Vasodilator

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

A vasodilator is a drug or chemical that relaxes the smooth muscle in blood vessels, which causes them to dilate. Dilation of arterial blood vessels (mainly arterioles) lead to a decrease in blood pressure.

## Contents

* 1 Function
* 2 Examples and individual mechanisms
* 2.1 Endogenous
* 2.2 Exogenous vasodilators
* 3 Therapeutic uses
* 4 References

## Function

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Vasodilation directly affects the relationship between Mean Arterial Pressure and Cardiac Output and Total Peripheral Resistance (TPR). Mathematically, cardiac output is computed by multiplying the heart rate (in beats/minute) and the stroke volume (the volume of blood ejected during systole). TPR depends on several factors including the length of the vessel, the viscosity of blood (determined by hematocrit), and the diameter of the blood vessel. The latter is the most important variable in determining resistance. An increase in either of these physiological components (cardiac output or TPR) cause a rise in the mean arterial pressure. Vasodilators work to decrease TPR and blood pressure through relaxation of smooth muscle cells in the tunica media layer of large arteries and smaller arterioles.[1]

Vasodilation occurs in superficial blood vessels of warm-blooded animals when their ambient environment is hot; this process diverts the flow of heated blood to the skin of the animal, where heat can be more easily released into the atmosphere. The opposite physiological process is vasoconstriction. These processes are naturally modulated by local paracrine agents from endothelial cells (e.g bradykinin, adenosine), as well as an organism's Autonomic Nervous System and adrenal glands, both of which secrete catecholamines such as norepinephrine and epinephrine, respectively.

## Examples and individual mechanisms

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Vasodilation is a result of relaxation in smooth muscle surrounding the blood vessels. This relaxation, in turn, relies on removing the stimulus for contraction, which depends predominately on intracellular calcium ion concentrations and phosphorylation of myosin light chain (MLC). Thus, vasodilation mainly works by either by lowering intracellular calcium concentration or dephosphorylation of MLC. This includes stimulation of myosin light chain phosphatase and induction of calcium symporters and antiporters that pump calcium ions out of the intracellular compartment. This is accomplished through retuptake of ions into the sarcoplasmic reticulum via exchangers and expulsion across the plasma membrane. [2] The specific mechanisms to accomplish these effects varies from vasodilator to vasodilator.

These may be grouped as endogenous and exogenous vasodilators;

### Endogenous

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Vasodilators [3] | Receptor
(↑ = opens. ↓ = closes) [3] | Transduction
(↑ = increases. ↓ = decreases) [3]

|
|

EDHF | ?  | hyperpolarization \--> ↓VDCC \--> ↓intracellular Ca2+
depolarization | ↑Voltage-gated K+ channel
interstitial K+ | directly
nitric oxide | ↑NO receptor | ↑cGMP \--> ↑PKG activity -->

* phosphorylation of MLCK \--> ↓MLCK activity --> dephosphorylation of MLC
* ↑SERCA \--> ↓intracellular Ca2+

β2 adrenergic agonists | β-2 adrenergic receptor | ↑Gs activity --> ↑AC activity --> ↑cAMP \--> ↑PKA activity --> phosphorylation of MLCK \--> ↓MLCK activity --> dephosphorylation of MLC
histamine | Histamine H2 receptor
prostacyclin | prostacyclin receptor
Prostaglandin D2 | PGD2 receptor
Prostaglandin E2 | PGE2 receptor
VIP | VIP receptor | ↑Gs activity --> ↑AC activity --> ↑cAMP \--> ↑PKA activity -->

* phosphorylation of MLCK \--> ↓MLCK activity --> dephosphorylation of MLC
* open Ca2+-activated and voltage-gated K+channel s \--> hyperpolarization --> close VDCC \--> ↓intracellular Ca2+

(extracellular) adenosine | A1, A2a and A2b adenosine receptors | ↑ATP-sensitive K+ channel \--> hyperpolarization --> close VDCC \--> ↓intracellular Ca2+

* (extracellular) ATP
* (extracellular) ADP

| ↑P2Y receptor | activate Gq \--> ↑PLC activity --> ↑intracellular Ca2+ \--> ↑NOS activity --> ↑NO \--> (see nitric oxide)
L-Arginine | imidazoline and α-2 receptor? [4] | Gi \--> ↓cAMP \--> activation of Na+/K+-ATPase[5] \--> ↓intracellular Na2+ \--> ↑Na+/Ca2+ exchanger activity --> ↓intracellular Ca2+
Bradykinin | Bradykinin receptor
Niacin (nicotinic acid) |  |
Platelet activating factor (PAF) |  |
CO2 | \-  | ↓interstitial pH \--> ?[6]
(probably) interstitial lactic acid | \-
muscle work | - |

* ↑vasodilators:
* ↑ATP consumption --> ↑adenosine
* ↑glucose usage --> CO2
* ↑interstitial K+
* ↑(extracellular) ATP
* ↑(extracellular) ADP
* ↑interstitial K+

* ↓vasoconstrictors:
* ↑ATP consumption --> ↓ ATP (intracellular)
* ↓oxygen \--> ↓oxidative phosphorylation \--> ↓ ATP (intracellular)

|  |

### Exogenous vasodilators

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* Absence of high levels of environmental noise
* Absence of high levels of illumination
* Adenocard - Adenosine agonist, primarily used as an anti-arrhythmic.
* Alpha blockers (block the vasoconstricting effect of adrenaline).
* Amyl nitrite and other nitrites are often used recreationally as a vasodilator, causing lightheadedness and a euphoric feeling.
* Atrial natriuretic peptide (ANP) - a weak vasodilator.
* Ethanol
* Histamine-inducers
* Complement proteins C3a, C4a and C5a work by triggering histamine release from mast cells and basophil granulocytes.
* Nitric oxide inducers
* Glyceryl trinitrate (commonly known as Nitroglycerin)
* Isosorbide mononitrate & Isosorbide dinitrate
* Pentaerythritol Tetranitrate (PETN)
* Sodium nitroprusside
* PDE5 inhibitors: these agents indirectly increase the effects of nitric oxide
* Sildenafil (Viagra)
* Tadalafil
* Vardenafil
* Terbutaline
* Tetrahydrocannabinol (THC) - the major active chemical in marijuana. Its mild vasodilating effects redden the eyes of cannabis smokers.
* Theobromine.
* Papaverine an alkaloid found in the opium poppy papaver somniferum
* Conjugated estrogens

## Therapeutic uses

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Vasodilators are used to treat conditions such as hypertension, where the patient has an abnormally high blood pressure, as well as angina and congestive heart failure, where a maintaining a lower blood pressure reduces the patient's risk of developing other cardiac problems.[7] Flushing may be a physiological response to vasodilators.

## References

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1. ↑ CVPharmacology
2. ↑ American Physiological Society
3. ↑ 3.0 3.1 3.2 Unless else specified in box, then ref is: Walter F., PhD. Boron. Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. ISBN 1-4160-2328-3. Page 479
4. ↑ Receptor-mediated activation of nitric oxide synthesis by arginine in endothelial cells Mahesh S. Joshi*,{dagger}, T. Bruce Ferguson, Jr.*, Fruzsina K. Johnson{ddagger}, Robert A. Johnson{ddagger}, Sampath Parthasarathy§, and Jack R. Lancaster, Jr.
5. ↑ Regulation of Na+-K+-ATPase by cAMP-dependent protein kinase anchored on membrane via its anchoring protein Kinji Kurihara, Nobuo Nakanishi, and Takao Ueha. Departments of 1 Oral Physiology and 2 Biochemistry, School of Dentistry, Meikai University, Sakado, Saitama 350-0283, Japan
6. ↑ Modin A, Björne H, Herulf M, Alving K, Weitzberg E, Lundberg JO (2001). "Nitrite-derived nitric oxide: a possible mediator of 'acidic-metabolic' vasodilation". Acta Physiol. Scand. 171 (1): 9–16. PMID 11350258.CS1 maint: Multiple names: authors list (link)
7. ↑ CVPharmacology

Template:Major Drug Groups

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Vasodilators used in cardiac diseases (C01D)

Nitrates|

Glyceryl trinitrate • Isosorbide dinitrate • Isosorbide mononitrate • Molsidomine • Pentaerythritol tetranitrate

Quinolone vasodilators|

Flosequinan

Others|

Itramin tosilate • Prenylamine • Oxyfedrine • Benziodarone • Carbocromen • Hexobendine • Etafenone • Heptaminol • Imolamine • Dilazep • Trapidil • Molsidomine • Efloxate • Cinepazet • Cloridarol • Nicorandil • Linsidomine • Nesiritide • Gapicomine

Template:Peripheral vasodilators

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Physiology of the cardiovascular system

Heart|

| Cardiac output|

* Cardiac cycle
* Cardiac output
* Heart rate
* Stroke volume
* Stroke volume
* End-diastolic volume
* End-systolic volume
* Afterload
* Preload
* Frank–Starling law
* Cardiac function curve
* Venous return curve
* Wiggers diagram
* Pressure volume diagram

|

Ultrasound|

* Fractional shortening = (End-diastolic dimension
* End-systolic dimension) / End-diastolic dimension
* Aortic valve area calculation
* Ejection fraction
* Cardiac index

Heart rate|

* Cardiac pacemaker
* Chronotropic (Heart rate)
* Dromotropic (Conduction velocity)
* Inotropic (Contractility)
* Bathmotropic (Excitability)
* Lusitropic (Relaxation)

Conduction|

* Conduction system
* Cardiac electrophysiology
* Action potential
* cardiac
* atrial
* ventricular
* Effective refractory period
* Pacemaker potential
* Electrocardiography
* P wave
* PR interval
* QRS complex
* QT interval
* ST segment
* T wave
* U wave
* Hexaxial reference system

Chamber pressure|

* Central venous
* Right
* atrial
* ventricular
* pulmonary artery
* wedge
* Left
* atrial
* ventricular
* Aortic

Other|

* Ventricular remodeling

Vascular system/
Hemodynamics|

| Blood flow|

* Compliance
* Vascular resistance
* Pulse
* Perfusion

|

Blood pressure|

* Pulse pressure
* Systolic
* Diastolic
* Mean arterial pressure
* Jugular venous pressure
* Portal venous pressure

Regulation of BP|

* Baroreflex
* Kinin–kallikrein system
* Renin–angiotensin system
* Vasoconstrictors
* Vasodilators
* Autoregulation
* Myogenic mechanism
* Tubuloglomerular feedback
* Cerebral autoregulation
* Paraganglia
* Aortic body
* Carotid body
* Glomus cell

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