Acute plasma volume reduction by atrial natriuretic peptide (ANP) may be mediated, at least in part, by increased exchange vessel water conductivity (Lp). The present study tests the hypothesis that physiological levels of ANP acutely and reversibly elevate single capillary Lp. Paired, in situ measurements of Lp were obtained using the modified Landis technique in individually perfused mesenteric capillaries of the frog, Rana pipiens. Control Lp measurements ranged from 0.1 to 40 x 10(-7) cm.s-1.cmH2O-1 (with a median value of 2.5 x 10(-7] in 81 microvessels perfused with frog Ringer solution containing dialyzed bovine serum albumin. Vessels were recannulated and perfused with one or more concentrations of human ANP (hANP) spanning the physiopathological range: 0.01, 0.1, 1, 10, and 100 nM. When possible, a final recannulation and Lp determination was performed in the absence of hANP. A median 2.2-fold rapid Lp increase was observed compared with control at each peptide concentration. Lp changes persisted for the duration of exposure to hANP, returning to control levels on withdrawal of the peptide. True and venular capillaries exhibited similar Lp responses: median 2.2- and 2.4-fold elevations, respectively. Sixty percent of true and venular capillaries exhibited twofold or greater hANP-induced increases in Lp, whereas only 25% of arteriolar capillaries exhibited such a response. Thus a differential sensitivity to the peptide exists across the exchange vessel network. The observations of this study demonstrate that physiological levels of ANP are capable of modulating exchange vessel Lp, one means by which the peptide may acutely alter plasma volume.(ABSTRACT TRUNCATED AT 250 WORDS)
Phosphorylation in situ of atrial natriuretic peptide prohormone at the cyclic AMP-dependent site.