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I was reading few articles that mention stress induced cortisol may contribute to vasoconstriction and contractility as if they are different. I did some searches on vasoconstriction and contractility but I kept getting the somewhat similar explanations of narrowing blood vessels and hence raising blood pressure. Could someone help explain and differentiate the two?

  • Although this has fairly low level of prior research, I decided to answer it. – DoctorWhom Aug 23 '19 at 5:59
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Although the term "contractility" can refer to contraction of any muscle, including skeletal muscle (e.g. biceps) and smooth muscle (e.g. muscles in arterial walls), in medicine contractility usually refers to cardiac contractility, which in most fundamental terms is the force with which the heart muscle squeezes.

According to the textbook Regulation of Cardiac Contractility by Solaro:

Contractility describes the relative ability of the heart to eject a stroke volume (SV) at a given prevailing afterload (arterial pressure) and preload (end-diastolic volume; EDV).

Vasoconstriction is a specific term for the squeezing of smooth muscle within the walls of blood vessels (arteries, arteroiles, veins, venuoles, etc). Vasoconstriction of arteries increases arterial blood pressure and cardiac afterload. Vasoconstriction of veins increases venous return to the heart by reducing venous pooling, thus increasing preload. Of note, most often vasoconstriction is used to refer to arterial vasoconstriction. There is a lot of good information on the pharmacology of modulating blood pressure including vasopressors (norepinephrine, levophed) that vasoconstrict to raise blood pressure in septic or hemorrhagic shock, etc.

Cortisol both increases cardiac contractility as well as increases arterial vasoconstriction.

Both increasing cardiac contractility (increased force of squeezing blood out of the heart) as well as increasing arterial vasoconstriction (decreasing diameter of arteries) will raise blood pressure.

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