.5 +/- 0.7, 7.3 +/- 0.8, and 6.0 +/- 1%, respectively). In addition, the coefficient of reflection, an index of the permeability to proteins, was higher in these three groups (0.41 +/- 0.06, 0.49 +/- 0.08, and 0.57 +/- 0.14, respectively) than in control rats infused with ANP (0.27 +/- 0.03), indicating an attenuation of the ANP-induced extravasation of proteins. Thus, in binephrectomized rats, the hypotensive activity of ANP requires a beta-adrenergic component, whereas its hemoconcentrating action is, at least in part, dependent upon dopaminergic and adrenergic activation.
authors.affiliation: Groupe rein et hypertension, Hôpital Saint-Charles, Montpellier, France.
authors.forename: J P
authors.initials: JP
authors.lastname: Valentin
authors.forename: J
authors.initials: J
authors.lastname: Ribstein
authors.forename: N
authors.initials: N
authors.lastname: Nafrialdi
authors.forename: A
authors.initials: A
authors.lastname: Mimran
mesh_terms: D018674:Adrenergic Antagonists / Q000494:pharmacology*; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000494:pharmacology / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects* / Q000502:physiology; D001798:Blood Proteins / Q000032:analysis; D018492:Dopamine Antagonists / Q000494:pharmacology*; D006339:Heart Rate / Q000187:drug effects; D006400:Hematocrit; D008297:Male; D009392:Nephrectomy; D009599:Nitroprusside / Q000494:pharmacology; D010953:Plasma Volume / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D018674:Adrenergic Antagonists; D001798:Blood Proteins; D018492:Dopamine Antagonists; D014665:Vasodilator Agents; D009599:Nitroprusside; D009320:Atrial Natriuretic Factor