title: Atrial natriuretic factor increases splenic microvascular pressure and fluid extravasation in the rat.
abstract: The spleen is an important site of atrial natriuretic factor (ANF)-induced fluid extravasation into the systemic lymphatic system. The mechanism underlying this process was studied in a blood-perfused (1 ml min(-1)) rat spleen using the double occlusion technique. To ensure that our observations were spleen specific, a similar protocol was repeated in the hindquarters. Rat ANF(1-28), infused into the splenic artery of anaesthetized male rats, caused a dose-dependent (0.3-59 pmol min(-1)) increase in microvascular pressure from 11.3 +/- 0.7 to 14.9 +/- 0.5 mmHg and in post-capillary resistance from 7.2 +/- 0.6 to 10.1 +/- 1.1 mmHg ml(-1). ANF elicited no change in splenic pre-capillary resistance or in hindquarter haemodynamics. Intrasplenic ANF (6.5 pmol min(-1)) caused a sustained increase in intrasplenic fluid efflux from 0.1 +/- 0.1 to 0.3 +/- 0.1 ml min(-1), and in capillary filtration coefficient (Kf) from 1.2 +/- 0.5 to 2.4 +/- 0.6 ml mmHg-1 min-1 (100 g tissue)-1. Mechanical elevation of splenic intravascular pressure (from 11.3 +/- 0.7 to 22.4 +/- 0.2 mmHg) significantly increased intrasplenic fluid extravasation (from 0.4 +/- 0.3 to 1.4 +/- 0.3 ml min(-1)). The natriuretic peptide receptor-C (NPRC)-specific agonist C-ANF(4-23) (12.5 and 125 pmol min(-1)) did not alter splenic intravascular pressure or pre-/post-capillary resistance. The ANF antagonist A71915 (8.3 and 83 pmol min-1), which blocks ANF-stimulated cGMP production via natriuretic peptide receptor-A (NPRA), inhibited the ANF-induced changes in splenic microvascular pressure and post-capillary resistance. It is concluded that ANF enhances the extravasation of isoncotic fluid from the splenic vasculature both by raising intrasplenic microvascular pressure (increased post-capillary resistance) and by increasing filtration area. The constrictive activity of ANF on the splenic vasculature is mediated through NPRA.
authors.affiliation: Department of Physiology, University of Alberta, Edmonton, Alberta, Canada T6G 2S2.
authors.forename: R
authors.initials: R
authors.lastname: Sultanian
authors.forename: Y
authors.initials: Y
authors.lastname: Deng
authors.forename: S
authors.initials: S
authors.lastname: Kaufman
mesh_terms: D000818:Animals; D009320:Atrial Natriuretic Factor / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001826:Body Fluids / Q000502:physiology*; D004305:Dose-Response Relationship, Drug; D006614:Hindlimb / Q000098:blood supply; D006975:Hypertension, Portal / Q000503:physiopathology; D008297:Male; D008833:Microcirculation / Q000187:drug effects; D011169:Portal Vein / Q000502:physiology; D051381:Rats; D020318:Rats, Long-Evans; D013154:Spleen / Q000098:blood supply*; D013157:Splenic Artery / Q000502:physiology; D014655:Vascular Resistance / Q000187:drug effects; D014882:Water-Electrolyte Balance / Q000187:drug effects* / Q000502:physiology
chemical_list: C472610:atrial natriuretic peptide, rat; D009320:Atrial Natriuretic Factor