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Substance P contributes to rapidly adapting receptor responses to pulmonary venous congestion in rabbits.
Author(s) -
Bonham A C,
Kott K S,
Ravi K,
Kappagoda C T,
Joad J P
Publication year - 1996
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1996.sp021378
Subject(s) - left atrial pressure , medicine , anesthesia , blood pressure , cardiology
1. This study tested the hypothesis that substance P stimulates rapidly adapting receptors (RARs), contributes to the increase in RAR activity produced by mild pulmonary congestion, and evokes an augmented response from RARs when combined with near‐threshold levels of pulmonary congestion. 2. RAR activity, peak tracheal pressure, arterial blood pressure and left atrial pressure were measured in paralysed, anaesthetized and ventilated rabbits. Substance P was given i.v. in one‐half log incremental doses to a maximum of 3 micrograms kg‐1. Mild pulmonary congestion was produced by inflating a balloon in the left atrium to increase left atrial pressure by 5 mmHg. Near‐threshold levels of pulmonary congestion were produced by increasing left atrial pressure by 2 mmHg. 3. Substance P produced dose‐dependent increases in RAR activity. The highest dose given increased the activity from 1.3 +/‐ 0.5 to 11.0 +/‐ 3.1 impulses bin‐1. Increases in left atrial pressure of 5 mmHg increased RAR activity from 3.8 +/‐ 1.4 to 14.7 +/‐ 3.9 impulses bin‐1. Blockade of NK1 receptors with CP 96345 significantly attenuated RAR responses to substance P and to mild pulmonary congestion. 4. Doses of substance P, which alone had no effect, stimulated the RARs when delivered during near‐threshold levels of pulmonary congestion. 5. The findings suggest that substance P augments the stimulatory effect of mild pulmonary congestion on RAR activity, most probably by enhancing hydraulically induced microvascular leak.