Page 10 - G43 ASSIGNMENT

Peripheral Vascular Resistance

Ezzaldin Aziz ID:1304

Introduction

Peripheral vascular resistance (systemic vascular resistance, SVR) is the resistance in the circulatory
system that is used to create blood pressure, the flow of blood and is also a component of cardiac
function. When blood vessels constrict (vasoconstriction) this leads to an increase in SVR. When blood
vessels dilate (vasodilation), this leads to a decrease in SVR. If referring to resistance within the
pulmonary vasculature, this is called pulmonary vascular resistance (PVR).

Issues of Concern

Vascular resistance is used to maintain organ perfusion. In certain disease states, such as congestive
heart failure, there is a hyper-adrenergic response, causing an increase in peripheral vascular resistance.
Prolonged increases in blood pressure affect several organs throughout the body. In conditions such as
shock, there is a decrease in vascular resistance thus causing decreased organ perfusion which leads to
organ malfunction.
Peripheral vascular resistance is mediated locally by metabolites, and over a distance on a neuro-
hormonal level, therefore, many different components may become altered leading to changes in
peripheral vascular resistance.
Cellular

The central dictation of peripheral vascular resistance occurs at the level of the arterioles. The arterioles
dilate and constrict in response to different neuronal and hormonal signals.

During an adrenergic response where norepinephrine gets released into the bloodstream, it binds to the
smooth muscle cells of the vasculature binding to an alpha-1 receptor (Gq protein); this causes an
increase in GTP in the cell, which activates phospholipase C, creating IP3. IP3 signals for release of the
intracellularly stored calcium as free calcium. This free calcium stimulates Calcium-dependent protein
kinases into activated protein kinases which leads to contraction of the smooth muscle.[1]

Other molecules that cause vasoconstriction on a cellular level include thromboxane, endothelin,
angiotensin II, vasopressin, dopamine, ATP.[1][2][3]

Epinephrine binds to vascular smooth muscles at the beta-2 receptor (Gs protein); this binding activity
increases adenylate cyclase activity, causing an increase in cAMP then increase in protein kinase A.
Protein kinase A phosphorylates myosin-light-chain kinase (MLCK), decreasing its activity, and thus
dephosphorylation of myosin light chain, and leading to vasodilation of the vasculature.[1][4]

Other molecules that cause vasodilation on a cellular level which include nitrous oxide, histamine,
prostacyclin, prostaglandin D2 and E2, adenosine, bradykinin, carbon dioxide, and vasoactive intestinal
peptide.[2][3][5]

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