Physiology, Peripheral Vascular Resistance

Article Author:
Claire Delong

Article Editor:
Sandeep Sharma

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Jeanie Skibiski
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Phillip Hynes

2/7/2019 11:30:08 PM


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.


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]

Organ Systems Involved

All organs systems in the body are affected by peripheral vascular resistance. The resistance of the blood vessels is a significant component of what dictates blood pressure and perfusion of the tissues.


In the human body there is very little change in blood pressure as it travels in the aorta and large arteries, but when the flow reaches the arterioles, there is a large drop in pressure, and the arterioles are the main regulators of SVR. 

The basis for the mechanism of peripheral vascular resistance is expressed by the Hagen-Poiseuille equation:

R = 8Ln/(pi*r^4) 

  • R is the resistance of blood flow [change in pressure between the starting point and end point]
  • L is the length of the vessel
  • n is the viscosity of blood
  • r is the radius of the blood vessel

This equation shows that modifying the radius of the vessel has drastic effects on the resistance to blood flow. As the vessel dilates (radius increases), the resistance is divided by the change to the fourth power; this goes for a decrease in radius as well, such as during an adrenergic state (e.g., exercise) when blood pressure must increase.

Related Testing

The calculation used to determine resistance in blood vessels (and all other liquid flow) is R = (change in pressure across the circulatory loop) / flow.

Concerning systemic vascular resistance, this would be: (pressure immediately leaving the left ventricle – pressure immediately upon entering the right atrium)/cardiac output. 

Blood pressure is calculated by multiplying the cardiac output by the systemic vascular resistance.

The mean arterial pressure (MAP) can be calculated by the following:

[(2/3) x (diastolic blood pressure)] + [(1/3) x (systolic blood pressure)]

Mean arterial pressure is normally between 65 and 110 mmHg, with a MAP of over 70mmHg needed for basic organ function.[6]

In septic shock, a MAP of 65 mmHg is considered sufficient for end-organ perfusion.[7]


Blood pressure mediation is by a balance of the cardiac output and the peripheral vascular resistance. In idiopathic hypertension, most patients will have a near normal cardiac output, but their peripheral resistance is elevated. As mentioned earlier, mediation of this resistance is at the level of the arteriole. As with other tissues in the body, if there is prolonged constriction of the smooth muscle within the arterioles, this will lead to hypertrophy and thickening of the vessel. There are several mechanisms by which the systemic vascular resistance may be altered.[2][3] 

The renin-angiotensin system is mediated by the renal system. Renin is a molecule released from the juxtaglomerular apparatus in response to under perfusion; renin may also be released via activation of the sympathetic nervous system. Renin converts angiotensinogen into angiotensin I, which subsequently converts into angiotensin II which acts as a vasoconstrictor on blood vessels, thus causing a rise in blood pressure.[2][3][8]

The autonomic nervous system causes both vasoconstriction and vasodilation. Alpha-1 receptor activation causes vasoconstriction, and beta-2 receptor activation causes vasodilation.[2][3] 

The endothelium, itself, can modulate blood pressure. The endothelium may release nitrous oxide (vasodilation) or endothelin (vasoconstrictor).[2][3] 

Several molecules have been found to place a role in blood pressure but have an unclear significance on the control of hypertension. Examples of these molecules are bradykinin, thromboxane, and atrial natriuretic peptide (ANP).[2][3]

Clinical Significance

The main concerns of peripheral vascular resistance are when it is at its extremes, called hypertension (too high) and hypotension (too low).

Hypertension (elevated peripheral vascular resistance) can be diagnosed when blood pressure measurements are greater than 140/90 on two separate clinical encounters. The majority of patients with hypertension are said to have essential hypertension, meaning there is no 'underlying' cause for the condition, and it is idiopathic. A minority of patients will have secondary hypertension, which is attributable to the underlying pathology. Examples of etiologies of secondary hypertension are renal disease (e.g., renal artery stenosis), endocrine conditions (e.g., Cushing’s disease), and drug-induced (e.g., oral contraceptives). Untreated hypertension can lead to chronic medical conditions consisting of coronary artery disease, renal disease, stroke, aneurysms, aortic dissection, congestive heart failure, peripheral vascular disease, and visual changes (e.g., retinal hemorrhages).[8][3]

Medications to lower peripheral vascular resistance include beta-blockers, diuretics, ACE-inhibitors, calcium-channel blockers, and alpha-blockers.

Hypotension is commonly associated with shock to which there are four main types. Hypovolemic shock is due to an excessive loss of blood resulting in a decreased cardiac output and increased SVR, as the body tries to maintain blood pressure. Cardiogenic shock is from a malfunction of the heart which results in decreased cardiac output and increased SVR. Neurogenic shock is from alterations in the autonomic nervous system that also results in decreased cardiac output and a decrease in SVR from a loss of the sympathetic innervation. Distributive shock reduces systemic vascular resistance from anaphylaxis or septic mediators, with an increase in cardiac output.[3][2]

Hypertensive urgency is a condition in which there is significantly elevated blood pressure (SBP greater than 180mmHg or DBP greater than 120mmHg) without evidence of any end-organ damage. A hypertensive emergency may correlate with end-organ damage (e.g., a headache, chest pain, focal neurologic deficits, altered mental status, SOB, pulmonary edema, renal failure, etc.).[9][10]

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Physiology, Peripheral Vascular Resistance - References


Webb RC, Smooth muscle contraction and relaxation. Advances in physiology education. 2003 Dec;     [PubMed]
Beevers G,Lip GY,O'Brien E, ABC of hypertension: The pathophysiology of hypertension. BMJ (Clinical research ed.). 2001 Apr 14;     [PubMed]
Bolívar JJ, Essential hypertension: an approach to its etiology and neurogenic pathophysiology. International journal of hypertension. 2013;     [PubMed]
Schindler C,Dobrev D,Grossmann M,Francke K,Pittrow D,Kirch W, Mechanisms of beta-adrenergic receptor-mediated venodilation in humans. Clinical pharmacology and therapeutics. 2004 Jan;     [PubMed]
Costa F,Biaggioni I, Role of nitric oxide in adenosine-induced vasodilation in humans. Hypertension (Dallas, Tex. : 1979). 1998 May;     [PubMed]
Moran D,Epstein Y,Keren G,Laor A,Sherez J,Shapiro Y, Calculation of mean arterial pressure during exercise as a function of heart rate. Applied human science : journal of physiological anthropology. 1995 Nov;     [PubMed]
Gargiulo R,Suhail F,Lerma EV, Hypertension and chronic kidney disease. Disease-a-month : DM. 2015 Sep;     [PubMed]
Rodriguez MA,Kumar SK,De Caro M, Hypertensive crisis. Cardiology in review. 2010 Mar-Apr;     [PubMed]
Henny-Fullin K,Buess D,Handschin A,Leuppi J,Dieterle T, [Hypertensive urgency and emergency]. Therapeutische Umschau. Revue therapeutique. 2015 Jun;     [PubMed]
Rodriguez R,Cucci M,Kane S,Fernandez E,Benken S, Novel Vasopressors in the Treatment of Vasodilatory Shock: A Systematic Review of Angiotensin II, Selepressin, and Terlipressin. Journal of intensive care medicine. 2018 Dec 18     [PubMed]


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