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Isolation of Intrapulmonary Artery and Smooth Muscle Cells to Investigate Vascular Responses

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Vasopressin-induced vasoconstriction: two concentration-dependent signaling pathways.

Kyle K Henderson¹, Kenneth L Byron

¹Department of Pharmacology and Experimental Therapeutics, Loyola University Chicago, Maywood, Illinois 60153, USA.

Journal of Applied Physiology (Bethesda, Md. : 1985)

|January 6, 2007

Summary

[Arg(8)]vasopressin (AVP) causes vasoconstriction through different calcium pathways. Low AVP concentrations activate protein kinase C (PKC) and L-type voltage-sensitive calcium channels (VSCC), unlike the phospholipase C pathway.

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Area of Science:

Physiology
Pharmacology
Cardiovascular Research

Background:

Current understanding links [Arg(8)]vasopressin (AVP) vasoconstriction to phospholipase C (PLC) activation.
This PLC pathway requires nanomolar AVP concentrations, which are higher than typical circulating levels.
Previous studies identified a novel, lower-concentration AVP pathway involving protein kinase C (PKC) and L-type voltage-sensitive calcium channels (VSCC) in smooth muscle cells.

Purpose of the Study:

To investigate the distinct calcium (Ca2+) signaling mechanisms underlying AVP-induced vasoconstriction in rat mesenteric arteries.
To determine the concentration-dependent roles of PLC, PKC, and VSCC in mediating AVP's vascular effects.

Main Methods:

Isolated, pressurized rat mesenteric arteries were used to measure vasoconstriction.
AVP concentration-response curves were generated (10^-14 to 10^-6 M).
The effects of VSCC blockade (verapamil) and PKC inhibition (calphostin-C, Ro-31-8220) on AVP-induced constriction were assessed at different AVP concentrations and time points.

Main Results:

AVP induced a concentration-dependent, V(1a) receptor-mediated constriction.
Half-maximal constriction (30 pM AVP) was blocked by VSCC and PKC inhibitors.
Acute maximal constriction (10 nM AVP) was initially insensitive to VSCC/PKC blockade but became dependent on both pathways with prolonged exposure.

Conclusions:

Different Ca2+ signaling pathways mediate AVP-induced vasoconstriction across varying AVP concentrations.
At physiologically relevant circulating concentrations, AVP's vasoconstrictor effects rely on a pathway involving PKC activation.
This low-concentration pathway is susceptible to inhibition by calcium channel blockers.