• Increased pressure due to more blood causes stretch of arteriolar wall and smooth muscle – the inherent property of smooth muscle causes it to contract when stretched, so the flow does not increase significantly


Blood vessels stay constricted unless in the presence of vasodilators. These are metabolites continuously produced by the endothelial cells lining the vessels, so:

  • If these cells metabolise more – they will produce more metabolites (CO2, H+, K+, NO) – and they will produce more vasodilatation

  • If there is less blood flow, then these produced metabolites (CO2, H+, K+, NO) will accumulate and keep the vessel dilated (the opposite is true, as more blood starts to flow with less resistance, these metabolites will start to wash away and then the vessels can constrict again to their resting tone)


  • Norepinephrine has a tonic influence (from sympathetic NS) on a receptors

  • In stress, sympathetic activation can evoke vasoconstriction, renal and splanchnic circulations

  • Epinephrine can cause vasodilation by binding to B2 receptors

  • Parasympathetic NS (with the exception of the penis) does not affect arteriolar tone

We need to understand that the vascular smooth muscle is always to some extent contracted: all vasodilatation is: simply reduction in tone!

How is this maintained?

  • In vessels with a high tone, each myocyte is tonically contracted, excessive ATP consumption is avoided by means of a ‘latch state’ (this means that the cross bridge does not quickly detach like in cardiac muscle, but remains attached, tense and flexed for a prolonged period)

  • In vessels with a low tone, individual myocytes show asynchronous, recurring contraction-relaxation cycles, associated with Ca2+ waves

#heart #ppp