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Humoral Control of the Circulation

Vasoconstrictor Agents
Ligand (hormone) Gprotein ReceptorPLC phospholipase C IP3--> release Ca++  Contraction
DAG PKCContraction
Hormone Receptos Uses Derived From
Endothelin 1 ETA- vasoconstriction When damage occurs to Big-endothelia 1
ET-1 ETB- vasodialation endothelium ETA receptor
Vasoconstriction Vascular endothelium
*Prevents Excessive
bleeding
Norepinephrin Alpha 1- constriction Sympathetic NS/ during Tyrosine (tyrosine
e/ Epinephrine Smooth muscle exercise  excited heart/ hydroxylase)Dopa
(α) Alpha 2 - inhibit NE contracts arterioles  Dopamine NE
release (auto receptor) (PNMT)
Eipinephrine
Beta 1- Increase HR/
Increase contraction/ Released by adrenal
increase conduction medulla (epinephrine)
velocity (heart/ Atria/
Ventricle/ AV Purkinje) NE produced in
NE/ Epi sympathetic nerve
Beta 2- relaxation (epi) terminals
Vascular smooth muscle
Coronary artery!

Angiotensin II AT1- vasoconstriction/ Hemorrhage renin release Angiotensinogen


angiogenisis  angiotensinogen cascade (renin) AngiotensinI
 Angio II works on AT1--> (ACE) 
AT2- Vasodialation/ constrict small arterioles, AngiotensinII (amino
vesel rerefaction blood flow severely peptidase)
depressed, works to increase AngiotensinIII
peripheral resistance;
increase arteriole pressure Made by Kidney
Increased BP

Vasopressin Hemorrhageantidiuretic Made in


hormone; Increase BP; Hypothalamus/
increase H2O absorption Excreted by posterior
from renal tubules back into pituitary gland
blood, control body fluid (neurohypophysis)
volume

O2 Constriction
Calcium Constriction
Vasodialator Agents
Ligand (hormone) Gprotein Receptor PLA2 phospholipase A2--> Arachodonic acid
1) COXProstanoids/PGE2/PGI2 Dialation
2) Epoxygenase EETs Vasodialation
Bradykinin *Relax vascular ACE (Angiotensin
smooth muscle via converting enzyme
release of NO Can stimulate
*Increase capillary Angiotensin II and
permeability inhibit Bradykinin
*Attract Leukocytes
*Kinins actions ACE blockers -
resemble those of reduce angiotension II
histamine and cause  reducing BP and
contraction of visceral increase levels of
smooth muscle (Effect Bradykinin
of Bronchi increase
cough) Blood/tissue fluids

Atrial Natriureic Peptides Naturesis (produce Cardiac atriocytes


Increase Na excretion ANP- circulating form
of Kidney); reduce BNP- human heart
Aldosterone sucretion; CNP- brain
vasodilatation

BNP used as marker


for heart failure, heart
failurestretch heart
 release BNP

Epinephrine β Beta 2- relaxation


Vascular smooth
muscle
Coronary artery!
Prostaglandins All tissues
Histamine Mast Cells
Serotonin Platelets, Nerve
terminal, Gut
Potassium K+ Small amounts Dilation
increase the rate of the
sodium potassium
pump/ net +1
extracellular to
hyperpolarize
dilation
CO2/ H+/ Lactic Acid Dilation

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