Key Points
- To compare the pharmacological characteristics of pre- and postjunctional receptors mediating responses to angiotensin II in canine mesenteric and pulmonary arteries.
- Measured electrical stimulation-evoked tritium overflow (prejunctional neurotransmitter release) and smooth muscle contractile force (postjunctional response) in isolated canine mesenteric and pulmonary arteries.
- Tested selective and nonselective receptor antagonists, including saralasin (nonselective peptide antagonist), losartan (AT1-selective antagonist), and PD123319 (AT2-selective antagonist).
- Angiotensin II enhanced stimulation-evoked tritium overflow in mesenteric (EC30% = 5 nM, maximal increase ~45%) and pulmonary arteries (EC30% = 1.54 nM, maximal increase ~80%), while inducing concentration-dependent postjunctional contractions in both tissues (pD2 = 8.57 and 8.52, respectively).
- Saralasin antagonized responses both prejunctionally (pA2 = 8.15 mesenteric, 8.10 pulmonary) and postjunctionally (pA2 = 9.51 mesenteric, 9.58 pulmonary), showing higher postjunctional potency.
- Losartan blocked only postjunctional contractile responses (pA2 = 8.15 mesenteric, 7.96 pulmonary) without affecting prejunctional tritium overflow, while the AT2 antagonist PD123319 was inactive at both sites.
Structured PICO
PPopulationCanine mesenteric and pulmonary arteries
IInterventionAngiotensin II with antagonists saralasin, losartan, and PD123319
OOutcomePrejunctional tritium overflow evoked by electrical stimulation and postjunctional contractile responsessurrogate
Pre- and postjunctional angiotensin II receptors in canine mesenteric and pulmonary arteries belong to different subtypes, with postjunctional being AT1 and prejunctional being a distinct, non-AT1/AT2 subtype.