Eta

Vasoconstriction

Vasodilation/vasoconstriction (ETB2)

cAMP inhibition; PLC/InsP3 calcium increase

Opioid

OP1 (delta), OP3 (mu)

Central cardiovascular regulation (OP1, 3); cardioprotection (OP1)

Gia1/3; Go

IK conductance activation; reduction in neuronal ICa; AC inhibition; PKC and KATP channel activation (cardioprotection)

AC, adenyl cyclase; ATI, AT2, angiotensin receptor 1, 2; ETA, endothelin A; ETB, endothelin B; Gi, inhibitory G protein; Gs, stimulatory G protein; Gq/11, Go, G15, other G proteins; ICa, voltage-dependent calcium channel (current); IK, voltage dependent potassium channel (current); InsP3, inositol triphosphate; KATP, potassium ATP channel; MAPK, MAP Kinase; OP1, delta-opioid receptor; OP3, mu-opioid receptor; PKC, protein kinase C; PLC, phospholipase C.

AC, adenyl cyclase; ATI, AT2, angiotensin receptor 1, 2; ETA, endothelin A; ETB, endothelin B; Gi, inhibitory G protein; Gs, stimulatory G protein; Gq/11, Go, G15, other G proteins; ICa, voltage-dependent calcium channel (current); IK, voltage dependent potassium channel (current); InsP3, inositol triphosphate; KATP, potassium ATP channel; MAPK, MAP Kinase; OP1, delta-opioid receptor; OP3, mu-opioid receptor; PKC, protein kinase C; PLC, phospholipase C.

ways characterize both p-AR (e.g., via Gs and AC) and ATI receptor signaling (e.g., via Gq/11 and PLC-p).

It was shown that selective blockade of p-AR inhibited angiotensin-induced contractility; selective blockade of ATI receptors reduced catecholamine-induced reduction in heart rate (30). These unusual transinhibitory effects were considered caused by underlying G protein-receptor uncoupling. Furthermore, direct interactions of these receptor systems were demonstrated in vivo, and it is speculated that such interactions may have a profound role in determining the ultimate responses to drugs designed to block a given receptor (e.g., pAR blockers, ATI receptor blockers). Cardiovascular receptor cross talk has been extensively reviewed by Dzimiri (31).

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