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Vasoactive Peptides and NO

kinins peptide autacoids that act locally to cause pain, vasodilation, increased vascular permeability, and synthesis of prostaglandins.
initiates synthesis of kinins tissue damage, allergic reactions, acute and chronic infammation
3 kinds of kinins bradykinin, kallidin, methionysl-lysylbradykinin
serine protease required for kinin synthesis kallikrens (exist as proenzyme "prekallikrein" until activated
substrate for kallikrein kininogens (either heavy-molecular-weight or low-molecular-weight)
formed by plasma kallikrein cleaving HMW-kininogen formed by tissue kallikrein cleaving LMW-kininogen
enzymes that metabolize kinins kinase I and kinase II (Angiotenisn Converting Enzyme; dipeptidyl carboxypeptidase)
half-life of kinins less than 15 seconds
receptors for kinins B1 and B2
kinin receptor upregulated during inflammation and seems to be responsible for most of kinins inflammatory effects B1
kinin recetor with high affinity for bradykinin B2
kinin receptor coupled to a G-protein and activates phospholipase A2 and phospholipase C B2
effects of kinins on arterial vascular beds vasodilation
mechanism of kinin effects on arterial vascular beds 1. Direct 2. Indirect (mediated through EDRF and synthesis of PGE2 and PGI1)
effect of kinins of veins vasoconstriction, probably due to PGF2alpha production)
main effect of kinins on the cardiovascular system edema due to arteriole vasodilation, venous constriction, and contraction of epithelial cells
role of kinins in inflammation edema and bronchospasm in asthmatics
role of kinins in pain B2 receptors mediate acute pain while B1 recetors mediate chronic inflammation
effects of bradykinin on neonates dilation of fetal pulmonary artery, closure of the ductus arteriosis, and constricture of umbilical arteries
clinical uses of kinins no approved uses yet, but ACE inhibitors block kinase II, which causes kinin elevation and subsequent hypotensive action
potent vasoconstriction peptide angiotensis
first enzyme in the biosynthesis of angitoensin II renin
location of synthesis, storage, and release of renin juxtaglomerular cells of kidney
renin substrate angiotensiogen
site of angiotensiongen synthesis liver
converts angiotensin I to angiotensin II Angiotensin Converting Enzyme (ACE)
location of ACE luminal surface of vascular endothelial cells
synthesis pathway of Angiotensin II Angiotensinogen cleaved by renin->angiotensin I->converted to Angiotenisn II by ACE
rate-limiting factors for Angiotensin II production renin secretion and circulating angiotensin
comounds that increase concentrations of angiotensinogen corticosteroids, thryoid hormones, estrogen
provides negative feedback for the production of angiotensin vascular stretch receptors, sodium, alpha adrenergic tonus
postive feedback on angiotensin II production beta 1 adrenergic receptors
metabolism of angiotensin rapidly removed from blood
mechanism of angiotensin II action AT1 is a G-protein coupled receptor-->activate PLC-->IP3 and DAG-->smooth muscle contraction. Also increases NE release and decreases NE reuptake. Stimulates release of NE and E from adrenals
effect of angiotensin II on the cardiovascular system very potent vasoconstrictor (via smooth muscle contraction, and some CNS and ANS). Its effects on NE potentiate sympathetic transmission
effect of angiotensin II on the adrenal cortex, kidney, and CNS stimulates aldosterone and glucocorticoid biosynthesis, renal vasoconstriction, renal sodium reabsorption, stimulation of drinking response, vasopressin release (ADH),
clinical effect of renin inhibitors suppress angiotensin II production-->lower blood pressure in HTN patients
clinical effect of ACE inhibitors block conversion of Angiotensin I to Angiotensin II, as well as inhibiting metabolism of bradykinin. Overall effect is to maintain vasodilation and decrease blood pressure
ACE inhibiting drugs captopril (Capoten) and enalapril (Vasotec)
side-effect of ACE inhibitors cough due to build-up of kinins in lung and edema
conditions treated by ACE inhibitors hypertension and congestive heart failure
angiotensin II agonists that are orally active and have the useful effects of ACE inhibitors without the coughing and edema non-peptide Angiotensin II agonists (losartan, valsartan)
ubiquitous short-lived vasodilator NO (also known as Endothelium Derived Relaxing Factor)
3 enzymes that produce NO cNOS(nNOS), iNOS, eNOS
constitutive NO enzyme present in neurons and epithelial cells cNOS (nNOS)
inducible NO enzyme present in macrophages and smooth muscle cells iNOS
constitutive NO enzyme present in endothelial cells eNOS
all three NOS isoforms are flavoproteins (T/F) True
substrate for NOS 1-arginine
cofactors required for NOS isoforms NADPH, flavine adenine dinucleotide, tetrahydrobiopterin
products of NOS 1-citrulline and NO
NO donors that spontaneously release NO nitroprusside, nitroglycerin
inactivate NO heme and superoxide (free radical)
increase potency and duration of NO antioxidants
product of glutathione interaction with NO S-nitrosoglutathione (long-lived carrier of NO)
NO mechanism activates soluble guanylyl cyclase-->produce cGMP-->activate protein kinase G-->smooth muscle relaxation
effects of NO on cardiovascular system maintenance of normal vascular tone
effect of NO inhibitors on cardiovascular system increase vascular tone, increase arterial pressure, potentiate vasopressor drugs.
effects of diabetes, atherosclerosis, and cardiac ischemia on NO decreased NO (and increased free radicals)
NO effect on LDL acts as an antioxidant to block its deposition on arterial walls (one of first steps in atherosclerosis)
NO effect on platelets decrease aggregation-->decrease chance of thrombus formation
NO effects on CNS diffusible second messenger that can facilitate the release of NTs-->potentiate developmental, learning, and memory functions
effect of excessive NO toxic to retinal neurons
type of neurons innervating the GI tract Non-adrenergic non-cholinergic (NANC) neurons that release NO
cause of penile erection NO release from NANC neruons-->increase cGMP-->relax smooth muscle-->allow blood influx-->erection
drug that potentiates NO-induced cGMP by inhibiting the phosphodiesterase that normally breaks down cGMP sildenafil (Viagra)
effect of NOS inhibitors on actue inflammation reduce edema and vascular permeability
effect of NOS inhibitors on arthritis reduce NO-induced COX2 activity-->decreased release of inflammatory prostaglandins
captopril (Capoten) drug type ACE inhibitor
enalapril (Vasotec) drug type ACE inhibitor
losartan (Cozaar) drug type AT1 receptor agonist
valsartan (Diovan) drug type AT1 receptor agonist
Nitroprusside drug type NO donor
Nitroglycerin drug type NO donor
sildenafil (Viagra) drug type selective inhibitor of the PDE that breaks down NO-dependent cGMP
Created by: stuschroff