Table 1.

Direct and indirect effects of endogenous Dynorphins on the cardiovascular system.

Dynorphin Fragment	Tissue	Effect	IC₅₀/ EC₅₀	Implication	Ref.

Big Dyn	Hela cells	Ability to cross plasma membrane	1 μM	Dyn molecules affect intracellular processes in absence of KOP	[140]
Dyn B 1–13	Rat cardiac sarcolemma membrane	Inhibit oubain binding site on Na⁺-K⁺ TPase	16.0 μM	Putative Mechanism for Na+-K+ ATPase inhibition	[39]
	Embryonic stem cells	Bind to KOP receptors on nuclei and upregulate GATA-4, Nkx-2.5 transcription		Intracellular actions of Dynorphins and involvement in cardiac differentiation	[53]
	Rat fetal Brain aggregates	Inhibited DNA synthesis 7 day old fetal brain aggregates, but stimulated DNA synthesis in 21 day old fetal brain aggregates	nM^*, 1 μM	Potential to modulate fetal glial cell proliferation in time-dependent manner	[54]
Dyn A 1–13	Hela cells	Ability to cross plasma membrane	10 μM	Demonstrates ability of Dyn molecules to affect intracellular processes in absence of KOP	[140]
	Cardiac	Inhibit Na⁺-K⁺ ATPase	30 μM	Increase intracellular [Na+]	[141]
	Cardiac	Indirect inhibitory effect on cardiac Dopamine Receptor 2-induced NE release	10 μM	Demonstrates direct, inhibitory role of sympathetic nervous system by dynorphins on cardiovascular tissue	[30]
	Rat cardiac sarcolemma membrane	Inhibit Oubain binding site on Na+-K+ ATPase	2.9 μM	Putative Mechanism for Na+-K+ ATPase inhibition	[39]

represents the IC₅₀ value for 7 day old fetal brain aggregates.