Article date: August 1981
By: BURTON M. ALTURA, NARESH CHAND in Volume 73, Issue 4, pages 819-827
The sensitivity and contractility of isolated canine intrapulmonary arteries and veins to a variety of primary prostaglandin compounds was studied.
Intrapulmonary arteries produced no measurable contractile responses to prostaglandin A1 (PGA,), PGA2, PGB1, PGD2, PGE,1, PGE2 or to PGFlα. However, high concentrations of both PGB2 (> 10−7 m) and PGF2α (> 10−6 m) elicited concentrated‐related, but weak, contractile responses, measuring only 5–25% of KCl‐induced maximum contractions.
Intrapulmonary arteries, partially contracted by 5‐hydroxytryptamine (5‐HT), exhibited concentration‐related relaxations in response to PGE,1 PGE2, PGA1, or PGA2 produced only weak superimposed contrtactions.
In contrast to intrapulmonary arteries, intrapulmonary veins contracted in a concentration‐related fashion to all prostaglandins tested, where the contractile sensitivity was (based on EC50 s and threshold concentrations): PGB2 > PGB1, > PGD2 > PGF2α > PGA2 »PGA1, > PGF1α > PGE2 > PGE1.
In terms of the ability to generate maximum contractile responses on intrapulmonary veins, the prostaglandins were also variable, with PGA2 and PGB2 being the most potent and PGD2 the least potent.
Intrapulmonary veins, partially contracted by 5‐HT, exhibited concentration‐related relaxations to PGE1 at low concentrations, followed by secondary contractile responses at higher concentrations.
Neither PGA1 nor PGA2 (3.4 × 10−8 to 3.4 × 10−5 m) inhibited or potentiated 5‐HT responses of intrapulmonary arteries.
These data suggest that there are species, regional and major qualitative and quantitative, differences in the responsiveness of intrapulmonary arteries and veins to prostaglandin.
The sensitivity and contractility of isolated canine intrapulmonary arteries and veins to a variety of primary prostaglandin compounds was studied.
Intrapulmonary arteries produced no measurable contractile responses to prostaglandin A1 (PGA,), PGA2, PGB1, PGD2, PGE,1, PGE2 or to PGFlα. However, high concentrations of both PGB2 (> 10−7 m) and PGF2α (> 10−6 m) elicited concentrated‐related, but weak, contractile responses, measuring only 5–25% of KCl‐induced maximum contractions.
Intrapulmonary arteries, partially contracted by 5‐hydroxytryptamine (5‐HT), exhibited concentration‐related relaxations in response to PGE,1 PGE2, PGA1, or PGA2 produced only weak superimposed contrtactions.
In contrast to intrapulmonary arteries, intrapulmonary veins contracted in a concentration‐related fashion to all prostaglandins tested, where the contractile sensitivity was (based on EC50 s and threshold concentrations): PGB2 > PGB1, > PGD2 > PGF2α > PGA2 »PGA1, > PGF1α > PGE2 > PGE1.
In terms of the ability to generate maximum contractile responses on intrapulmonary veins, the prostaglandins were also variable, with PGA2 and PGB2 being the most potent and PGD2 the least potent.
Intrapulmonary veins, partially contracted by 5‐HT, exhibited concentration‐related relaxations to PGE1 at low concentrations, followed by secondary contractile responses at higher concentrations.
Neither PGA1 nor PGA2 (3.4 × 10−8 to 3.4 × 10−5 m) inhibited or potentiated 5‐HT responses of intrapulmonary arteries.
These data suggest that there are species, regional and major qualitative and quantitative, differences in the responsiveness of intrapulmonary arteries and veins to prostaglandin.
DOI: 10.1111/j.1476-5381.1981.tb08734.x
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